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From: TSS ()
Subject: Prion disease found lurking in deer muscle
Date: January 26, 2006 at 11:44 am PST


Prion disease found lurking in deer muscle
19:00 26 January 2006
NewScientist.com news service
Debora MacKenzie

The infectious prions that cause Chronic Wasting Disease, an infection similar to BSE that afflicts North American deer and elk have been found in the parts of the animals that people eat. No one knows if CWD can jump to humans, but if it does hunters in affected areas might be at risk.

CWD was first diagnosed as a spongiform encephalopathy in captive deer and elk in Colorado in the 1970s, and in wild deer and elk in the region in the 1980s. But in the 1990s it spread widely within the elk farming industry, jumped to wild deer, and now affects two provinces of Canada and 13 US states.

Like the related sheep disease scrapie – though unlike BSE – CWD spreads from animal to animal, says Glenn Telling of the University of Kentucky at Lexington, US. Deer housed with infected animals, or fed infected brain experimentally, contract the disease.

Because of this there are fears that the CWD prion might be distributed widely in the deer’s tissues – as scrapie is in sheep. Efforts to find the infectious prion in the muscle of infected animals, by seeing whether antibodies to the prion could find any and bind on, have previously failed.

But Telling’s lab has now shown that diseased prions can reside in muscle of deer infected with CWD, by using transgenic mice.

Transgenic mice
The team replaced the gene for the normal mouse version of the prion protein with the normal gene from deer, so the mice made the normal, healthy deer protein. They then injected the mouse brains with tissue from infected deer. Twelve to 18 months later, the mice developed encephalopathy.

Tissues from both the infected deers' brains and thigh muscle caused disease. Muscle took slightly longer to cause disease than brain tissue, showing it had slightly less prion.

“We don’t know that it is transmitted in the wild by animals eating muscle from infected animals,” cautions Telling. “We now have to see where else the prion might be,” including saliva and even excrement, using more transgenic mice.

Brain warnings
“Because we tested deer that were already ill,” he told New Scientist, “we don’t know what the distribution of prion is in animals that are still incubating the disease.” Hunters have been warned by wildlife agencies not to kill and eat obviously ill animals, but an animal not yet showing signs of the disease might still carry the abnormal prion, albeit less of it.

It is also unknown whether people can catch encephalopathy by eating CWD-infected meat, as they can from eating BSE-tainted meat. Anecdotal reports that hunters develop the human prion disease CJD in unusual numbers have never been confirmed. State officials have issued warnings to hunters not to eat brain or spinal cord – the tissues most affected.

“If I were a hunter I would be cautious about eating deer in areas affected,” says Telling. But he notes that not much testing of wildlife has been done, and it is not clear how prevalent the infection is.

Journal reference: Science (DOI: 10.1126/science.1122864)

http://www.newscientist.com/article.ns?id=dn8638

-------- Original Message --------
Subject: BSE IN NON-NEURAL TISSUE ???
Date: Wed, 6 Oct 2004 12:27:10 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@UNI-KARLSRUHE.DE


