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From: TSS (216-119-143-50.ipset23.wt.net)
Subject: Docket No. 2004N-0081 and or RIN number RIN-0910-AF47 Use of Materials Derived From Cattle in Human Food and Cosmetics [TSS SUBMISSION]
Date: July 13, 2004 at 2:54 pm PST
-------- Original Message --------
Subject: Docket No. 2004N-0081 and or RIN number RIN-0910-AF47 Use of Materials Derived From Cattle in Human Food and Cosmetics [comment submission]
Date: Tue, 13 Jul 2004 16:08:38 -0500
From: "Terry S. Singeltary Sr."
To: fdadockets@oc.fda.gov
CC: burt.pritchett@fda.gov, Agriculture@mail.house.govCOMMENT SUBMISSION
[Docket No. 2004N-O081]
RIN-0910--AF47
Use of Materials Derived From Cattle in Human Food and Cosmetics
http://www.fda.gov/OHRMS/DOCKETS/98fr/04n-0081-nir0001.pdf Greetings FDA, I would kindly like to comment on the potential for TSE transmission from
cosmetics to humans and why I think that ALL animal by-products should be
excluded from cosmetics. IF we look at the TSE 'KURU'. Kuru is a
transmissible spongiform encephalopathy that was identified in Papua New
Guinea in the late 1950s. Several thousand cases of the disease occurred
during a period of several decades. Epidemiologic investigations
implicated ritual endocannibalistic funeral feasts as the likely route
through which the infectious agent was spread. The incubation period in
females was estimated to be shorter than that in males. The shortest
incubation periods were estimated in adult women, who may have been
exposed to the largest doses of infectious material.
MY question is, was the woman exposed to larger doses, are was it the
route of the
agent that may have been the factor of shorter incubation in woman, or both? What is Kuru?
Kuru is a rare and fatal brain disorder that occurred at epidemic levels
during the 1950s-60s among the Fore people in the highlands of New
Guinea. The disease was the result of the practice of ritualistic
cannibalism among the Fore, in which relatives prepared and consumed the
tissues (including brain) of deceased family members. Brain tissue from
individuals with kuru was highly infectious, and the disease was
transmitted either through eating or by contact with open sores or
wounds. Government discouragement of the practice of cannibalism led to
a continuing decline in the disease, which has now mostly disappeared. snip... PLEASE NOTE the later ''or by contact with open sores or wounds.'' > and the disease was transmitted either through eating or by contact
> with open sores or wounds.
http://www.ninds.nih.gov/health_and_medical/disorders/kuru.htm
> the Fore women would scoop the brains of their dead relatives out of
> their skulls by hand before cooking. They then wiped the residual
> liquid and cadaver tissue over their paint-daubed bodies, leaving it
> caked in their hair and on their bodies for weeks after a mortuary feast.
Jennifer Cooke: kuru deaths continue in 1999
Sydney Morning Herald, Saturday, August 28, 1999
TSE INFECTION does takes place when the skin surface has been broken by
scarification (Taylor et al, 1996).
The transmission of KURU into animals supported the belief that the
disease had
been transmitted through ceremonial cannibalistic rituals in New Guinea
with a
possible route of spread involving handling fresh tissue and inoculation
through
mucous membranes and wounds including skin abrasions (Gajdusek, 1977) Masters, C.J., Gajdusek, D.C. and Gibbs, C.J., (1980). The spongiform
encephalopathies: the natural history of CJD and its relationship to
kuru and scrapie.
* Gajdusek D.C. (1996). Kuru: From the New Guinea field journals
1957-1962. Grand Street, 15:6-33
* Gajdusek D.C. (1973). Kuru in the New Guinea Highlands. In
Spillane JD (ed): Tropical Neurology. New York, Oxford University
Press.
* Gajdusek D.C., Gibbs C.J., and M. Alpers (1966). Experimental
transmission of a kuru-like syndrome to chimpanzees. Nature, 209:794.
* Lindenbaum S. (1979). Kuru Sorcery. Mountain View, Ca, Mayfield
Publishing Company.
SCCNFP/0724/03, final
THE SCIENTIFIC COMMITTEE ON COSMETIC PRODUCTS AND NON-FOOD PRODUCTS
INTENDED FOR CONSUMERS
OPINION
CONCERNING
USE OF SPECIFIED RISK MATERIAL IN COSMETICS
CLARIFICATION FOR TALLOW DERIVATIVES
adopted by the SCCNFP on 30 July 2003
by means of the written procedure
SCCNFP/0724/03, final
Opinion on the Use of specified risk material in cosmetics -
Clarification for tallow derivatives
_____________________________________________________________________________________________
2
1. Background
1. Entry n° 419 stipulates that Bovine, ovine and caprine tissues and
fluids from the
encephalon, the spinal cord and the eyes, and ingredients derived
therefrom must not form
part of the composition of cosmetic products, was first added to Annex
II to Cosmetics
Directive 76/768/EEC1 by Commission Directive 97/1/EC2 following an
opinion of the
Scientific Committee on Cosmetology.
2. Entry n° 419 was further amended by Commission Directives 98/16/EC3,
and 2000/6/EC4 in
order to align the list of prohibited animal materials to that contained
in Commission
Decisions defining Specified Risk Materials (SRM) as regards
transmissible spongiform
encephalopathies (TSEs).
3. Entry n° 419 stipulates that From the date referred to in Article 22
of Regulation (EC) No
999/2001 (8) of the European Parliament and of the Council, the
specified risk materials as
designated in Annex V to that Regulation, and ingredients derived therefrom.
Until that date, the specified risk materials as designated in Annex XI
Part A to Regulation
(EC) no 999/2001 and ingredients derived therefrom.
However, tallow derivatives may be used provided that the following
methods have been used
and strictly certified by the producer:
- transesterification or hydrolysis at least: 200 °C, 40 bars (40,000
hPa) for 20 minutes
(glycerol and fatty acids and esters),
- saponification with NaOH 12M (glycerol and soap) :
batch process: at 95 °C for 3 hours
or
continuous process: at 140 °C, 2 bars (2 000 hPa) for 8 minutes or
equivalent conditions.
4. Based on the opinions of the SSC5 and on Commission Decision
2001/2/EC6 regulating the
use of material presenting risks as regards TSEs, the SCCNFP adopted 2
further opinions on
the amendment to entry n° 419 (SCCNFP/0451/01 of 12 June 2001 and
SCCNFP/0521/01 of
25 September 2001).
5. Consequently, the SCCNFP recommended that the list referred to in
Regulation n° 999/2001
should be supplemented by the ingredients derived therefrom and that no
exceptions should
be made regarding tallow derivatives.
1 OJ L 262, 27.09.1976, p. 169
2 OJ L 16, 18.01.1997, p. 85
3 OJ L 77, 14.03.1998, p. 44
4 OJ L 56, 1.03.2000, p. 42
5 Opinion of the SSC on TSE infectivity distribution in ruminant tissues
(state of knowledge December 2001),
adopted 10-11 January 2002
6 OJ L 001, 4.01.2001, p. 21
SCCNFP/0724/03, final
Opinion on the Use of specified risk material in cosmetics -
Clarification for tallow derivatives
_____________________________________________________________________________________________
3
6. In its opinion adopted by the SCCNFP during the 22nd Plenary Meeting
of 17 December
2002 the SCCNFP (SCCNFP/0612/02) stated that
the exceptions made for tallow derivatives in its latest opinion
concerning the
amendment to entry n° 419 of Annex II to Directive 76/768/EEC on
cosmetic products
(SCCNFP/0552/02 of 27 February 2002) are no longer scientifically
consistent with
the scientific opinions of the Scientific Steering Committee on the
safety of tallow.
7. Recently the SSC adopted on its last meeting on 10 - 11 April 2003 an
opinion on the safety
of tallow derivatives from cattle tallow based on an updated report by
the European
Oleochemicals and Allied Products Group (APAG) on The safety of tallow
derivatives
with respect to Bovine Spongiform Encephalopathy
8. Due to the cosmetic applications of tallow derivatives the SSC stated
that it is justified to
modulate the risk reduction according to the source of the tallow used
for the production of
the derivatives and the geographical BSE risk level.
2. Terms of Reference
Commission Decision 2001/2/EC was repealed by Commission Regulation (EC) n°
1326/2001/EC7 of 29.6.2001 laying down transitional measures to permit
the changeover to the
Regulation (EC) No 999/20018 of the European Parliament and of the
Council of 22 May 2001
laying down rules for the prevention, control and eradication of certain
transmissible spongiform
encephalopathies.
The current definition for Specified Risk Material is found in Annex V
of the latter legislative
text and according to Article 3 1(g) does not include products
containing or derived from those
tissues unless indicated otherwise. There is also no exception made for
tallow derivatives that
may be used if defined methods have been used to prepare.
Because the designation of specified risk material is dynamic progress
and in order to avoid the
systematic consultation of the SCCNFP each time the designation of
specified risk material is
updated, the SCCNFP was asked to give advice on the following questions:
1. Are tallow derivatives safe for use in cosmetic products with regard
to BSE risk regardless of
the production process if they are derived from food- or feed- grade
tallow and if cross
contamination is prevented?
2. Are tallow derivatives safe for use in cosmetic products with regard
to BSE risk regardless of
the production process if they are derived cattle from GBR-C I
countries9 and fallen stock
are excluded?
3. For GBR-C II countries, are tallow derivatives safe for use in
cosmetic products if fallen
stock are excluded, the animals from which the tallow is sourced are fit
for human
7 OJ L 177, 30.6.2001, p. 60
8 OJ L 147, 31.5.2001, p.1
9 GBR-C stays for Geographical BSE risk in cattle .
SCCNFP/0724/03, final
Opinion on the Use of specified risk material in cosmetics -
Clarification for tallow derivatives
_____________________________________________________________________________________________
4
consumption, the raw tallow is produced according to the standards
indicated in the SSC
opinion of 28-29 June 2001 on the safety of tallow (including
filtration), and the following
processing conditions have been used:
to obtain glycerol and fatty acids and esters: transesterification or
hydrolysis at at least
200°C and an appropriate corresponding pressure for 20 minutes, followed
by a
purification to remove (insoluble) impurities;
to obtain glycerol and soap: saponification with NaOH 12M : batch
process: at 95°C for 3
hours; or: continuous process: at 140°C, 2 bars (2000 hPa) for 8 minutes
or equivalent
conditions, followed by a purification to remove (insoluble) impurities;
and cross contamination is prevented?
4. For GBR-C III and IV countries, are tallow derivatives safe for use
in cosmetic products if,
in addition to the conditions described under (3), the specified risk
materials have been
removed and are not used for the production of tallow / tallow derivatives?
3. Opinion of the SCCNFP
Based on the information presented in the last opinion adopted by the
Scientific Steering
Committee and in the respective EU legislative texts concerning
specified risk material (SMR)
and concerning certain transmissible spongiform encephalophathies, the
SCCNFP is of the
opinion that tallow derivatives are safe for use as ingredients in
cosmetic products.
It is justified to modulate the risk reduction according to the source
of the tallow used for the
production of the derivatives and the geographical BSE risk level.
1. Tallow derivatives are safe with regard to BSE risk regardless of the
production process
if they are derived from food- or feed- grade tallow and if cross
contamination is
prevented. The criteria for food- and feed- grade tallow are detailed in
the SSC opinion of
28-29 June 2001 on the safety of tallow obtained from ruminant slaughter
by products.
2. Tallow derivatives are safe with regard to BSE risk regardless of the
production process
if they are derived from cattle from GBR-C I countries and fallen stock
are excluded.
3. For GBR-C II countries, tallow derivatives are safe if fallen stock
are excluded, the
animals from which the tallow is sourced are fit for human consumption,
the raw tallow
is produced according to the standards indicated in the SSC opinion of
28-29 June 2001
on the safety tallow (including filtration), the processing conditions
described in the
mandate have been used and cross contamination is preserved.
4. For GBR-C III and IV countries, tallow derivatives are safe if, in
addition to the above
(3), the specific risk materials have been removed and are not used for
the production of
tallow/tallow derivatives.
http://europa.eu.int/comm/health/ph_risk/committees/sccp/documents/out229_en.pdf > 4. For GBR-C III and IV countries, tallow derivatives are safe if, in
> addition to the above
> (3), the specific risk materials have been removed and are not used
> for the production of
> tallow/tallow derivatives.
PLEASE NOTE, under the old BSE GBR, the USA would be re-classified as at
least a GBR III
risk assessment, if not a GBR IV in my opinion due to the misgivings
from USDA/APHIS et al,
some documented below in my references from Docket No, 04-047-l
Regulatory Identification
No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission).
