Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (TSS SUBMISSION)

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From: TSS (216-119-143-167.ipset23.wt.net)
Subject: Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (TSS SUBMISSION)
Date: July 11, 2004 at 7:56 pm PST

-------- 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]

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.

In addition the researchers showed that this new sub-clinical infection
could be easily passed on when injected into healthy mice and hamsters.

ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS
SET BY THE JOURNAL.

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.

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 Â£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 Â£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

======================================

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

CJD WATCH

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