##################### Bovine Spongiform Encephalopathy #####################[PDF] ACGM Compendium of Guidance, Part 2a Annex III, Additional ...FileFormat: PDF/Adobe Acrobat - View as HTML... of the agents associated with BSE and other ... example, may maketransmission to neural tissues more ... Work involving non-pathogenichost micro-organisms containing ...www.hse.gov.uk/infection/gmo/acgm/acgmcomp/2a3.pdfsnip...26 (4 of 14)Implications for health issuessnip...IN field cases of BSE, infectivity in 'peripheral' (i.e. non-CNS)tissues is lower than in scrapie to the extent of being undetectablein mouse bioassay (129). In cattle experimentally infected by the oralroute, infectivity in the lymphoid tissues of BSE-infected cattle has been_impossible_ to determine due to lack of a sufficiently sensitiveinfectivity test. Responses may arise from ongoing cattle-to-cattleinoculation experiments as well as from novel, more sensitivebiochemical tests (114). However, the fact that with BSE, the CNS-peripheral tissue differential is higher than that found in sheep scrapieis important for decision takers who apply the worst-case scenerio...snip...http://www.oie.int/eng/publicat/rt/2201/3.%20Lasmezas.pdfGreetings list members,I am most anxious to see what studies in this day and age(much more sensitive) and with the new phenotypes of TSEshowing up in the bovine (not that BSE will not show up inthe non-neural tissue once looked at again with better testing),they really have no idea.THE TSEs''not least whether it is transmissible to primates(133)''(please note CWD has transmitted to primate, cattle and sheep byinoculation...TSS)http://www.oie.int/eng/publicat/rt/2201/3.%20Lasmezas.pdfeverytime there is a study that shows somethingthey do not want (as in the case with sporadic CJD and blood Transmissionof Creutzfeldt-Jakob Disease from Blood and Urine Into Mice The Lancet,November 9, 1985 JUN TATEISHI et al;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Retrieve&list_uids=2865558&dopt=Citationthey just claim that the testing protocol had been tainted or some stufflikethat. AS the case of the studies of scrapie and muscle tissue long agoby Pattison et al;J69CVO BSE 1 5SCRAPIE AGENT IN MUSCLE - PATTISON I A (1990) VETERINARY RECORD, 20JANUARY 1990, p.68Background1 Dr Pattison, a retired but eminent worker on scrapie for many years inthe AFRC, has pointed out that in one of his experimental studies ofscrapie in goats he found scrapie agent in the biceps femoris (rump)muscle of one animal with clinical disease but not in 2 others withclinical disease and in none with pre-clinical disease. MAFF have basedtheir policy on BSE in regard to meat (beef) on the results of studiesof natural scrapie (ie disease occurring under farm conditions) in bothsheep and goats by Hadlow 1979, 80, 81.Other Infectivity Studies2. These studies on 52 animals by equally eminent scrapie workers(Hadlow et al) revealed no evidence whatever of infectivity in skeletalmuscle from these natural cases either in the pre-clinical or evenclinical stages of disease.It is clear that the pathogenesis of experimental (Pattison) and natural(Hadlow) scrapie may be different and it was therefore considered wiseto base present policy on knowledge of the natural disease.3. Pattison exposed his 14 goats to intracerebral inoculation of thricepassaged scrapie virus (in goats). This may have resulted in strainselection and/or mutation of the natural agent. In contrast Hadlow'sstudy involved natural strains (probably multiple) in a flock with ahigh incidence of disease in which exposure would almost certainly havebeen by the mouth.4. The fact that Hadlow identified no infectivity in muscle by mouseinoculation (whereas some other tissues not normally consumed haddetectable infectivifcy) shows that cross contamination of his tissuesdid not occur. Pattison's experiments were reported about 20 yearsearlier when much less was known about Scrapie. In the interveningperiod the knowledge available to Hadlow on the insensitivity of scrapieagent to heat became available. There is therefore at least thepossibility that Pattison's instruments were not sterilised effectively,thus possibly giving the false positive result for muscle.5. Pattison used a more sensitive model for the detection ofinfectivifcy, namely goats, whereas Hadlow used mice ie necessitatingcrossing the species barrier and possibly reducing the test sensitivity.90/1.19/9.1CVO BSE 1 56. In regard to the choice of species for agent assay, mice (Hadlow),these would be guaranteed free of pre-existing Scrapie infection.Pattison could offer no such guarantee that this was the case in theanimal to which muscle was passaged and disease could have developedfrom exposure from a source other than muscle.7. Pattison did not report that his recipient animals, including the oneinoculated with muscle, were examined by histopathology to confirm thepresence of disease. This is a significant deficit. Clinical diagnosisalone is not acceptable as adequate evidence for the existence of scrapie.8. Even in Pattison's studies only in 1 out of 14 goats was infectivitydetected in muscle and that was in a CLINICAL case. In BSE all clinicalcases are notified and do not enter any food chain.9. The last paragraph of Pattison's letter is illogical. Furthermore,this is no evidence whatsoever that scrapie or BSE is a danger to man.W A WATSON 19 January 1990Private Offices Mr K C Meldrum Mrs E Attridge Mr R Lowson Ms L Austin MrR Bradley90/1.19/9.2http://www.bseinquiry.gov.uk/files/yb/1990/01/19009001.pdfCOURSE this was blown smooth out of the water with moresensitve testing recently;EMBO reports AOP Published online: 11 April 2003 Widespread