Report on the
Assessment of the Geographical BSE - Risk of USA (July 2000) (220kb) http://europa.eu.int/comm/food/fs/sc/ssc/out137_en.pdf NOW, with these findings and the fact I will probably never live long
enough to
know exactly what the source of infection that killed my mother from the
Heidenhain Variant of Creutzfeldt Jakob Disease, I only ponder if the
potential
route of infection could have come from cosmetics. My mother used those
expensive facial creams all her life. SHE was an avid fisherwoman and would
layer herself with these creams for wrinkles, all over her face and around
her eyes. WITH these creams containing SRMs i.e. 'brain, eyes,
pituitary, CNS'
tissues, the fact that the hvCJD is a TSE that manifests itself directly
behind the
eyes (occipital brain region), in the front part of the brain, the fact
it is an exceedingly
rare strain/phenotype of the CJD, I only ponder the potential for
cosmetics as to be
a potential source of some human TSE? I also ponder the thought of
accumulation
of the TSE agent over a period of time from a multitude of routes and
sources, and
finally after a long period of time and accumulation, the 'threshold' is
met (whatever
that may be), and one becomes clinical with TSE? WITH new studies showing
the TSE agent in muscle tissue, the fact that the sensitivity of TSE
testing is
'not that sensitive', and the fact that Prusiner et al have a test that
they claim
is some 1000 times more sensitive than existing TSE test. The fact that new
'atypical' cases of TSEs are showing in in cattle and sheep in different
parts of
the globe, with the new 'atypical' TSE in cattle called 'BASE' being
very similar
to sporadic CJD as opposed to nv/v CJD, I think it paramount that we act
now
and ban ALL animal TSEs in Cosmetics. AS testing becomes more sensitive,
change
the rules as applicable. TO wait and continue to expose millions and
millions and
then later on, after finding out the worse case scenario is correct,
then to act, will be
much too late. WE MUST ACT NOW! How many humans are the Industry/Gov.
willing to expose to this agent that is 100% fatal, all for money, just
to come up
years or decades later saying, ''oops, sorry, we wish to submit the
following
docket to discuss further BSE/TSE precautions to remove all animal
Tissues from
cosmetics etc." due to all reasons I have stated in these federal
dockets over the years? WE must act now to remove all animal TSEs from cosmetics! SEE more relevant references pertaining to new atypical TSEs in cattle
and sheep
very similar to sporadic CJD in humans and new studies on TSE
infectivity in muscle
tissue below in my previous submission to Docket No, 04-047-l Regulatory
Identification
No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission) and why
it is paramount to BAN ALL ANIMAL TISSUES IN COSMETICS;
-------- Original Message --------
Subject: Docket No, 04-047-l Regulatory Identification No. (RIN)
091O-AF46 NEW BSE SAFEGUARDS (comment submission)
Date: Sun, 11 Jul 2004 21:34:22 -0500
From: "Terry S. Singeltary Sr."
To: fdadockets@oc.fda.gov
CC: regulations@aphis.usda.gov, burt.pritchett@fda.gov
Docket No. 04-047-l No. 04-021ANPR No. 2004N-0264 NEW BSE SAFEGUARDS
Federal Measures to Mitigate BSE Risks: Considerations for Further
Action http://www.fda.gov/cvm/index/updates/bseanprm.htm Greetings FDA,
USDA and APHIS et al, I would kindly like to comment on the continued
delay of the regulations that have been proposed for years to reduce the
risk of BSE/TSE in the USA. Each day that is wasted debating this issue
allows this agent to spread, and many many more humans and animals
become needlessly exposed to this agent via a multitude of potential
routes and sources right here in the USA. TO continue to ignore the new
findings from several scientists about the fact that BSE is not the only
strain of TSE in cattle, the fact that new atypical strains of TSE are
showing up in not only cattle, but sheep and the fact that the new
strain of TSE in cattle seems to be more similar to sporadic CJD as
opposed to the nv/v CJD, to continue to ignore these findings will only
further spread this agent. CWD and Scrapie have been running rampant in
the USA for decades. BOTH of which have been rendered and fed back to
animals for human/animal consumption for decades. All of which transmits
to primates by the natural and non-forced oral consumption of TSE
scrapie, CJD, Kuru agent (and CWD by inoculation). Strong Scientific
evidence discovered back in the 80s support the fact that a TSE has been
prevalent in the USA bovine for decades, either undetected or ignored.
IF you consider the recent stumbling and staggering TEXAS cow that was
showing all signs of a CNS/TSE disorder that was ordered to be rendered
without BSE/TSE test, brains, spinal cord, head and all (as to no
possible evidence left of TSE), I would think the 'ignored' or 'covered
up' to be the better terminology. Then you have the Downer in Washington
state that was actually a good walker and then all the banned Canadian
products that some how found it's way across the border into the USA,
considering all this, it is very difficult for me to believe that the
FDA/USDA/APHIS et al are doing everything possible to protect the
'consumer'. Hardly the case; Congressman Henry Waxmans Letter to the
Honorable Ann Veneman
http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_may_13_let.pdf
-------- Original Message -------- Subject: Re: Congressman Henry
Waxmans Letter to the Honorable Ann Veneman on failure by USDA/APHIS TO
TEST TEXAS MAD COW Date: Wed, 9 Jun 2004 16:48:31 -0500 From: "Terry S.
Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To:
BSE-L@uni-karlsruhe.de References: <40A8CD52.1070308@wt.net> ########
Bovine Spongiform Encephalopathy ######### USA BSE RED BOOK > October
1998 > > BSE Red Book 2.1-36 > > 7.2.1.7 Laboratory Coordination--The
Laboratory Coordination Officer > will advise the READE(3 Director
concerning laboratory capabilities and > appropriate laboratory
examinations to be conducted to provide needed > results as rapidly as
possible. This individual will assist with > interpretation of results.
seems that if the 'enhanced BSE/TSE testing program' is to test some
400,000+ animals in 1 1/2 years, they better hurry up, times a wasting.
> BSE Red Book 2.1-39 > > 7.6 Depopulation Procedures > > Under no >
circumstances may BSE suspects be sent fo slaughhter or rendering.
snip... > BSE Red Book 2.1-40 > > 7.7 Disposal > Under no circumstances
may BSE suspects be sent to slaughter or > rendering. Notify FDA, CVM if
you suspect that the carcass of a > BSE-confirmed animal has moved to
rendering or animal feed > manufacturing. Field personel should arrange
for the carcass to be > transported to and examined by a qualified
veterinary pathologist or > field veterinary medical officer. After the
pathologic examination has > been completed and the necessary diagnostic
specimens have been > obtained, field personnel should arrange for
disposal of the carcass. > Before a method of disposal is selected,
there are many factors that > must be considered, and often other State
and Federal agencies must be > consulted. The environmental and legal
impacts of the operation must be > considered. Upon recommendation of
the State or Federal agencies, VS may > consider other disposal methods.
> snip... > 7.7.3 Rendering > Because BSE is spread by rendered animal
protein, BSE-suspect and > confirmed carcasses must not be rendered,
unless the rendered material > is incinerated. Notify FDA, CVM if you
suspect that dead BSE animals or > carcasses have moved to rendering or
animal feed manufacturing. > snip... > 7.10.11 Prevention--Suspects and
animals confirmed to have BSE must not > be rendered. Producers, feed
mills, and rendering establishments should > adhere to U.S. State and
local rendering policies and FDA regulations > concerning the feeding of
rendered animal protein to ruminants. TSS Terry S. Singeltary Sr. wrote:
> ######## Bovine Spongiform Encephalopathy > ######### > > ONE HUNDRED
EIGHTH CONGRESS > CONGRESS OF THE UNITED STATES > HOUSE OF
REPRESENTATIVES > COMMITTEE ON GOVERNMENT REFORM > 2157 RAYBURN HOUSE
OFFICE BUILDING > WASHINGTON, DC 20515-6143 > > > www.house.gov/reform >
> May 13, 2004 > > > The Honorable Ann M. Veneman > Secretary of
Agriculture > Department of Agriculture > 1400 Independence Avenue, SW >
Washington, DC 20250 > > Dear Madam Secretary: > > 1 am writing to
express concern that the recent failure of the U.S. > Department of >
Agriculture (USDA) to test a Texas cow with neurological symptoms for >
bovine spongiform > encephalopathy (BSE) may reflect wider problems in
the surveillance > program. USDA > apparently does not keep track of how
many cows condemned for central > nervous system > symptoms are tested
for BSE nor does it require that suspect carcasses > be held pending
testing. > Effective surveillance and control of BSE in the United
States require > a reliable system for > ensuring that potentially
infected cows are tested and that no > infected materials enter the
animal or human food supply. > > Under USDA regulations, any cow that
exhibits signs of central nervous > system (CNS) > problems must be
condemned by Food Safety Inspection Service (FSIS) > personnel at the
plant.1 > According to a 1997 Animal and Plant Health Inspection Service
(APHIS) > Memorandum, brain > samples all of such animals should be sent
for BSE testing.2 The > memorandum notes that "[i]t is > essential that
brain specimens be collected from adult cattle > condemned for CNS signs
as part of > our national surveillance of BSE."3 > > The cow slaughtered
at the Lone Star Beef slaughterhouse last week > staggered and fell, >
and was condemned ante mortem by FSIS personnel.4 Despite a request >
from APHIS personnel > > 1 9 CFR 309.4. > > 2 USDA APHIS, Veterinary
Services Memorandum No. 580.16. Procedures/or > Investigation of Adult
Cattle With Clinical Signs of Central Nervous > System (CNS) Disease and
> Procedures for Surveillance of Downer Cows for Bovine Spongiform >
Encephalopathy (BSE) > (June 11,1997). > > 3 Id. > > 4 U.S. Confirms a
Failure to Use Mad Cow Test, Wall Street Journal > (May 4, 2004). > >
The Honorable Ann M. Veneman > May 13,2004 > Page 2 > > at the plant to
conduct BSE testing, however, an APHIS supervisor in > Austin reportedly
refused > the test and instructed the plant to send the carcass for
rendering.5 > > This sequence of events is troubling, and it raises the
question of > whether this is an > isolated incident. In 1997, USDA
noted a major gap between the number > of cattle condemned > for CNS
symptoms and the number of these cows actually tested for mad > cow
disease. The > Department found: > > Based on information provided by
the Food Safety and Inspection > Service (FSIS), the > number of adult
cattle (2 years of age or greater) condemned at > slaughter due to CNS >
signs is much greater than the number whose brains have been collected >
for testing.6 > > Despite recognizing the problem more than six years
ago, however, USDA > apparently did > not adopt procedures to ensure
that these samples would be collected. > In March 2004, the > Government
Reform Committee asked USDA to provide, for each of the > last five
years, the > number of BSE tests performed on cattle condemned by FSIS
inspectors > on the basis of CNS > symptoms.7 In response, USDA provided
information on the numbers of > cattle condemned for > CNS symptoms by
FSIS, but replied that "[i]t is not possible to > determine, from the
data we > currently collect, how many of these cattle were tested by
APHIS for > BSE."8 It thus appears that > not only does USDA not
routinely track the gap between the number of > condemned and tested >
cattle, but that USDA could not even calculate this gap when requested >
to do so by Congress. > > There also appears to be a lack of clarity
regarding the disposition > of cattle with CNS > symptoms while BSE
tests are pending. In the past, companies could > send cattle awaiting
BSE > testing results for rendering, which would allow their remains to
be > used in feed for animals > other than ruminants, such as pigs and
chickens. After this incident, > both FDA and USDA > policy appear to
have changed in different ways. > > USDA policy has apparently shifted
to requesting that companies not > send cattle to > rendering while
awaiting test results. A May 5, 2004 memo from APHIS > states, "it is
requested > though not required that [the cattle] not go to inedible
rendering > until the sample comes > > USDA's San Angelo Vets and Techs
Ordered Not to Test Suspect Cow, > Meating Place > (May 5, 2004). > > 6
USDA APHIS, supra note 2. > > 7 Letter from Rep. Tom Davis and Rep.
Henry A- Waxman to Secretary of > Agriculture > Ann M. Veneman (Mar. 8,
2004). > > 8 Letter from Ronald F. Hicks, Assistant Administrator,
Office of > Program Evaluation, > Enforcement, and Review- FSIS. to Reo.
Henrv A. Waxman- Attachment 1 > (Mar. 22- 2004). > > The Honorable Ann
M. Veneman > May 13,2004 > Page 3 > > back negative."9 There is no
explanation of why this course of action > is requested, but not >
required. > > FDA policy also appears to have shifted towards
prohibiting the use of > carcasses of cattle > with CNS symptoms and
indeterminate BSE status in certain types of > animal feed. On April 30,
> FDA requested that the rendering company holding the remains of the >
Texas cow either destroy > them or use them exclusively in swine feed. m
the case that the > remains are included in swine > feed, FDA "will
track the material all the way through the supply > chain from the
processor to the farm to ensure that the feed is > properly monitored
and used only as feed for pigs."10 > > Any confusion over what to do
with cattle condemned for CNS symptoms > awaiting > testing for BSE
seems unnecessary. The obvious approach is to require > companies either
to > destroy the carcasses or hold them until test results become >
available. Such a policy would avoid any need for complicated >
traceback procedures after the discovery of a positive result. >
According to the information provided to the Committee by USDA, the >
FSIS has condemned > only 200 to 250 cows per year because of signs of
central nervous > system damage." Mandating > the destruction or holding
of their carcasses would have minimal > economic impact. > > The
experience with the BSE-infected cow in Washington State > illustrates
the prudence > of waiting for the results of BSE tests. Prior to
December 2003, USDA > permitted cattle that > were sampled as part of
the BSE surveillance program to enter commerce > even while BSE tests >
were pending. As a result, when the BSE-infected cow was discovered, >
it had already entered > the food supply. This led to a complicated and
partially successful > traceback procedure in which > hundreds of
thousands of pounds of beef had to be destroyed. Because > of this
debacle, USDA > quickly developed a new policy to require holding all
carcasses from > the human food chain > during BSE testing. > > I
appreciate that you have taken steps to enhance the safety of the > U.S.
food supply since > the discovery of BSE in the United States. I urge
you to consider the > lessons of this latest > > 9 Memo from John R.
Clifford, Acting Deputy Administrator, Veterinary > Services, and >
William Smith, Assistant Administrator, Office of Field Operations, >
Food Safety and Inspection > Service, to VSMT, Regional Directors, Area
Veterinarians in Charge, > and Veterinary Services, > Subject: Policy
Statement Regarding BSE Sampling of Condemned Cattle > at Slaughter
Plants - > for Immediate Implementation (May 5, 2004) (online at >
http://www.aphis.usda.gov/lpa/issues/bse/BSE_APHIS-FSIS.pdf). > > 10
FDA, Statement on Cow -with Central Nervous System Symptoms (Apr. > 20,
2004) > (online at
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html). > > 11 The
yearly totals of FSIS antemortem CNS condemnation for all adult > cattle
were 233 > (1999), 220 (2000), 201 (2001), 249 (2002), and 247 (2003).
The > database for 2003 had not yet > closed. > > The Honorable Ann M.
Veneman > May 13,2004 > Page 4 > > incident. USDA should develop a
process that ensures the tracking of > cattle condemned for CNS > signs
and should institute a policy requiring all carcasses with > pending BSE
tests to be destroyed or held. If there are any statutory > barriers to
these steps, please do not hesitate to let me know. > > Sincerely, > >
XXXXX X. XXXXXX > > Henry A. Waxman > Ranking Minority Member > >
Congressman Henry Waxmans's Letter to the Honorable Ann Veneman >
http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_may_13_let.pdf
> > > TSS > > #########
http://mailhost-alt.rz.uni-karlsruhe.de/warc/bse-l.html > ########## >
######### http://mailhost-alt.rz.uni-karlsruhe.de/warc/bse-l.html
########## NOW, after being told that last year that strict TSE
guidelines would be put into place to plug any leaks in the triple TSE
fire walls that have been leaking, we see again the same old industry
backed rhetoric 'protect the industry at all cost', and again, measures
to protect the American consumer from a horrible disease has been set
back due to corporate greed. OF course it was said long ago; It is clear
that USDA have little information and _no_ regulatory responsibility for
rendering plants in the US... snip... 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_... snip...
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf A New Incidence of
TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin
reported that many of his mink were "acting funny", and some had died.
At this time, we visited the farm and found that approximately 10% of
all adult mink were showing typical signs of TME: insidious onset
characterized by subtle behavioral changes, loss of normal habits of
cleanliness, deposition of droppings throughout the pen rather than in a
single area, hyperexcitability, difficulty in chewing and swallowing,
and tails arched over their _backs like squirrels. These signs were
followed by progressive deterioration of neurologic function beginning
with locomoior incoordination, long periods of somnolence in which the
affected mink would stand motionless with its head in the corner of the
cage, complete debilitation, and death. Over the next 8-10 weeks,
approximately 40% of all the adult mink on the farm died from TME. Since
previous incidences of TME were associated with common or shared feeding
practices, we obtained a careful history of feed ingredients used over
the past 12-18 months. The rancher was a "dead stock" feeder using
mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had
never been fed. http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf DUE
to the new 'atypical' TSEs showing up in different species, it is
paramount that removing specified risk materials (SRMs) from all animal
feed, including pet food, in order to control the risks of cross
contamination throughout feed manufacture and distribution and on the
farm due to misfeeding is a no brainer. FAILING to do this will only
continue to spread this agent. AGAIN, due to the findings of new
'atypical' TSEs showing up in different species, we must require
dedicated equipment or facilities for handling and storing feed and
ingredients during manufacturing and transportation, to prevent cross
contamination. WE must not let the industry and politics dictate
science. BASE in cattle in Italy of Identification of a second bovine
amyloidotic spongiform encephalopathy: Molecular similarities with
sporadic Creutzfeldt-Jakob disease
http://www.pnas.org/cgi/content/abstract/0305777101v1 Identification of
possible animal origins of prion disease in human beings snip... A
further comparison6 of BASE with sCJD in people revealed that, at least
in terms of PrPSc characteristics, BASE was similar to a particular
type of sCJD sCJD(MV2) (figure). These researchers conclude not only
that BASE is a new strain of BSE, but also that characteristics of human
and animal PrPSc could help to identify potential risk factors for
disease in individuals with sCJD of unknown origin. snip... THE LANCET "
Vol 363 " June 19, 2004 " www.thelancet.com 2013 Characterization of two
distinct prion strains derived from bovine spongiform encephalopathy
transmissions to inbred mice S. E. Lloyd, J. M. Linehan, M. Desbruslais,
S. Joiner, J. Buckell, S. Brandner, J. D. F. Wadsworth and J. Collinge J
Gen Virol 2004 85 (8): p. 2471-2478 J Gen Virol -- Future Table of
Contents Alert (not yet published...TSS) Journal of Virological Methods
117 (2004) 2736 Atypical scrapie cases in Germany and France are
identified by discrepant reaction patterns in BSE rapid tests A.
Buschmanna, A.-G. Biacabe b, U. Ziegler a, A. Bencsik b, J.-Y. Madecb,
G. Erhardt c, G. Lühken c, T. Baron b, M.H. Groschup a,? a Federal
Research Centre for Virus Diseases of Animals, Institute for Novel and
Emerging Infectious Diseases, Boddenblick 5a, 17493 Greifswald-Insel
Riems, Germany b AFSSA-Lyon Unité Virologie-ATNC , 31 Avenue Tony
Garnier, 69364 Lyon Cedex 07, France c Department of Animal Breeding and
Genetics, Justus-Liebig University Giessen, Ludwigstr. 21B, 35390
Giessen, Germany Received 27 August 2003; received in revised form 13
November 2003; accepted 18 November 2003 Abstract The intensified
surveillance of scrapie in small ruminants in the European Union (EU)
has resulted in a substantial increase of the number of diagnosed cases.
Four rapid tests which have passed the EU evaluation for BSE testing of
cattle are also recommended currently and used for the testing of small
ruminants by the EU authorities. These tests include an indirect ELISA
(cELISA), a colorimetric sandwich ELISA (sELISA I), a chemiluminescent
sandwich ELISA (sELISA II), and a Western blot (WB). To this point, the
majority of samples have been screened by using either sELISA I
(predominantly in Germany) or WB (predominantly in France). In this
study, it is shown that a number of the German and French scrapie cases
show inconsistent results using rapid and confirmatory test methods.
Forty-eight German sheep, 209 French sheep and 19 French goat
transmissible spongiform encephalopathy (TSE) cases were tested. All
cases were recognised by the sELISA I and either one of the confirmatory
methods (scrapie-associated fibrils (SAF)-immunoblot or
immunohistochemistry). Surprisingly, three rapid tests failed to detect
a significant number of scrapie cases (29 in France and 24 in Germany).
The possible reasons for these inconsistent reaction patterns of scrapie
cases are discussed. Similar discrepancies have not been observed during
rapid testing of cattle for BSE, the disease for which all diagnostic
methods applied have been evaluated. © 2003 Elsevier B.V. All rights
reserved. Keywords: Scrapie; Prion protein; Rapid test; Confirmatory
method 1. Introduction snip... 4. Discussion Since the spring of 2002,
rapid tests are being used for active surveillance of scrapie in the
national sheep herds of the EU member states. These tests have been
approved by the European commission and they include a colorimetric
sandwich ELISA, a luminescence sandwich ELISA, an indirect ELISA using
chemiluminescence as well as a rapid Western blotting assay. According
to EU legislation (EC regulation 999/2001 and amendments), rapid tests
are only approved for screening brain samples. In case of a reactive
result, the sample has to be examined in the national reference
laboratory using one of the OIE approved confirmatory methods which are
SAF-immunoblotting and immunohistochemistry. The introduction of this
active surveillance programme in the EU using BSE rapid tests
demonstrated that scrapie in small ruminants is much more prevalent than
had been previously estimated. Moreover, we found that not all scrapie
cases are detected equally well by the four applied rapid tests as a
significant portion of the samples were found positive with the sELISA I
test but were not reactive with the rapid WB and sELISA II. The cELISA
could only be used on a rather small number of samples, however, it must
be assumed from the available results that it shows a performance
similar to that of the rapid WB and sELISA II. Although some of the
sELISA I results were weak positive, all cases that were initially
detected using this method were confirmed by using OIE-recommended
methods. It is therefore concluded that the sELISA I results are true
positive, whereas the rapid WB, sELISA II and cELISA results of the same
samples must be considered as false negative. This of course presupposes
that the currently applied con- firmatory methods do not produce any
false positive results. All samples that were first detected by using
the rapid WB also gave positive results using the other rapid test
methods. This observation supports the hypothesis that the rapid WB
fails to detect certain positive sheep. Regrettably, it was not feasible
during this study to retest small ruminant field samples that had
initially been negative in the rapid WB with the sELISA I test in order
to check if any positive samples had been ignored during the first
screening. Non-uniform rapid test results were reproducible when
selected coded samples were exchanged between the German and French
national TSE reference laboratories and the samples were repeatedly
positive in the sELISA I. Furthermore, it should be emphasised that the
reactivity using this test was generally high (more than four times the
cut-off level in most cases), showing that negative results obtained
with other methods cannot be explained by threshold levels of protease
resistant prion protein in these particular samples alone. Brainstem
samples collected in abattoirs and rendering plants do not always
fulfill the desired diagnostic quality standards in terms of freshness
and in sampling localisation. In the beginning, we therefore could not
exclude the possibility that single incongruent test results were due to
varying PrPSc concentrations in the brainstems. However, the large
number of such samples and the variety of the sample histories argue
against such artefacts. However, such effects may explain why a few
cases were negative by immunohistochemistry, but positive by
SAF-immunoblotting, a diagnostic method where PrPSc is concentrated from
larger brain areas. These 53 atypical scrapie cases in France and
Germany out of a set of 276 may represent a novel strain of this disease
in the field. Similar observations have also been made by the Norwegian
National TSE Reference Laboratory, where some sheep scrapie samples were
not reactive using the rapid WB (Benestad et al., 2003). However, not
all characteristics described for those Nor98 designated cases match the
atypical scrapie cases reported here. In particular, all Nor98 cases
display a strong signal at 12 kDa that seems to be absent in a number of
the German and French cases. We therefore postulate that at least three
different scrapie phenotypes A. Buschmann et al. / Journal of
Virological Methods 117 (2004) 2736 35 (typical scrapie and two
atypical strains) exist within the European sheep flock. To determine
critical factors affecting the rapid WB detection of PrPSc, we undertook
a series of exchange experiments. The detection of atypical cases was
improved after replacing the rapid WB homogenisation buffer supplied
within the testkit of which the composition is undisclosed by an
in-house homogenisation buffer containing desoxycholate and NP40 as
detergents. Attempts were also made to replace the proteinase K
solution, the detection antibody (by mab L42 that is directed to the
same epitope as mab 6H4), and the conjugate antibody. Although no single
critical step was revealed that alone enabled the detection of samples,
these modifications altogether led to positive results for almost all
atypical samples. It became also evident that minor changes in the
sample treatment may have major effects when the modified
SAF-immunoblotting technique was applied: while some of the atypical
samples were negative with this method in which the first
ultracentrifugation step is omitted and PK digestion is performed prior
to SAF preparation, the same samples became clearly positive when the
other SAF preparation protocol was applied. However, the physiochemical
characteristics of ovine PrPSc derived from different scrapie isolates
that are the basis for the observed effects still need further research
efforts. PrP molecules derived from animals affected with different TSE
strains vary in their cleavage sites for proteinase K digestion and
therefore display different molecular weights when analysed in
immunoblot (Hill et al., 1998; Baron et al., 2000; Stack et al., 2002).
For example, the N-terminus of PrP derived from BSE-affected sheep is
digested further by proteinase K than PrP derived from scrapie-affected
sheep and therefore leads to a residual PrP of a lower molecular mass.