PrPScaccumulation in muscles of hamsters orally infected with scrapie AchimThomzig, Christine Kratzel, Gudrun Lenz, Dominique KrĂĽger & MichaelBeekes Robert Koch-Institut, P26, Nordufer 20, D-13353 Berlin, GermanyReceived 13 February 2003; Accepted 13 March 2003; Published online 11April 2003.Abstract :Scrapie, bovine spongiform encephalopathy and chronic wasting diseaseare orally communicable, transmissible spongiform encephalopathies(TSEs). As zoonotic transmissions of TSE agents may pose a risk to humanhealth, the identification of reservoirs for infectivity in animaltissues and their exclusion from human consumption has become a matterof great importance for consumer protection. In this study, a variety ofmuscles from hamsters that were orally challenged with scrapie wasscreened for the presence of a molecular marker for TSE infection, PrPSc(the pathological isoform of the prion protein PrP). Sensitive westernblotting revealed consistent PrPSc accumulation in skeletal muscles fromforelimb and hindlimb, head, back and shoulder, and in tongue.Previously, our animal model has provided substantial baselineinformation about the peripheral routing of infection in naturallyoccurring and orally acquired ruminant TSEs. Therefore, the findingsdescribed here highlight further the necessity to investigate thoroughlywhether muscles of TSE-infected sheep, cattle, elk and deer containinfectious agents.http://www.emboreports.org/Prions in skeletal musclePatrick J. Bosque*,dagger ,Dagger , Chongsuk Ryou*, Glenn Telling*,§,David Peretz*,dagger , Giuseppe Legname*,dagger , Stephen J.DeArmond*,dagger ,¶, and Stanley B. Prusiner*,dagger ,||,*** Institute for Neurodegenerative Diseases and Departments of daggerNeurology, ¶ Pathology, and || Biochemistry and Biophysics, Universityof California, San Francisco, CA 94143Contributed by Stanley B. Prusiner, December 28, 2001Considerable evidence argues that consumption of beef products fromcattle infected with bovine spongiform encephalopathy (BSE) prionscauses new variant Creutzfeldt-Jakob disease. In an effort to preventnew variant Creutzfeldt-Jakob disease, certain "specified offals,"including neural and lymphatic tissues, thought to contain high titersof prions have been excluded from foods destined for human consumption[Phillips, N. A., Bridgeman, J. & Ferguson-Smith, M. (2000) in The BSEInquiry (Stationery Office, London), Vol. 6, pp. 413-451]. Here wereport that mouse skeletal muscle can propagate prions and accumulatesubstantial titers of these pathogens. We found both high prion titersand the disease-causing isoform of the prion protein (PrPSc) in theskeletal muscle of wild-type mice inoculated with either the Me7 orRocky Mountain Laboratory strain of murine prions. Particular musclesaccumulated distinct levels of PrPSc, with the highest levels observedin muscle from the hind limb. To determine whether prions are producedor merely accumulate intramuscularly, we established transgenic miceexpressing either mouse or Syrian hamster PrP exclusively in muscle.Inoculating these mice intramuscularly with prions resulted in theformation of high titers of nascent prions in muscle. In contrast,inoculating mice in which PrP expression was targeted to hepatocytesresulted in low prion titers. Our data demonstrate that factors inaddition to the amount of PrP expressed determine the tropism of prionsfor certain tissues. That some muscles are intrinsically capable ofaccumulating substantial titers of prions is of particular concern.Because significant dietary exposure to prions might occur through theconsumption of meat, even if it is largely free of neural and lymphatictissue, a comprehensive effort to map the distribution of prions in themuscle of infected livestock is needed. Furthermore, muscle may providea readily biopsied tissue from which to diagnose prion disease inasymptomatic animals and even humans. Dagger Present address: Departmentof Medicine, Denver Health Medical Center, Denver, CO 80204.§ Present address: Department of Microbiology and Immunology, Universityof Kentucky, Lexington, KY 40536-0230.** To whom reprint requests should be addressed. E-mail: vann@cgl.ucsf.edu.www.pnas.org/cgi/doi/10.1073/pnas.052707499http://www.pnas.org/cgi/content/abstract/99/6/3812?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=prusiner&author2=prusiner&titleabstract=prions+meat+tissue+mice&fulltext=prions+meat+tissue+mice&searchid=1024346978866_6016&stored_search=&FIRSTINDEX=0&fdate=1/1/2002FULL TEXT;http://www.pnas.org/cgi/content/full/99/6/3812?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=prusiner&author2=prusiner&titleabstract=prions+meat+tissue+mice&fulltext=prions+meat+tissue+mice&searchid=1050249844061_1953&stored_search=&FIRSTINDEX=0&fdate=1/1/2002http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=11904434http://www.unizh.ch/pathol/neuropathologie/d/pdf_pub01/AguzziA_et_al_2001_Prions_health_scare___NatReviews2_118-126.pdfNOW, the most frightening findings of late are these findings that;Extraneural Pathologic Prion Protein in Sporadic Creutzfeldt ¬Jakob DiseaseMarkus Glatzel, M.D., Eugenio Abela, Manuela Maissen, M.S., and AdrianoAguzzi, M.D., Ph.D.snip...Conclusions Using sensitive techniques, we identified extraneuraldepositionof PrPSc in spleen and muscle samples from approximately one third ofpatientswho died with sporadic Creutzfeldt ¬Jakob disease. Extraneural PrPScappearsto correlate with a long duration of disease.http://content.nejm.org/cgi/content/short/349/19/1812?query=TOCTHESE findings above by Aguzzi et al have major implications on themedical andsurgical arena...kind regards,terry################# BSE-L-subscribe-request@uni-karlsruhe.de #################


Content-Type: text/plain; charset=ISO-8859-1
Message-ID:
Date: Mon, 29 Dec 2003 19:26:39 +0100
Reply-To: Bovine Spongiform Encephalopathy
Sender: Bovine Spongiform Encephalopathy
From: TSS
Subject: WIDESPREAD ACCUMULATION IN MUSCLES OF HAMSTERS ORALLY INFECTED
WITH SCRAPIE (other studies)


######## Bovine Spongiform Encephalopathy #########

Greeings List Members,

i am sure most has been watching this 3 ring circus with Bozo
himself leading the bunch. if it was not so serious it would be
most comical. has not anyone in the USA Gov Scientist read any
of these studies. how many studies have been with BSE and muscle?
how many studies have been done with these new phenotypes of BSE
in cattle in France, Italy and Japan? has there been testing
with these phenotypes? All the Feds seem to be doing is running
strictly on 'fear-fact-control' and to hell science. they would
rather just spew out half truths and some flat out lies. save the
industry at all cost. why do they not mention these studies below?
all we hear about is the 20,000+ cattle tested last year, but they
fail to tell you that only some 57,000+ cattle have ever been tested
in the USA since the inception of the BSE surveillance program began
some 13 or 14 YEARS AGO for Pete's sake, no they dont mention this.
nor do they mention the sporadic CJD and the findings from Asante/Collinge
et al that BSE transmission to the 129-methionine genotype can lead
to an alternate phenotype which is indistinguishable from type 2 PrPSc,
the commonest sporadic CJD. NO, they would rather feed the public
half-truths and lies...TSS