This effect has been proposed as a possible diagnostic marker to
differentiate between BSE and scrapie infections in sheep. Our
experiments showed that this variation in the PK cleavage site between
scrapie and BSE in sheep has no impact on the performance of the rapid
tests on ovine BSE PrPSc since all commercial rapid tests detect PrPSc
derived from experimentally BSE infected sheep of the PrPARQ/ARQ
genotype (data not shown). Moreover, WB and sELISA II use the same
monoclonal antibody (mab 6H4; Korth et al., 1997) which binds to an
epitope far away from the PK cleavage site (aa 144148) and would
therefore not be expected to react differently with scrapie- and
BSE-derived PrPSc. The same is the case with the French immunoblot test
that uses mab SAF 84 (Demart et al., 1999), binding to an epitope in the
same region of the protein (aa 125163). No information is available on
the PrP epitopes that are targeted in the sELISA I and cELISA. TSE
infectivity can only be confined reliably, to date, by transmission
experiments to an appropriate host. As it cannot be ruled out completely
at this stage that non-infectious PrPC may also form intracellular
aggregates with increased protease resistance and hydrophobicity that
may lead to false positive results in diagnostic tests, the level of
infectivity of such atypical cases is currently being examined by
inoculation into RIII, C57B1 and VM95 mice. In case of a transmission to
these mouse strains, the lesion profile scores will be determined and
PrPSc will be analysed concerning its glycotype and PK resistance. The
use of rapid tests for small ruminants was introduced by the EU
Commission on the basis of their successful evaluation for BSE testing
in cattle (Moynagh and Schimmel, 1999) in order to achieve an overview
of the scrapie prevalence in the EU. Unfortunately, no independent
evaluation has been performed in the EU to date to reveal the individual
rapid tests performance on small ruminant scrapie cases. Therefore,
their specificity and sensitivity for this use can only be estimated by
the results of samples selected randomly that have been tested
individually by the manufacturers. Inconsistencies in the ability of
rapid tests to identify positive cases would question the current
efforts to intensify and standardise the scrapie surveillance in the EU
member states. Our data show that the actual numbers of scrapie cases
and the prevalence of scrapie may be seriously underestimated in
countries where rapid tests that may produce false-negative results are
used. In the German epidemiosurveillance scheme for scrapie, the sELISA
I is applied for testing of more than 80% of the samples, while in
France 60% of the samples are tested with the rapid WB. Therefore, it
must be accepted that the current EU-wide epidemiosurveillance programme
can only give a general impression of the scrapie situation but may miss
on average up to 12% of the true number of German scrapie cases and up
to 16% of the French cases (estimated numbers take into account the
applied test methods and the numbers of atypical cases since 2002). This
must be kept in mind when scrapie prevalence data obtained by BSE rapid
testing are interpreted. Acknowledgements We wish to acknowledge
Matthias Kramer and Sandra Göbel (FRCVDA-Wusterhausen, Germany) and
Didier Calavas (AFSSA-Lyon, France) for epidemiological data, Bertrand
Bedhom (LABOGENA, France) for genotype analysis of French scrapie cases
and J. Grassi (C.E.A.-Saclay, France) for supply of SAF 70 and SAF 84
antibody. This work was partly funded by the German Ministry of Consumer
Protection, Nutrition and Agriculture (BMVEL). References snip...END Vet
Pathol -- Ersdal et al. 40 (2): 164 ... up PrP rapidly at a young age,
as Heggebø et al. ... Ersdal, MJ Ulvund) and 133449/111 (SL Benestad)
from the ... Vet Rec 147:439-441, 2000[ISI][Medline]; Bendheim PE ...
http://www.vetpathology.org/cgi/content/full/40/2/164 - [PDF]
Accumulation of Pathogenic Prion Protein (PrP ) in Nervous and ... File
Format: PDF/Adobe Acrobat ... 166 Vet Pathol 40:2, 2003 Ersdal, Ulvund,
Benestad, and Tranulis ... RPLN Ileum Lambs RPLN DJLN Ileum Spleen
F89/160.1.5 L42 R521 R505 ORourke et al. ...
http://www.vetpathology.org/cgi/reprint/40/2/164.pdf - [PDF] SCIENTIFIC
PAPERS File Format: PDF/Adobe Acrobat ... 2003 Mar- 2003 Mar 31;
34(2):185-92. SEAC/SCI/79/17 Ersdal C, Ulvund MJ, Benestad SL, Tranulis
MA. ... Vet Rec. ... SEAC/SCI/79/25 He L, Lu XY, Jolly AF et al. ...
http://www.seac.gov.uk/papers/SEAC-SCI-79.pdf - SCRAPIE - NORWAY: NEW
PHENOTYPE ***************************************** A ProMED-mail post
ProMED-mail, a program of the International Society for Infectious
Diseases Date: 16 Nov 2003 From: Terry Singletary Source: The Veterinary
Record, 16 Aug 2003 [edited] [With new information, it appears there is
potentially a new phenotype of atypical' BSE/TSE in animals in Japan
and France. The article below indicates a new strain of Scrapie, the
'Nor98', which also has negative IHC and histology. Although this
article does not suggest a link to the atypical forms seen in cattle, it
does seem more than coincidence that there are also appearing different
strains, or perhaps atypical strains of scrapie as well. It has been
believed for years that there is a link between BSE and scrapie; perhaps
this is another bit of research that should be carefully examined.
Mod.TG] Cases of scrapie with unusual features in Norway and designation
of a new type, Nor98. The Veterinary Record, 16 August 2003, vol. 153,
no. 7, pp. 202-208(7) Benestad S.L.; Sarradin P.; Thu B.; Schonheit J.;
Tranulis M.A.; Bratberg B. Abstract: 5 cases of scrapie with unusual
features have been diagnosed in Norway since 1998. The affected sheep
showed neurological signs dominated by ataxia, and had the PrP genotypes
homozygous A136 H154 Q171/ A136H154Q171 or heterozygous
A136H154Q171/A136R154Q171, which are rarely associated with scrapie.
Brain histopathology revealed neuropil vacuolisation essentially in the
cerebellar and cerebral cortices; vacuolation was less prominent in the
brainstem, and no lesions were observed at the level of the obex. The
deposits of PrPSc were mainly in the cortex of the cerebellum and
cerebrum, and no PrPSc was detectable by immunohistochemistry or ELISA
in the lymphoid tissues investigated. Western blot analysis showed that
the glycotype was different from other known scrapie strains and from
the BSE strain. From a diagnostic point of view, these features indicate
that this type of scrapie, designated Nor98, could have been overlooked
and may be of significance for sampling in scrapie surveillance
programmes. Document Type: Research article ISSN: 0042-4900 DOI
(article): NO_DOI SICI (online): 0042-4900(20030816)153:7L.202;1-
Publisher: BVA Publications -- ProMED-mail NOT to forget the 'atypical'
VERMONT USA' sheep scrapie/BSE/TSE? back in 2000 with the testing
conveniently ignored and put off once again with animal TSEs. Why I ask?
SCRAPIE ''ATYPICAL'' TSE IN SHEEP VERMONT UPDATE 2004 Greetings, IN the
year 2000, some sheep in Vermont were confiscated due to what the
USDA/APHIS said was an 'atypical TSE'. WE were told there would be
additional testing to confirm exactly what TSE we were dealing with;
Release No. 0141.02 Ed Curlett (301) 734-3256 Jerry Redding (202)
720-6959 TESTING TO CONTINUE ON IMPORTED SHEEP CONFISCATED LAST YEAR
WASHINGTON, April 11, 2002 -- The U.S. Department of Agriculture today
announced that tests conducted on a flock of sheep confiscated last year
from a farm in Vermont confirm that two of the 125 sheep tested positive
for an atypical undifferentiated transmissible spongiform encephalopathy
(TSE) of foreign origin. The flock of 125 sheep was confiscated in March
2001 after four animals from an associated flock tested positive for TSE
in July 2000. USDA will continue to conduct additional tests to
determine the type of TSE in these sheep. "These results confirm our
previous conclusions were correct and that we took the appropriate
preventative actions in confiscating these animals," said Bobby Acord,
administrator of USDAs Animal and Plant Health Inspection Service.
"USDAs actions to confiscate, sample and destroy these sheep were on
target. As a result of our vigilance, none of these confiscated animals
entered the animal or human food supply." The sheep, imported from
Belgium and the Netherlands in 1996, were placed under certain federal
restrictions when they entered the country as part of USDA's scrapie
control efforts. In 1998, USDA learned that it was likely that sheep
from Europe were exposed to feed contaminated with bovine spongiform
encephalopathy. At that time, the state of Vermont, at the request of
USDA, imposed a quarantine on these flocks, which prohibited slaughter
or sale for breeding purposes. On July 10, 2000, several sheep from the
flock tested positive for a TSE, a class of degenerative neurological
diseases that is characterized by a very long incubation period and a
100 percent mortality rate in infected sheep. Two of the better known
varieties of TSE are scrapie in sheep and BSE in cattle. There is no
evidence that scrapie poses a risk to human health. On July 14, 2000,
USDA issued a declaration of extraordinary emergency to acquire the
sheep. This action was contested by the flock owners. A federal district
court judge ruled in favor of USDA based on the merits of the case. The
flock owners appealed to the Second Circuit Court requesting a stay,
which was denied. The sheep were confiscated by USDA in March 2001 and
transported to USDA's National Veterinary Services Laboratories in Ames,
Iowa, where they were humanely euthanized. Tissue samples were collected
from the sheep for diagnostic testing and USDA will continue with
additional tests which could take up to 2 - 3 years to complete. In all,
USDA has acquired 380 sheep from a total of three flocks. All of the
animals were humanely euthanized, sampled and disposed and did not enter
the animal or human food supply. Our goal continues to be to prevent,
detect and eradicate foreign animal diseases to protect American
agriculture, natural resources and consumers," said Acord. "We will
continue to utilize the scientific results of these and other tests
conducted during the last several years to strengthen our extensive
surveillance, monitoring and prevention efforts." For more information
about USDAs ongoing surveillance, monitoring and prevention efforts as
it relates to this situation, please visit
www.aphis.usda.gov/oa/tse/index.html # NOW, June 2004 those same test
that we were told would start in 2002, have yet to be started. THE TSE
those VERMONT sheep was supposedly to have had, has yet to be confirmed.
WHY? IGNORING the fact Scrapie does transmit to primates by their non
forced consumption of known infectious scrapie tissues. 1: J Infect Dis
1980 Aug;142(2):205-8 Oral transmission of kuru, Creutzfeldt-Jakob
disease, and scrapie to nonhuman primates. Gibbs CJ Jr, Amyx HL, Bacote
A, Masters CL, Gajdusek DC. Kuru and Creutzfeldt-Jakob disease of humans
and scrapie disease of sheep and goats were transmitted to squirrel
monkeys (Saimiri sciureus) that were exposed to the infectious agents
only by their nonforced consumption of known infectious tissues. The
asymptomatic incubation period in the one monkey exposed to the virus of
kuru was 36 months; that in the two monkeys exposed to the virus of
Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that
in the two monkeys exposed to the virus of scrapie was 25 and 32 months,
respectively. Careful physical examination of the buccal cavities of all
of the monkeys failed to reveal signs or oral lesions. One additional
monkey similarly exposed to kuru has remained asymptomatic during the 39
months that it has been under observation. PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
IGNORING the fact Scrapie transmission studies have never been done on
man. IGNORING the fact surveillance for TSE in man in the USA and other
places around the globe is terribly under funded and lacking in
guidance. to date some 25 states make it reportable, with some states
having an age bracket only documenting the younger victims. leaving the
door open to spread the agent through the medical and surgical arena.
With the recent announcement of the UK contingency plan for the
emergence of naturally occurring BSE in sheep June 2004, and the
terrible implications for human health this would cause, full text some
31 pages;
http://www.defra.gov.uk/corporate/consult/bseinsheep/bseinsheep.pdf you
would have thought that this would have been at the top of someone's
priority list. However, it does not look that way. I ask again, WHY? I
wish to submit the following; -------- Original Message --------
Subject: Re: AW: [BSE-L] USDA did not test possible mad cows - Dr.
Detwiler, what about those sheep? Date: Sun, 13 Jun 2004 11:27:24 -0500
From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform
Encephalopathy To: BSE-L@uni-karlsruhe.de References:
<13.2d20eaae.2df84fb9@aol.com> <40C8C7A0.1080107@wt.net> ######## Bovine
Spongiform Encephalopathy ######### Greetings list members, Thought I
should let the list know that Dr. Detwiler kindly replied to my question
about the delayed 'atypical' TSE testing in the Vermont sheep and tried
to explain what caused the delay. If I interpreted it correctly, seems
it was the fault of the U.K. ; -------- Original Message --------
Subject: Sheep Date: Sat, 12 Jun 2004 14:26:04 EDT From: LAVET22@aol.com
To: flounder@wt.net Mr. Singeltary. I hope this finds you well. As you
are aware I left the USDA last year. I can only update you on the sheep
before that time. Contact was established with the UK on doing the
bioassay studies. They agreed. However, we were prioritized after their
own needs, hence the delay. I am aware that there are now additional
labs in Europe running the mouse bioassay strain typing. You will have
to contact USDA for further word. Linda Detwiler ========= My reply to
Dr. Detwiler; -------- Original Message -------- Subject: Re: Sheep
Date: Sat, 12 Jun 2004 13:53:57 -0500 From: "Terry S. Singeltary Sr."