EMBO reports AOP Published online: 11 April 2003 Widespread PrPSc
accumulation in muscles of hamsters orally infected with scrapie Achim
Thomzig, Christine Kratzel, Gudrun Lenz, Dominique KrĂĽger & Michael
Beekes Robert Koch-Institut, P26, Nordufer 20, D-13353 Berlin, Germany

Received 13 February 2003; Accepted 13 March 2003; Published online 11
April 2003.

Abstract :

Scrapie, bovine spongiform encephalopathy and chronic wasting disease
are orally communicable, transmissible spongiform encephalopathies
(TSEs). As zoonotic transmissions of TSE agents may pose a risk to human
health, the identification of reservoirs for infectivity in animal
tissues and their exclusion from human consumption has become a matter
of great importance for consumer protection. In this study, a variety of
muscles from hamsters that were orally challenged with scrapie was
screened for the presence of a molecular marker for TSE infection, PrPSc
(the pathological isoform of the prion protein PrP). Sensitive western
blotting revealed consistent PrPSc accumulation in skeletal muscles from
forelimb and hindlimb, head, back and shoulder, and in tongue.
Previously, our animal model has provided substantial baseline
information about the peripheral routing of infection in naturally
occurring and orally acquired ruminant TSEs. Therefore, the findings
described here highlight further the necessity to investigate thoroughly
whether muscles of TSE-infected sheep, cattle, elk and deer contain
infectious agents.

http://www.emboreports.org/

some previous data on TSE in muscle;

J69

CVO BSE 1 5

SCRAPIE AGENT IN MUSCLE - PATTISON I A (1990) VETERINARY RECORD, 20
JANUARY 1990, p.68

Background

1 Dr Pattison, a retired but eminent worker on scrapie for many years in
the AFRC, has pointed out that in one of his experimental studies of
scrapie in goats he found scrapie agent in the biceps femoris (rump)
muscle of one animal with clinical disease but not in 2 others with
clinical disease and in none with pre-clinical disease. MAFF have based
their policy on BSE in regard to meat (beef) on the results of studies
of natural scrapie (ie disease occurring under farm conditions) in both
sheep and goats by Hadlow 1979, 80, 81.

Other Infectivity Studies

2. These studies on 52 animals by equally eminent scrapie workers
(Hadlow et al) revealed no evidence whatever of infectivity in skeletal
muscle from these natural cases either in the pre-clinical or even
clinical stages of disease.

It is clear that the pathogenesis of experimental (Pattison) and natural
(Hadlow) scrapie may be different and it was therefore considered wise
to base present policy on knowledge of the natural disease.

3. Pattison exposed his 14 goats to intracerebral inoculation of thrice
passaged scrapie virus (in goats). This may have resulted in strain
selection and/or mutation of the natural agent. In contrast Hadlow's
study involved natural strains (probably multiple) in a flock with a
high incidence of disease in which exposure would almost certainly have
been by the mouth.

4. The fact that Hadlow identified no infectivity in muscle by mouse
inoculation (whereas some other tissues not normally consumed had
detectable infectivifcy) shows that cross contamination of his tissues
did not occur. Pattison's experiments were reported about 20 years
earlier when much less was known about Scrapie. In the intervening
period the knowledge available to Hadlow on the insensitivity of scrapie
agent to heat became available. There is therefore at least the
possibility that Pattison's instruments were not sterilised effectively,
thus possibly giving the false positive result for muscle.

5. Pattison used a more sensitive model for the detection of
infectivifcy, namely goats, whereas Hadlow used mice ie necessitating
crossing the species barrier and possibly reducing the test sensitivity.

90/1.19/9.1

CVO BSE 1 5

6. In regard to the choice of species for agent assay, mice (Hadlow),
these would be guaranteed free of pre-existing Scrapie infection.
Pattison could offer no such guarantee that this was the case in the
animal to which muscle was passaged and disease could have developed
from exposure from a source other than muscle.

7. Pattison did not report that his recipient animals, including the one
inoculated with muscle, were examined by histopathology to confirm the
presence of disease. This is a significant deficit. Clinical diagnosis
alone is not acceptable as adequate evidence for the existence of scrapie.

8. Even in Pattison's studies only in 1 out of 14 goats was infectivity
detected in muscle and that was in a CLINICAL case. In BSE all clinical
cases are notified and do not enter any food chain.

9. The last paragraph of Pattison's letter is illogical. Furthermore,
this is no evidence whatsoever that scrapie or BSE is a danger to man.

W A WATSON 19 January 1990

Private Offices Mr K C Meldrum Mrs E Attridge Mr R Lowson Ms L Austin Mr
R Bradley

90/1.19/9.2

http://www.bseinquiry.gov.uk/files/yb/1990/01/19009001.pdf

Prions in skeletal muscle

Patrick J. Bosque*,dagger ,Dagger , Chongsuk Ryou*, Glenn Telling*,§,
David Peretz*,dagger , Giuseppe Legname*,dagger , Stephen J.
DeArmond*,dagger ,¶, and Stanley B. Prusiner*,dagger ,||,**

* Institute for Neurodegenerative Diseases and Departments of dagger
Neurology, ¶ Pathology, and || Biochemistry and Biophysics, University
of California, San Francisco, CA 94143

Contributed by Stanley B. Prusiner, December 28, 2001

Considerable evidence argues that consumption of beef products from
cattle infected with bovine spongiform encephalopathy (BSE) prions
causes new variant Creutzfeldt-Jakob disease. In an effort to prevent
new variant Creutzfeldt-Jakob disease, certain "specified offals,"
including neural and lymphatic tissues, thought to contain high titers
of prions have been excluded from foods destined for human consumption
[Phillips, N. A., Bridgeman, J. & Ferguson-Smith, M. (2000) in The BSE
Inquiry (Stationery Office, London), Vol. 6, pp. 413-451]. Here we
report that mouse skeletal muscle can propagate prions and accumulate
substantial titers of these pathogens. We found both high prion titers
and the disease-causing isoform of the prion protein (PrPSc) in the
skeletal muscle of wild-type mice inoculated with either the Me7 or
Rocky Mountain Laboratory strain of murine prions. Particular muscles
accumulated distinct levels of PrPSc, with the highest levels observed
in muscle from the hind limb. To determine whether prions are produced
or merely accumulate intramuscularly, we established transgenic mice
expressing either mouse or Syrian hamster PrP exclusively in muscle.
Inoculating these mice intramuscularly with prions resulted in the
formation of high titers of nascent prions in muscle. In contrast,
inoculating mice in which PrP expression was targeted to hepatocytes
resulted in low prion titers. Our data demonstrate that factors in
addition to the amount of PrP expressed determine the tropism of prions
for certain tissues. That some muscles are intrinsically capable of
accumulating substantial titers of prions is of particular concern.
Because significant dietary exposure to prions might occur through the
consumption of meat, even if it is largely free of neural and lymphatic
tissue, a comprehensive effort to map the distribution of prions in the
muscle of infected livestock is needed. Furthermore, muscle may provide
a readily biopsied tissue from which to diagnose prion disease in
asymptomatic animals and even humans. Dagger Present address: Department
of Medicine, Denver Health Medical Center, Denver, CO 80204.

§ Present address: Department of Microbiology and Immunology, University
of Kentucky, Lexington, KY 40536-0230.