To: LAVET22@aol.com References: <54.2bd2ac1e.2dfca4bc@aol.com> hello Dr.
Detwiler, thanks for your kind reply. > However, we were prioritized
after their own needs, hence the delay. not sure i understand that? >
You will have to contact USDA for further word. already done that, and
there answer was; >5/20/04 > >Dear Mr. Singeltary, > >The Western blot
tests on these animals were completed in April of this >year. That means
that we can begin the mouse inoculations. To get the >results of the
Western blot tests, you will need to submit a Freedom of >Information
Act request through our FOIA office. The FAX number there is
>301-734-5941. > >Have a nice day, > >Jim Rogers >APHIS LPA > and with
my previous attempts for information via the FOIA through this
administration (as you are probably very well aware of) they have all
been ignored/refused. so any further attempts would be fruitless i am
sure. thanks anyway... kindest regards, Terry LAVET22@aol.com wrote: >
Mr. Singeltary. snip... TSS Terry S. Singeltary Sr. wrote: > ########
Bovine Spongiform Encephalopathy > ######### > > Greetings Dr. Detwiler,
> > glad to see you are still with us, you had become very silent
lately. > hope you are enjoying semi retirement. > > recently, i
inquired through the BSE-L and via USDA official about > those Vermont
sheep via belgium which there was an Extraordinary > Declaration of
Emergency declared here in the USA due to > atypical scrapie. The thread
is; > > Confiscation of Sheep in Vermont and testing results ? Thu, 20
May 2004 > 12:10:03 -0500 "Terry S. Singeltary Sr." Bovine > Spongiform
Encephalopathy BSE-L > > > >> Imported >> Belgium/Netherlands >> Sheep
Test Results >> Background >> Factsheet >> Veterinary Services April
2002 >> APHIS > > > > snip... > >> Additional tests will be conducted to
determine >> exactly what TSE the animals haveBSE or scrapie. >> These
tests involve the use of bioassays that consist >> of injecting mice
with tissue from the infected animals >> and waiting for them to develop
disease. This testing >> may take at least 2 to 3 years to complete. > >
> >
http://www.aphis.usda.gov/lpa/pubs/fsheet_faq_notice/fs_ahvtsheeptr.pdf
> > DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL
T.S.E. > (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES > >
http://frwebgate.access.gpo.gov/cgi-bin/getdoc.cgi?dbname=2000_register&doci
> > d=fr20jy00-32 > > > DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE
OF AN ATYPICAL T.S.E > (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED
STATES [2] > >
http://frwebgate.access.gpo.gov/cgi-bin/getdoc.cgi?dbname=2000_register&doci
> > d=fr20jy00-31 > > > or if those old urls dont work, go here; > >
DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E >
(PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES > - Terry S. >
Singeltary Sr. 7/20/00 (0) > > [Federal Register: July 20, 2000 (Volume
65, Number 140)] [Notices] > [Page 45018] >From the Federal Register
Online via GPO Access > [wais.access.gpo.gov] [DOCID:fr20jy00-32] > >
-----------------------------------------------------------------------
> > DEPARTMENT OF AGRICULTURE > > Office of the Secretary > > [Docket
No. 00-072-1] > > Declaration of Extraordinary Emergency Because of an
Atypical > Transmissible Spongiform Encephalopathy (Prion Disease) of
Foreign Origin > > A transmissible spongiform encephalopathy (TSE)
(prion disease) of > foreign origin has been detected in the United
States. It is different > from TSE's previously diagnosed in the United
States. The TSE was > detected in the progeny of imported sheep. The
imported sheep and > their progeny are under quarantine in Vermont.
Transmissible > spongiform encephalopathies are degenerative fatal
diseases that can > affect livestock. TSE's are caused by similar, as
yet uncharacterized, > agents that usually produce spongiform changes in
the brain. > Post-mortem analysis has indicated positive results for an
atypical > TSE of foreign origin in four sheep in Vermont. Because of
the > potentially serious consequences of allowing the disease to spread
to > other livestock in the United States, it is necessary to seize and
> dispose of those flocks of sheep in Vermont that are affected with or
> exposed to the disease, and their germ plasm. The existence of the >
atypical TSE of foreign origin represents a threat to U.S. livestock. >
It constitutes a real danger to the national economy and a potential >
serious burden on interstate and foreign commerce. The Department has >
reviewed the measures being taken by Vermont to quarantine and >
regulate the flocks in question and has consulted with appropriate >
officials in the State of Vermont. Based on such review and >
consultation, the Department has determined that Vermont does not have >
the funds to compensate flock owners for the seizure and disposal of >
flocks affected with or exposed to the disease, and their germ plasm. >
Without such funds, it will be unlikely to achieve expeditious >
disposal of the flocks and germ plasm. Therefore, the Department has >
determined that an extraordinary emergency exists because of the >
existence of the atypical TSE in Vermont. This declaration of >
extraordinary emergency authorizes the Secretary to seize, quarantine, >
and dispose of, in such manner as he deems necessary, any animals that >
he finds are affected with or exposed to the disease in question, and >
their germ plasm, and otherwise to carry out the provisions and >
purposes of the Act of July 2, 1962 (21 U.S.C. 134-134h). The State of >
Vermont has been informed of these facts. > > Dated: This declaration of
extraordinary emergency shall become > effective July 14, 2000. Dan
Glickman, Secretary of Agriculture. [FR > Doc. 00-18367 Filed 7-19-00;
8:45 am] BILLING CODE 3410-34-P > >
http://frwebgate.access.gpo.gov/cgi-bin/getdoc.cgi?dbname= >
2000_register&docid=fr20jy00-32 ================================ >
[Federal Register: July 20, 2000 (Volume 65, Number 140)] [Notices] >
[Page 45018] >From the Federal Register Online via GPO Access >
[wais.access.gpo.gov] [DOCID:fr20jy00-31] > >
========================================================================
> Notices Federal Register >
________________________________________________________________________
> > This section of the FEDERAL REGISTER contains documents other than
> rules or proposed rules that are applicable to the public. Notices of
> hearings and investigations, committee meetings, agency decisions and
> rulings, delegations of authority, filing of petitions and >
applications and agency statements of organization and functions are >
examples of documents appearing in this section. > >
========================================================================
> > [[Page 45018]] > >
-----------------------------------------------------------------------
> > DEPARTMENT OF AGRICULTURE > > Office of the Secretary > > [Docket
No. 00-072-2] > > Declaration of Emergency Because of an Atypical
Transmissible > Spongiform Encephalopathy (Prion Disease) of Foreign
Origin > > A transmissible spongiform encephalopathy (TSE) (prion
disease) of > foreign origin has been detected in the United States. It
is different > from TSE's previously diagnosed in the United States. The
TSE was > detected in the progeny of imported sheep. The imported sheep
and > their progeny are under quarantine in Vermont. Transmissible >
spongiform encephalopathies are degenerative fatal diseases that can >
affect livestock. TSE's are caused by similar, as yet uncharacterized, >
agents that usually produce spongiform changes in the brain. >
Post-mortem analysis has indicated positive results for an atypical >
TSE of foreign origin in four sheep in Vermont. Because of the >
potentially serious consequences of allowing the disease to spread to >
other livestock in the United States, it is necessary to seize and >
dispose of those flocks of sheep in Vermont that are affected with or >
exposed to the disease, and their germ plasm. The existence of the >
atypical TSE of foreign origin represents a threat to U.S. livestock. >
It constitutes a real danger to the national economy and a potential >
serious burden on interstate and foreign commerce. APHIS has >
insufficient funds to carry out the seizure and disposal of animals >
and germ plasm necessary to eliminate this disease risk. These funds >
would be used to compensate the owners of the animals and germ plasm >
for their seizure and disposal in accordance with 21 U.S.C. 134a. >
Therefore, in accordance with the provisions of the Act of September >
25, 1981, as amended (7 U.S.C. 147b), I declare that there is an >
emergency that threatens the livestock industry of this country and >
hereby authorize the transfer and use of such funds as may be >
necessary from appropriations or other funds available to agencies or >
corporations of the United States Department of Agriculture to seize >
and dispose of animals that are affected with or exposed to this TSE, >
and their germplasm, in accordance with 21 U.S.C. 134a. > > Dated: This
declaration of emergency shall become effective July 14, > 2000. Dan
Glickman, Secretary of Agriculture. [FR Doc. 00-18368 Filed > 7-19-00;
8:45 am] BILLING CODE 3410-34-P > > I was told that ; > > > --------
Original Message -------- > Subject: Re: hello Dr. Sutton...question
please...scrapie...TSS > Date: Thu, 20 May 2004 14:36:09 -0400 > From:
Jim.D.Rogers@aphis.usda.gov > To: flounder@wt.net > > > > Dear Mr.
Singeltary, > > The Western blot tests on these animals were completed
in April of this > year. That means that we can begin the mouse
inoculations. To get the > results of the Western blot tests, you will
need to submit a Freedom of > Information Act request through our FOIA
office. The FAX number there is > 301-734-5941. > > Have a nice day, > >
Jim Rogers > APHIS LPA > ========= > > > Dr. Detwiler, my question is,
why have these very important test been > delayed for so long when we
were told they were to have been started > some 2+ years ago? > > who
made this call to delay these very important test and why ? > > thank
you, > with kindest regards, > > Terry > > > Linda Detwiler wrote: > >>
######## Bovine Spongiform Encephalopathy >> ######### >> snip...
######### http://mailhost-alt.rz.uni-karlsruhe.de/warc/bse-l.html
########## WHAT ABOUT THE POTENTIAL FOR BSE IN SHEEP AND GOATS OR ANY OF
THE OTHER NEW ''ATYPICAL'' TSEs SHOWING UP? 02-Jun-04, 10:45 BSE IN
SHEEP CONTINGENCY PLAN - CONSULTATION LAUNCH Defra and the other UK
Agriculture and Rural Affairs Departments today launched a consultation
on the UK contingency plan on possible actions if BSE were confirmed in
sheep. http://www.wired-gov.net/WGLaunch.aspx?ARTCL=24789 The total
prevalence of scrapie in the USA is really unknown. USA SCRAPIE Infected
and Source Flocks; As of September 30, 2003, there were 50 scrapie
infected and source flocks (figure 3 ). There were 73 newly infected
flocks reported in FY 2003 (figure 4 ). In addition, 351 scrapie cases
were also confirmed and reported by the National Veterinary Services
Laboratories (NVSL) (figures 5 and 6 ). No case of scrapie in goats was
reported in FY 2003. The last case was confirmed in August 2002. New
infected and source flock numbers and the number of these flocks
released in FY 2003 are depicted in chart 4 . Sixty flocks, which is
equivalent to 82 percent of the new scrapie infected and source flocks
identified in FY 2003, were released or put on clean-up plans in FY
2003.
http://www.aphis.usda.gov/vs/nahps/scrapie/yearly_report/yearly-report.html
CWD USA Current Distribution of CWD among Captive Cervid Herds Map Image
Click on the Picture above to See a Larger Image Bullet Represents
captive elk herds that are currently CWD-positive. Bullet Represents
captive deer herds that are currently CWD-positive. Depopulated Captive
Cervid Herds Map Image Click on the Picture above to See a Larger Image
Bullet Represents CWD-positive captive elk herds that were depopulated
due to CWD. Bullet Represents CWD-positive captive deer herds that were
depopulated due to CWD. Current Distribution of Chronic Wasting Disease
in Free-Ranging Cervids Map Image Click on the Picture above to See a
Larger Image Bullet Represents counties in which CWD has been identified
in free-ranging cervids. Note that large counties in the western states
make the CWD area appear larger than actual extent. Refer to state
wildlife agencies (links on the State Information page) for more
detailed information on wildlife occurrances.
http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html DUE to the
new 'atypical' TSEs showing up, prohibiting the use of all mammalian and
poultry protein in ruminant feed, to prevent cross contamination, is the
only way to assure that CWD, Scrapie, BSE and all new 'atypical' TSEs
will not cross-contaminate. CATTLE have gone clinical with TSE as young
as 20 months, to only be concerned and to set regulations only for the
30 month and older cattle is not sufficient to prevent the spread of
this agent. The age limit should be 12 months; DEAD STOCK DOWNERS are of
major concern for TSEs. DUE not ignore the sub clinical TSE population.
TO change regulations and to only focus on the CNS (stumbling,
staggering and twitching cow), will further help spread this agent by
ignoring the younger documented cows that have been documented (as young
as 20 month, see documentation of these young cattle with BSE/TSE);
Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL
IMPORTS FROM CANADA [takes a few minutes to load]
https://web01.aphis.usda.gov/BSEcom.nsf/BSEFrameset?OpenFrameSet&Frame=BottomFrame&Src=_25t156hb3dtmisrjjconjcc9n6ph6ccr66oqjgdpo74qm6e1l68qjcp9hc4o30dhgckq34phfc8rjgoj16orjep9ic8o66c9i64s3achl6pi68cpg60r38eb675i3ujrgcln48rr3elmmarjk4p0nat3f8pp62rb5cg0_
THE BSE/TSE SUB CLINICAL COW Broken bones and such may be the first
signs of a sub clinical BSE/TSE cow; SUB CLINICAL PRION INFECTION
MRC-43-00 Issued: Monday, 28 August 2000 NEW EVIDENCE OF SUB-CLINICAL
PRION INFECTION: IMPORTANT RESEARCH FINDINGS RELEVANT TO CJD AND BSE A
team of researchers led by Professor John Collinge at the Medical
Research Council Prion Unit1 report today in the Proceedings of the
National Academy of Sciences, on new evidence for the existence of a
?sub-clinical? form of BSE in mice which was unknown until now. The
scientists took a closer look at what is known as the ?species barrier?
- the main protective factor which limits the ability of prions2 to jump
from one species to infect another. They found the mice had a
?sub-clinical? form of disease where they carried high levels of
infectivity but did not develop the clinical disease during their normal
lifespan. The idea that individuals can carry a disease and show no
clinical symptoms is not new. It is commonly seen in conventional
infectious diseases. Researchers tried to infect laboratory mice with
hamster prions3 called Sc237 and found that the mice showed no apparent
signs of disease. However, on closer inspection they found that the mice
had high levels of mouse prions in their brains. This was surprising
because it has always been assumed that hamster prions could not cause
the disease in mice, even when injected directly into the brain. In
addition the researchers showed that this new sub-clinical infection
could be easily passed on when injected into healthy mice and hamsters.
The height of the species barrier varies widely between different
combinations of animals and also varies with the type or strain of
prions. While some barriers are quite small (for instance BSE easily
infects mice), other combinations of strain and species show a seemingly
impenetrable barrier. Traditionally, the particular barrier studied here
was assumed to be robust. Professor John Collinge said: "These results
have a number of important implications. They suggest that we should
re-think how we measure species barriers in the laboratory, and that we
should not assume that just because one species appears resistant to a
strain of prions they have been exposed to, that they do not silently
carry the infection. This research raises the possibility, which has
been mentioned before, that apparently healthy cattle could harbour, but
never show signs of, BSE. "This is a timely and unexpected result,
increasing what we know about prion disease. These new findings have
important implications for those researching prion disease, those
responsible for preventing infected material getting into the food chain
and for those considering how best to safeguard health and reduce the
risk that theoretically, prion disease could be contracted through
medical and surgical procedures." ISSUED FRIDAY 25 AUGUST UNDER EMBARGO.
PLEASE NOTE THAT THE EMBARGO IS SET BY THE JOURNAL. FOR FURTHER
INFORMATION CONTACT THE MRC PRESS OFFICE ON 020 7637 6011 (OFFICE HOURS)
OR 07818 428297 OR 0385 774357 (OUT-OF-OFFICE-HOURS) OR PROFESSOR JOHN
COLLINGE ON 020 7594 3760. PLEASE NOTE THAT OWING TO TRAVEL COMMITMENTS
PROFESSOR COLLINGE WILL ONLY BE AVAILABLE UNTIL 16.30 ON FRIDAY 25
AUGUST AND CONTACTABLE AGAIN ON MONDAY 28 AUGUST VIA THE MRC PRESS
OFFICE. DR ANDREW HILL (A CO-AUTHOR ON THE PAPER) FROM THE DEPARTMENT OF
PATHOLOGY AT THE UNIVERSITY OF MELBOURNE WILL BE AVAILABLE ON 00 61 3
8344 3995 (DURING OFFICE HOURS) OR 00 61 3 9443 0009 (OUT-OF-OFFICE
HOURS). PLEASE NOTE THAT AUSTRALIA IS TEN HOURS AHEAD OF UK TIME. NOTES
FOR EDITORS Professor Collinge is a consultant neurologist and Director
of the newly formed MRC Prion Unit based at The Imperial College School
of Medicine at St Mary?s Hospital. He is also a member of the UK
Government?s Spongiform Encephalopathy Advisory Committee (SEAC). The
MRC prion unit is was set up in 1999, and its work includes molecular
genetic studies of human prion disease and transgenic modelling of human
prion diseases. Prions are unique infectious agents that cause fatal
brain diseases such as Creutzfeldt-Jakob disease (CJD) in humans and
scrapie and BSE (mad cow disease) in animals. In some circumstances
prions from one species of animals can infect another and it is clear
that BSE has done this to cause the disease variant CJD in the UK and
France. It remains unclear how large an epidemic of variant CJD will
occur over the years ahead. The strain of prion used here to infect the
mice is the Sc237 strain (also known as 263K) which infects hamsters,
and until now was assumed not to infect mice. This research was funded
by the Medical Research Council and Wellcome Trust. The Medical Research
Council (MRC) is a national organisation funded by the UK tax-payer. Its
business is medical research aimed at improving human health; everyone
stands to benefit from the outputs. The research it supports and the
scientists it trains meet the needs of the health services, the
pharmaceutical and other health-related industries and the academic
world. MRC has funded work which has led to some of the most significant
discoveries and achievements in medicine in the UK. About half of the
MRC?s expenditure of £345 million is invested in over 50 of its
Institutes and Units, where it employs its own research staff. The
remaining half goes in the form of grant support and training awards to
individuals and teams in universities and medical schools. The Wellcome
Trust is the world's largest medical research charity with a spend of
some £600 million in the current financial year 1999/2000. The Wellcome
Trust supports more than 5,000 researchers, at 400 locations, in 42
different countries to promote and foster research with the aim of
improving human and animal health. As well as funding major initiatives
in the public understanding of science, the Wellcome Trust is the
country's leading supporter of research into the history of medicine.
http://www.mrc.ac.uk/index/public_interest/public-press_office/public-press_releases_2000/public-mrc-43-00.htm
USDA/APHIS ET AL MUST GET BSE/TSE TESTING DONE CORRECTLY THE recent
findings of positive 'inconclusives' that turned up negative was not
only a nightmare to the consumer, but also to the farmers and industry
as well. Using Prionics or Bio-Rad or whatever rapid TSE test will never
eliminate the potential for human error. IF we look at the recent
discovery of the BSE in Switzerland in the Zoo Zebu, the testing they
perform would have eliminated this mix-up; Diagnosis: A. Laboratory
where diagnosis was made: Institute of Animal Neurology, University of
Bern (OIE Reference Laboratory for bovine spongiform encephalopathy). B.
Diagnostic tests used: - histology; - immunohistochemistry; - ELISA (two
different kits); - western blot. All tests gave positive results.
http://www.oie.int/eng/info/hebdo/AIS_38.HTM#Sec9 ALSO, if we look at
the USA BSE EMERGENCY RESPONSE PLAN, where it states; Subject: U.S.
Emergency Bovine Spongiform Encephalopathy Response Plan Summary Date:
Tue, 4 May 1999 18:25:12 -0500 From: "Terry S. Singeltary Sr." Reply-To:
BSEL To: BSEL snip... If additional tests do suggest a presumptive
diagnosis of BSE, an NVSL pathologist will hand carry the sample to the
United Kingdom for confirmation. It is at this critical point, when NVSL
suggests a diagnosis of BSE and is preparing to send the sample to the
United Kingdom, that this BSE Response Plan is initiated. The Plan
begins the preliminary notification from NVSL to APHIS. Preliminary
Notification The director of NVSL is responsible for immediately
notifying the APHIS, Veterinary Services (VS) deputy administrator when
tests suggest a presumptive diagnosis of BSE. Once NVSL has made a
presumptive diagnosis of BSE, APHIS and FSIS field activities will also
be initiated. APHIS will receive notification (either confirming or not
confirming NVSL's diagnosis) from the United Kingdom anywhere between 24
and 96 hours. (The international animal health community has recognized
the United Kingdom's Central Veterinary Laboratory {CVL} as the world's
reference laboratory for diagnosing BSE. Other countries, including
Belgium, France, Ireland, Luxembourg, the Netherlands, Portugal, and
Switzerland, have all sent samples to this lab to confirm their first
case of BSE). snip...end...TSS WHY is the UK not going to verify the
findings of BSE/TSE in tissue samples as the original BSE emergency
response plan told them too? I think that having several different rapid
TSE test kits (Prionics, Bio-Rad etc.) along with the IHC and finally
the OIE reference laboratory for confirmation is the best possible
answer. Prusiner et al have a test that is some 1,000 times more
sensitive and I only ponder why we are not using it? My fear is that
once testing becomes more sensitive, more tissue/organ will become known
to hold infectivity of some titre of the TSE agent. THEN we must ponder
if _accumulation_ may play a role? With the threat from new atypical
TSEs in many species and the real threat from iatrogenic CJD, the fact
that we do not yet know how these new 'atypical' phenotpyes will
transmit and how infectious there tissues may be, we must act now, we
cannot flounder any longer. Docket No. 03-080-1 -- USDA ISSUES PROPOSED
RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA [takes a few minutes to
load]
https://web01.aphis.usda.gov/BSEcom.nsf/BSEFrameset?OpenFrameSet&Frame=BottomFrame&Src=_25t156hb3dtmisrjjconjcc9n6ph6ccr66oqjgdpo74qm6e1l68qjcp9hc4o30dhgckq34phfc8rjgoj16orjep9ic8o66c9i64s3achl6pi68cpg60r38eb675i3ujrgcln48rr3elmmarjk4p0nat3f8pp62rb5cg0_
Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]
http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt
Docket Management Docket: 02N-0273 - Substances Prohibited From Use in
Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed Comment
Number: EC -10 Accepted - Volume 2
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html
PART 2
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html
PDF]Freas, William TSS SUBMISSION File Format: PDF/Adobe Acrobat - Page
1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary Sr.
[flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf
Asante/Collinge et al, 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;
http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm Docket
Management Docket: 96N-0417 - Current Good Manufacturing Practice in
Manufacturing, Packing, or Holding Dietary Ingredients a Comment Number:
EC -2 Accepted - Volume 7
http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm
[PDF] Appendices to PL107-9 Inter-agency Working Group Final Report 1-1
File Format: PDF/Adobe Acrobat - View as HTML Agent, Weapons of Mass
Destruction Operations Unit Federal Bureau of those who provided
comments in response to Docket No. ... Meager 8/18/01 Terry S.
Singeltary Sr ... www.aphis.usda.gov/lpa/pubs/pubs/PL107-9_Appen.pdf
Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION TO
DOCKET 2003N-0312]
http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt
# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of
2002; [TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] -
TSS 1/27/03 (0) Docket Management Docket: 02N-0276 - Bioterrorism
Preparedness; Registration of Food Facilities, Section 305 Comment
Number: EC-254 [TSS SUBMISSION]
http://www.fda.gov/ohrms/dockets/dockets/02n0276/02N-0276-EC-254.htm
Dockets Entered On October 2, 2003 Table of Contents, Docket #, Title,
1978N-0301, OTC External Analgesic Drug Products, ... EMC 7, Terry S.
Singeltary Sr. Vol #: 1, ...
www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm Daily
Dockets Entered on 02/05/03 DOCKETS ENTERED on 2/5/03. ... EMC 4 Terry
S. Singeltary Sr. Vol#: 2. ... Vol#: 1. 03N-0009 Federal Preemption of
State & Local Medical Device Requireme. ...
www.fda.gov/ohrms/dockets/dailys/03/Feb03/020503/020503.htm Docket
Management Docket: 02N-0370 - Neurological Devices; Classification of
Human Dura Mater Comment Number: EC -1 Accepted - Volume 1
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be11.html
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfe.html
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfc.html
Daily Dockets - 04/10/03 ... 00D-1662 Use of Xenotransplantation
Products in Humans. EMC 98 Terry S. Singeltary Sr. Vol#: 3. 01F ...
www.fda.gov/ohrms/dockets/dailys/03/Apr03/041003/041003.htm - 05-20-2003
- Cached 2003D-0186 Guidance for Industry: Use of Material From Deer and
Elk In Animal Feed EMC 1 Terry S. Singeltary Sr. Vol #: 1 --------
Original Message -------- Subject: DOCKET-- 03D-0186 -- FDA Issues Draft
Guidance on Use of Material >From Deer and Elk in Animal Feed;
Availability Date: Fri, 16 May 2003 11:47:37 -0500 From: "Terry S.