** To whom reprint requests should be addressed. E-mail: vann@cgl.ucsf.edu.

www.pnas.org/cgi/doi/10.1073/pnas.052707499

http://www.pnas.org/cgi/content/abstract/99/6/3812?
maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=prusiner&author2=prusiner&t
itle
abstract=prions+meat+tissue+mice&fulltext=prions+meat+tissue+mice&searchid=1
0243
46978866_6016&stored_search=&FIRSTINDEX=0&fdate=1/1/2002


FULL TEXT;

http://www.pnas.org/cgi/content/full/99/6/3812?
maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=prusiner&author2=prusiner&t
itle
abstract=prions+meat+tissue+mice&fulltext=prions+meat+tissue+mice&searchid=1
0502
49844061_1953&stored_search=&FIRSTINDEX=0&fdate=1/1/2002

full text to;

From: TSS (216-119-136-53.ipset16.wt.net)
Subject: Re: Guidance for Industry on Use of Material From Deer and Elk in
Animal Feed; Availability [TSS SUBMISSION Docket No. 2003D-0186]
Date: September 16, 2003 at 1:50 pm PST

In Reply to: Guidance for Industry on Use of Material From Deer and Elk in
Animal Feed; Availability [Docket No. 2003D-0186] posted by TSS on
September
16, 2003 at 7:34 am:


-------- Original Message --------
Subject: Guidance for Industry on Use of Material From Deer and Elk in
Animal
Feed; Availability [Docket No. 2003D-0186]
Date: Tue, 16 Sep 2003 15:29:37 -0500
From: "Terry S. Singeltary Sr."
To: fdadockets@oc.fda.gov
CC: bpritche@cvm.fda.gov


Guidance for Industry on Use of Material From Deer and Elk in
Animal Feed; Availability [Docket No. 2003D-0186]


To: fdadockets@oc.fda.gov


Greetings FDA,

I would kindly like to comment on;

Guidance for Industry on Use of Material From Deer and Elk in
Animal Feed; Availability [Docket No. 2003D-0186]

Several factors on this apparent voluntary proposal disturbs me greatly,
please allow me to point them out;

I am greatly concerned about the apparent lack of desire to truly combat
human/animal TSEs in the USA (all of them). we have floundered too long.
someone must step up to the plate to combat all human/animal TSEs in the
USA, North America and the Globe. A study that just came out;

Nature 425, 35 - 36 (04 September 2003); doi:10.1038/425035a

Prion disease: Horizontal prion transmission in mule deer...(see full
text in references
below...TSS)

THIS has been suspected for decades. so the feeding of deer and elk and the
''gathering and co-mingling'' would inhance this route of this agent...

WHAT about 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...

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. if this is not done, they system will fail...

WE must ban not only CNS SRMs (specified risk materials),
but ALL tissues. recent new and old findings support infectivity
in the rump muscle. whether it be low or high titre of infectivity,
accumulation may play a crucial role in TSEs (who knows when the
threshold of infection will accure?)...

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. we now have documented
the transmission of CWD to 5 cattle and CWD transmission to one
sheep (personal communication Dr. Janice Miller BSE-List). So it is
not out of the question that the potential of CWD transmission
via the oral route (feed) is possible. could it not just be a longer
incubation period due to the route? i will document this data below
in my references...

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 to the public, 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. with an agent that has an incubation
period that could be from 10 to 50 years (depending which TSE you
are speaking of), to wait for facts, when some of those facts have been
staring you in the face for decades, will only continue to spread this
agent...

NOW we have a documented case of BSE in North America
(Canada), so you see, we are not as immune as everyone would
have us think we are. if anyone thinks there is only one case of BSE/TSE
in cattle in North America, then they are being very naive indeed.

Canadian Bulls Imported to the United States;

* On Tuesday, June 3, 2003, Canada reported to USDA’s Animal and
Plant Health Inspection Service (APHIS) that their investigation
indicated that 5 bulls from one of the possible birth herds of the
BSE index animal in Saskatchewan were sold to a ranch in Montana.
* Records indicate that the five bulls were born in Saskatchewan in
1996 and left Canada for Montana on April 28, 1997.