Singeltary Sr." To: fdadockets@oc.fda.gov Greetings FDA, i would kindly
like to comment on; Docket 03D-0186 FDA Issues Draft Guidance on Use of
Material From Deer and Elk in Animal Feed; Availability Several factors
on this apparent voluntary proposal disturbs me greatly, please allow me
to point them out; 1. MY first point is the failure of the partial
ruminant-to-ruminant feed ban of 8/4/97. this partial and voluntary feed
ban of some ruminant materials being fed back to cattle is terribly
flawed. without the _total_ and _mandatory_ ban of all ruminant
materials being fed back to ruminants including cattle, sheep, goat,
deer, elk and mink, chickens, fish (all farmed animals for human/animal
consumption), this half ass measure will fail terribly, as in the past
decades... 2. WHAT about sub-clinical TSE in deer and elk? with the
recent findings of deer fawns being infected with CWD, how many could
possibly be sub-clinically infected. until we have a rapid TSE test to
assure us that all deer/elk are free of disease (clinical and
sub-clinical), we must ban not only documented CWD infected deer/elk,
but healthy ones as well. it this is not done, they system will fail...
3. WE must ban not only CNS (SRMs specified risk materials), but ALL
tissues. recent new and old findings support infectivity in the rump or
ass muscle. wether it be low or high, accumulation will play a crucial
role in TSEs. 4. THERE are and have been for some time many TSEs in the
USA. TME in mink, Scrapie in Sheep and Goats, and unidentified TSE in
USA cattle. all this has been proven, but the TSE in USA cattle has been
totally ignored for decades. i will document this data below in my
references. 5. UNTIL we ban all ruminant by-products from being fed back
to ALL ruminants, until we rapid TSE test (not only deer/elk) but cattle
in sufficient numbers to find (1 million rapid TSE test in USA cattle
annually for 5 years), any partial measures such as the ones proposed
while ignoring sub-clinical TSEs and not rapid TSE testing cattle, not
closing down feed mills that continue to violate the FDA's BSE feed
regulation (21 CFR 589.2000) and not making freely available those
violations, will only continue to spread these TSE mad cow agents in the
USA. I am curious what we will call a phenotype in a species that is
mixed with who knows how many strains of scrapie, who knows what strain
or how many strains of TSE in USA cattle, and the CWD in deer and elk
(no telling how many strains there), but all of this has been rendered
for animal feeds in the USA for decades. it will get interesting once
someone starts looking in all species, including humans here in the USA,
but this has yet to happen... 6. IT is paramount that CJD be made
reportable in every state (especially ''sporadic'' cjd), and that a CJD
Questionnaire must be issued to every family of a victim of TSE. only
checking death certificates will not be sufficient. this has been proven
as well (see below HISTORY OF CJD -- CJD QUESTIONNAIRE) 7. WE must learn
from our past mistakes, not continue to make the same mistakes...
REFERENCES Six white-tailed deer fawns test positive for CWD MADISON --
Six fawns in the area of south central Wisconsin where chronic wasting
disease has been found in white-tailed deer have tested positive for the
disease, according to Department of Natural Resources wildlife health
officials. These are the youngest wild white-tailed deer detected with
chronic wasting disease (CWD) to date. Approximately 4,200 fawns,
defined as deer under 1 year of age, were sampled from the eradication
zone over the last year. The majority of fawns sampled were between the
ages of 5 to 9 months, though some were as young as 1 month. Two of the
six fawns with CWD detected were 5 to 6 months old. All six of the
positive fawns were taken from the core area of the CWD eradication zone
where the highest numbers of positive deer have been identified. snip...
http://www.dnr.state.wi.us/org/caer/ce/news/on/2003/on20030513.htm#art4
=================================================== Issued: Monday, 28
August 2000 NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT
RESEARCH FINDINGS RELEVANT TO CJD AND BSE A team of researchers led by
Professor John Collinge at the Medical Research Council Prion Unit1
report today in the Proceedings of the National Academy of Sciences, on
new evidence for the existence of a 'sub-clinical' form of BSE in mice
which was unknown until now. The scientists took a closer look at what
is known as the 'species barrier' - the main protective factor which
limits the ability of prions2 to jump from one species to infect
another. They found the mice had a 'sub-clinical' form of disease where
they carried high levels of infectivity but did not develop the clinical
disease during their normal lifespan. The idea that individuals can
carry a disease and show no clinical symptoms is not new. It is commonly
seen in conventional infectious diseases. Researchers tried to infect
laboratory mice with hamster prions3 called Sc237 and found that the
mice showed no apparent signs of disease. However, on closer inspection
they found that the mice had high levels of mouse prions in their
brains. This was surprising because it has always been assumed that
hamster prions could not cause the disease in mice, even when injected
directly into the brain. In addition the researchers showed that this
new sub-clinical infection could be easily passed on when injected into
healthy mice and hamsters. The height of the species barrier varies
widely between different combinations of animals and also varies with
the type or strain of prions. While some barriers are quite small (for
instance BSE easily infects mice), other combinations of strain and
species show a seemingly impenetrable barrier. Traditionally, the
particular barrier studied here was assumed to be robust. Professor John
Collinge said: "These results have a number of important implications.
They suggest that we should re-think how we measure species barriers in
the laboratory, and that we should not assume that just because one
species appears resistant to a strain of prions they have been exposed
to, that they do not silently carry the infection. This research raises
the possibility, which has been mentioned before, that apparently
healthy cattle could harbour, but never show signs of, BSE. "This is a
timely and unexpected result, increasing what we know about prion
disease. These new findings have important implications for those
researching prion disease, those responsible for preventing infected
material getting into the food chain and for those considering how best
to safeguard health and reduce the risk that theoretically, prion
disease could be contracted through medical and surgical procedures."
ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS
SET BY THE JOURNAL. FOR FURTHER INFORMATION CONTACT THE MRC PRESS OFFICE
ON 020 7637 6011 (OFFICE HOURS) OR 07818 428297 OR 0385 774357
(OUT-OF-OFFICE-HOURS) OR PROFESSOR JOHN COLLINGE ON 020 7594 3760.
PLEASE NOTE THAT OWING TO TRAVEL COMMITMENTS PROFESSOR COLLINGE WILL
ONLY BE AVAILABLE UNTIL 16.30 ON FRIDAY 25 AUGUST AND CONTACTABLE AGAIN
ON MONDAY 28 AUGUST VIA THE MRC PRESS OFFICE. DR ANDREW HILL (A
CO-AUTHOR ON THE PAPER) FROM THE DEPARTMENT OF PATHOLOGY AT THE
UNIVERSITY OF MELBOURNE WILL BE AVAILABLE ON 00 61 3 8344 3995 (DURING
OFFICE HOURS) OR 00 61 3 9443 0009 (OUT-OF-OFFICE HOURS). PLEASE NOTE
THAT AUSTRALIA IS TEN HOURS AHEAD OF UK TIME. NOTES FOR EDITORS
Professor Collinge is a consultant neurologist and Director of the newly
formed MRC Prion Unit based at The Imperial College School of Medicine
at St Mary's Hospital. He is also a member of the UK Government's
Spongiform Encephalopathy Advisory Committee (SEAC). The MRC prion unit
is was set up in 1999, and its work includes molecular genetic studies
of human prion disease and transgenic modelling of human prion diseases.
Prions are unique infectious agents that cause fatal brain diseases such
as Creutzfeldt-Jakob disease (CJD) in humans and scrapie and BSE (mad
cow disease) in animals. In some circumstances prions from one species
of animals can infect another and it is clear that BSE has done this to
cause the disease variant CJD in the UK and France. It remains unclear
how large an epidemic of variant CJD will occur over the years ahead.
The strain of prion used here to infect the mice is the Sc237 strain
(also known as 263K) which infects hamsters, and until now was assumed
not to infect mice. This research was funded by the Medical Research
Council and Wellcome Trust. The Medical Research Council (MRC) is a
national organisation funded by the UK tax-payer. Its business is
medical research aimed at improving human health; everyone stands to
benefit from the outputs. The research it supports and the scientists it
trains meet the needs of the health services, the pharmaceutical and
other health-related industries and the academic world. MRC has funded
work which has led to some of the most significant discoveries and
achievements in medicine in the UK. About half of the MRC's expenditure
of £345 million is invested in over 50 of its Institutes and Units,
where it employs its own research staff. The remaining half goes in the
form of grant support and training awards to individuals and teams in
universities and medical schools. The Wellcome Trust is the world's
largest medical research charity with a spend of some £600 million in
the current financial year 1999/2000. The Wellcome Trust supports more
than 5,000 researchers, at 400 locations, in 42 different countries to
promote and foster research with the aim of improving human and animal
health. As well as funding major initiatives in the public understanding
of science, the Wellcome Trust is the country's leading supporter of
research into the history of medicine. ©2002 Medical Research Council
Data Protection policy | Contact the MRC
http://www.mrc.ac.uk/index/public_interest/public-press_office/public-press_releases_2000/public-mrc-43-00.htm
====================================== Oral transmission and early
lymphoid tropism of chronic wasting disease PrPres in mule deer fawns
(Odocoileus hemionus ) Christina J. Sigurdson1, Elizabeth S. Williams2,
Michael W. Miller3, Terry R. Spraker1,4, Katherine I. O'Rourke5 and
Edward A. Hoover1 Department of Pathology, College of Veterinary
Medicine and Biomedical Sciences, Colorado State University, Fort
Collins, CO 80523- 1671, USA1 Department of Veterinary Sciences,
University of Wyoming, 1174 Snowy Range Road, University of Wyoming,
Laramie, WY 82070, USA 2 Colorado Division of Wildlife, Wildlife
Research Center, 317 West Prospect Road, Fort Collins, CO 80526-2097,
USA3 Colorado State University Veterinary Diagnostic Laboratory, 300
West Drake Road, Fort Collins, CO 80523-1671, USA4 Animal Disease
Research Unit, Agricultural Research Service, US Department of
Agriculture, 337 Bustad Hall, Washington State University, Pullman, WA
99164-7030, USA5 Author for correspondence: Edward Hoover.Fax +1 970 491
0523. e-mail ehoover@lamar.colostate.edu Mule deer fawns (Odocoileus
hemionus) were inoculated orally with a brain homogenate prepared from
mule deer with naturally occurring chronic wasting disease (CWD), a
prion-induced transmissible spongiform encephalopathy. Fawns were
necropsied and examined for PrP res, the abnormal prion protein isoform,
at 10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an
immunohistochemistry assay modified to enhance sensitivity. PrPres was
detected in alimentary-tract-associated lymphoid tissues (one or more of
the following: retropharyngeal lymph node, tonsil, Peyer's patch and
ileocaecal lymph node) as early as 42 days p.i. and in all fawns
examined thereafter (53 to 80 days p.i.). No PrPres staining was
detected in lymphoid tissue of three control fawns receiving a control
brain inoculum, nor was PrPres detectable in neural tissue of any fawn.
PrPres-specific staining was markedly enhanced by sequential tissue
treatment with formic acid, proteinase K and hydrated autoclaving prior
to immunohistochemical staining with monoclonal antibody F89/160.1.5.
These results indicate that CWD PrP res can be detected in lymphoid
tissues draining the alimentary tract within a few weeks after oral
exposure to infectious prions and may reflect the initial pathway of CWD
infection in deer. The rapid infection of deer fawns following exposure
by the most plausible natural route is consistent with the efficient
horizontal transmission of CWD in nature and enables accelerated studies
of transmission and pathogenesis in the native species. snip... These
results indicate that mule deer fawns develop detectable PrP res after
oral exposure to an inoculum containing CWD prions. In the earliest
post-exposure period, CWD PrPres was traced to the lymphoid tissues
draining the oral and intestinal mucosa (i.e. the retropharyngeal lymph
nodes, tonsil, ileal Peyer's patches and ileocaecal lymph nodes), which
probably received the highest initial exposure to the inoculum. Hadlow
et al. (1982) demonstrated scrapie agent in the tonsil, retropharyngeal
and mesenteric lymph nodes, ileum and spleen in a 10-month-old naturally
infected lamb by mouse bioassay. Eight of nine sheep had infectivity in
the retropharyngeal lymph node. He concluded that the tissue
distribution suggested primary infection via the gastrointestinal tract.
The tissue distribution of PrPres in the early stages of infection in
the fawns is strikingly similar to that seen in naturally infected sheep
with scrapie. These findings support oral exposure as a natural route of
CWD infection in deer and support oral inoculation as a reasonable
exposure route for experimental studies of CWD. snip...
http://vir.sgmjournals.org/cgi/content/full/80/10/2757
=================================== now, just what is in that deer feed?
_ANIMAL PROTEIN_ Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 -0700 From: "Terry S. Singeltary Sr."
Reply-To: BSE-L To: BSE-L 8420-20.5% Antler Developer For Deer and Game
in the wild Guaranteed Analysis Ingredients / Products Feeding
Directions snip... _animal protein_ http://www.surefed.com/deer.htm
BODE'S GAME FEED SUPPLEMENT #400 A RATION FOR DEER NET WEIGHT 50 POUNDS
22.6 KG. snip... _animal protein_ http://www.bodefeed.com/prod7.htm
Ingredients Grain Products, Plant Protein Products, Processed Grain
By-Products, Forage Products, Roughage Products 15%, Molasses Products,
__Animal Protein Products__, Monocalcium Phosphate, Dicalcium Pyosphate,
Salt, Calcium Carbonate, Vitamin A Acetate with D-activated Animal
Sterol (source of Vitamin D3), Vitamin E Supplement, Vitamin B12
Supplement, Riboflavin Supplement, Niacin Supplement, Calcium
Panothenate, Choline Chloride, Folic Acid, Menadione Soduim Bisulfite
Complex, Pyridoxine Hydorchloride, Thiamine Mononitrate, d-Biotin,
Manganous Oxide, Zinc Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt
Carbonate, Dried Sacchoromyces Berevisiae Fermentation Solubles,
Cellulose gum, Artificial Flavors added.
http://www.bodefeed.com/prod6.htm ===================================
MORE ANIMAL PROTEIN PRODUCTS FOR DEER Bode's #1 Game Pellets A RATION
FOR DEER F3153 GUARANTEED ANALYSIS Crude Protein (Min) 16% Crude Fat
(Min) 2.0% Crude Fiber (Max) 19% Calcium (Ca) (Min) 1.25% Calcium (Ca)
(Max) 1.75% Phosphorus (P) (Min) 1.0% Salt (Min) .30% Salt (Max) .70%
Ingredients Grain Products, Plant Protein Products, Processed Grain
By-Products, Forage Products, Roughage Products, 15% Molasses Products,
__Animal Protein Products__, Monocalcium Phosphate, Dicalcium Phosphate,
Salt, Calcium Carbonate, Vitamin A Acetate with D-activated Animal
Sterol (source of Vitamin D3) Vitamin E Supplement, Vitamin B12
Supplement, Roboflavin Supplement, Niacin Supplement, Calcium
Pantothenate, Choline Chloride, Folic Acid, Menadione Sodium Bisulfite
Complex, Pyridoxine Hydrochloride, Thiamine Mononitrate, e - Biotin,
Manganous Oxide, Zinc Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt
Carbonate, Dried Saccharyomyces Cerevisiae Fermentation Solubles,
Cellulose gum, Artificial Flavors added. FEEDING DIRECTIONS Feed as
Creep Feed with Normal Diet http://www.bodefeed.com/prod8.htm
INGREDIENTS Grain Products, Roughage Products (not more than 35%),
Processed Grain By-Products, Plant Protein Products, Forage Products,
__Animal Protein Products__, L-Lysine, Calcium Carbonate, Salt,
Monocalcium/Dicalcium Phosphate, Yeast Culture, Magnesium Oxide, Cobalt
Carbonate, Basic Copper Chloride, Manganese Sulfate, Manganous Oxide,
Sodium Selenite, Zinc Sulfate, Zinc Oxide, Sodium Selenite, Potassium
Iodide, Ethylenediamine Dihydriodide, Vitamin E Supplement, Vitamin A
Supplement, Vitamin D3 Supplement, Mineral Oil, Mold Inhibitor, Calcium
Lignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium Bisulfite
Complex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid,
Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate DIRECTIONS
FOR USE Deer Builder Pellets is designed to be fed to deer under range
conditions or deer that require higher levels of protein. Feed to deer
during gestation, fawning, lactation, antler growth and pre-rut, all
phases which require a higher level of nutrition. Provide adequate
amounts of good quality roughage and fresh water at all times.
http://www.profilenutrition.com/Products/Specialty/deer_builder_pellets.html
=================================================== DEPARTMENT OF HEALTH
& HUMAN SERVICES PUBLIC HEALTH SERVICE FOOD AND DRUG ADMINISTRATION
April 9, 2001 WARNING LETTER 01-PHI-12 CERTIFIED MAIL RETURN RECEIPT
REQUESTED Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O.
Box 117 Sandy Lake, PA 16145 PHILADELPHIA DISTRICT Tel: 215-597-4390
Dear Mr. Raymond: Food and Drug Administration Investigator Gregory E.
Beichner conducted an inspection of your animal feed manufacturing
operation, located in Sandy Lake, Pennsylvania, on March 23, 2001, and
determined that your firm manufactures animal feeds including feeds
containing prohibited materials. The inspection found significant
deviations from the requirements set forth in Title 21, code of Federal
Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant
Feed. The regulation is intended to prevent the establishment and
amplification of Bovine Spongiform Encephalopathy (BSE) . Such
deviations cause products being manufactured at this facility to be
misbranded within the meaning of Section 403(f), of the Federal Food,
Drug, and Cosmetic Act (the Act). Our investigation found failure to
label your swine feed with the required cautionary statement "Do Not
Feed to cattle or other Ruminants" The FDA suggests that the statement
be distinguished by different type-size or color or other means of
highlighting the statement so that it is easily noticed by a purchaser.
In addition, we note that you are using approximately 140 pounds of
cracked corn to flush your mixer used in the manufacture of animal feeds
containing prohibited material. This flushed material is fed to wild
game including deer, a ruminant animal. Feed material which may
potentially contain prohibited material should not be fed to ruminant
animals which may become part of the food chain. The above is not
intended to be an all-inclusive list of deviations from the regulations.
As a manufacturer of materials intended for animal feed use, you are
responsible for assuring that your overall operation and the products
you manufacture and distribute are in compliance with the law. We have
enclosed a copy of FDA's Small Entity Compliance Guide to assist you
with complying with the regulation... blah, blah, blah...
http://www.fda.gov/foi/warning_letters/g1115d.pdf
================================== snip... posted here;
http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In
Animal Feed EMC 7 Terry S. Singeltary Sr. Vol #: 1 2003D-0186 Guidance
for Industry: Use of Material From Deer and Elk In Animal Feed EMC 7
Terry S. Singeltary Sr. Vol #: 1
http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm
Chronic Wasting Disease and Potential Transmission to Humans Ermias D.
Belay,*Comments Ryan A. Maddox,* Elizabeth S. Williams, Michael W.
Miller,! Pierluigi Gambetti,§ and Lawrence B. Schonberger* *Centers for
Disease Control and Prevention, Atlanta, Georgia, USA; University of
Wyoming, Laramie, Wyoming, USA; !Colorado Division of Wildlife, Fort
Collins, Colorado, USA; and §Case Western Reserve University, Cleveland,
Ohio, USA Suggested citation for this article: Belay ED, Maddox RA,
Williams ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting
disease and potential transmission to humans. Emerg Infect Dis [serial
on the Internet]. 2004 Jun [date cited]. Available from:
http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm
------------------------------------------------------------------------
Chronic wasting disease (CWD) of deer and elk is endemic in a tri-corner
area of Colorado, Wyoming, and Nebraska, and new foci of CWD have been
detected in other parts of the United States. Although detection in some
areas may be related to increased surveillance, introduction of CWD due
to translocation or natural migration of animals may account for some
new foci of infection. Increasing spread of CWD has raised concerns
about the potential for increasing human exposure to the CWD agent. The
foodborne transmission of bovine spongiform encephalopathy to humans
indicates that the species barrier may not completely protect humans
from animal prion diseases. Conversion of human prion protein by
CWD-associated prions has been demonstrated in an in vitro cell-free
experiment, but limited investigations have not identified strong
evidence for CWD transmission to humans. More epidemiologic and
laboratory studies are needed to monitor the possibility of such
transmissions. snip... Transmission to Other Animals Concerns have been
raised about the possible transmission of the CWD agent to domestic
animals, such as cattle and sheep, which may come in contact with
infected deer and elk or CWD-contaminated environments. If such
transmissions were to occur, they would potentially increase the extent
and frequency of human exposure to the CWD agent. In addition, passage
of the agent through a secondary host could alter its infectious
properties, increasing its potential for becoming more pathogenic to
humans. This phenomenon may have occurred with BSE when a strain of
scrapie, a possible original source of the BSE outbreak, changed its
pathogenic properties for humans after infecting cattle. However, the
exact origin of BSE remains unknown. Although CWD does not appear to
occur naturally outside the cervid family, it has been transmitted
experimentally by intracerebral injection to a number of animals,
including laboratory mice, ferrets, mink, squirrel monkeys, and goats (1
,26 ). In an experimental study, the CWD agent was transmitted to 3 of
13 intracerebrally injected cattle after an incubation period of 22 to
27 months (27 ). The susceptibility of cattle intracerebrally challenged
with the agent of this disease was substantially less than that observed
after intracerebral scrapie challenge: nine of nine cattle succumbed to
scrapie challenge after intracerebral injection (28 ). In ongoing
experimental studies, after >6 years of observation, no prion disease
has developed in 11 cattle orally challenged with the CWD agent or 24
cattle living with infected deer herds (E.S. Williams and M.W. Miller,
unpub. data) (1 ). In addition, domestic cattle, sheep, and goat
residing in research facilities in close contact with infected cervids
did not develop a prion disease. [PLEASE NOTE, THIS HAS BEEN UPDATED TO
AN ADDITIONAL 2 COWS AND ONE SHEEP, making the total transmission of CWD
to cattle at 5 and one transmission of CWD to one sheep, MILLER ET AL
BSE-L...TSS] Conclusions The lack of evidence of a link between CWD
transmission and unusual cases of CJD, despite several epidemiologic
investigations, and the absence of an increase in CJD incidence in
Colorado and Wyoming suggest that the risk, if any, of transmission of
CWD to humans is low. Although the in vitro studies indicating
inefficient conversion of human prion protein by CWD-associated prions
raise the possibility of low-level transmission of CWD to humans, no
human cases of prion disease with strong evidence of a link with CWD
have been identified. However, the transmission of BSE to humans and the
resulting vCJD indicate that, provided sufficient exposure, the species
barrier may not completely protect humans from animal prion diseases.
Because CWD has occurred in a limited geographic area for decades, an
adequate number of people may not have been exposed to the CWD agent to
result in a clinically recognizable human disease. The level and
frequency of human exposure to the CWD agent may increase with the
spread of CWD in the United States. Because the number of studies
seeking evidence for CWD transmission to humans is limited, more
epidemiologic and laboratory studies should be conducted to monitor the
possibility of such transmissions. Studies involving transgenic mice
expressing human and cervid prion protein are in progress to further
assess the potential for the CWD agent to cause human disease.
Epidemiologic studies have also been initiated to identify human cases
of prion disease among persons with an increased risk for exposure to
potentially CWD-infected deer or elk meat (47 ). If such cases are
identified, laboratory data showing similarities of the etiologic agent
to that of the CWD agent would strengthen the conclusion for a causal
link. Surveillance for human prion diseases, particularly in areas where
CWD has been detected, remains important to effectively monitor the
possible transmission of CWD to humans. Because of the long incubation
period associated with prion diseases, convincing negative results from
epidemiologic and experimental laboratory studies would likely require
years of follow-up. In the meantime, to minimize the risk for exposure
to the CWD agent, hunters should consult with their state wildlife
agencies to identify areas where CWD occurs and continue to follow
advice provided by public health and wildlife agencies. Hunters should
avoid eating meat from deer and elk that look sick or test positive for
CWD. They should wear gloves when field-dressing carcasses, bone-out the
meat from the animal, and minimize handling of brain and spinal cord
tissues. As a precaution, hunters should avoid eating deer and elk
tissues known to harbor the CWD agent (e.g., brain, spinal cord, eyes,
spleen, tonsils, lymph nodes) from areas where CWD has been identified.
snip... see full text ;
http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm Diagnosis and
Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001;
285: 733-734.
http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States Email Terry S. Singeltary: flounder@wt.net
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?
http://www.neurology.org/cgi/eletters/60/2/176#535 BRITISH MEDICAL
JOURNAL http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2
http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1 IN SHORT, we have
floundered to long in the regulation of human/animal TSEs. EACH day
longer, more and more people will become exposed. YOU can step up to the
plate and act now, forget about corporate/political interest, act in the
best of public health, with the available science to date (it's all
there), or you can pay later. AT what cost you ask, depends which loved
one you loose to this agent. THIS goes far beyond the bad hamburger.
85%+ of all CJD (sporadic), did not just happen. sporadic CJD simply
means CJD from unknown route and source of agent, and we have many of
both right here in the USA. What phenotype is anyone's guess? ALL SRM
must be removed. ALL animals for human/animal consumption must be tested
for TSE. ALL human TSEs must be made reportable Nationally and
Internationally. with CJD/TSE questionnaire asking real questions as to
route and source of agent. THIS must pertain to all ages! CJD WATCH
http://www.fortunecity.com/healthclub/cpr/349/part1cjd.htm CJD Watch
message board http://disc.server.com/Indices/167318.html TERRY S.
SINGELTARY SR. P.O. BOX 42 BACLIFF, TEXAS 77518
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