* Individual records on the bulls were not kept by the owners of the
Montana farm. As a result it was not possible to determine the
exact date the Canadian bulls were removed from the ranch. Through
a review of brand inspection records and interviews with the
Montana rancher, investigators have determined that 24 bulls were
moved off of this ranch from 1997 to 2002. These sales would have
included the imported bulls. Eleven of the bulls were moved to a
market in Montana and 12 of the bulls moved to two markets in
South Dakota. One bull was slaughtered for personal consumption.
* A joint effort among USDA, the U.S. Food and Drug Administration,
and state veterinary officials in Montana, Nebraska, Minnesota,
South Dakota, Texas, and Wyoming traced all 24 of the bulls to
determine their final disposition. This investigation is
consistent with the actions taken in Canada and will contribute to
that overall investigation.

· All 24 bulls were traced to their most likely point of slaughter by
June 12.

1. Three bulls were purchased by a slaughter facility in Nebraska; two
of these animals were ruled out as not being from Canada due to age and
size at the time of slaughter, the other bull was slaughtered for human
consumption and the offal went to a rendering company.

2. Five bulls were purchased by a slaughter facility in Minnesota; all
five bulls were verified as slaughtered for human consumption and the
offal went to a rendering company. One of these bulls was ruled out as
not being from Canada as it was a different breed.

3. Two bulls were sold to a slaughter plant in Texas where they were
slaughtered for human consumption. The offal went to two different
renderers. The final rendered product was shipped to a pet food company

4. Twelve bulls were sold to two slaughter facilities in South Dakota;
two of these bulls were ruled out as being of Canadian origin due to
age, weight, or other characteristics. Two went to a slaughter facility
for human consumption and the offal went to a renderer; because this
facility was destroyed by fire records to verify animal identification
were not available. The other eight were verified as slaughtered for
human consumption and the offal went to a renderer.

5. One bull initially sold in Wyoming was traced to a feedyard in NE
where he was fed with a large number of other bulls. He was later
shipped to slaughter for human consumption and the offal went to a renderer.

6. One bull was slaughtered for home consumption by the ranch owner at a
local custom slaughter facility in Montana and the offal went to a land
fill...

snip...

Backgrounder

Release No. bg0166.03
Updated Information in BOLD


Backgrounder
Bovine Spongiform Encephalopathy (BSE)
from the U.S. Department of Agriculture and Food and Drug Administration

Updated July 10, 2003

http://www.usda.gov/news/releases/2003/05/bg0166.htm

THE FDA learned that the pet food that the firm received may have
included rendered material from the BSE positive cow (USA firm).
we know that cats are susceptible to TSEs and there is some interesting
findings on dogs and TSEs as well. however this was never followed up
on. regardless,
these animals are rendered and fed back to cattle, sheep, deer, elk,
dogs and cats
and eventually, some humans will consume those animals that were fed those
dogs and cats...

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). there are new findings from
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. how many of these such phenotypes of sCJD
are in the USA? We must learn from our past mistakes, not
continue to make the same mistakes...

REFERENCES

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

Nature 425, 35 - 36 (04 September 2003); doi:10.1038/425035a

Prion disease: Horizontal prion transmission in mule deer

The gathering of deer during winter may foster the spread of chronic
wasting disease.

Epidemics of contagious prion1


diseases can be perpetuated by horizontal (animal to animal) and
maternal (dam to offspring, before or after birth) transmission2-7
,

but the relative importance of each mechanism is unclear. Here we
compare the incidence of chronic wasting disease (CWD) in captive mule
deer (Odocoileus hemionus) that is attributable to horizontal or
maternal transmission. We find that horizontal transmission is
remarkably efficient, producing a high incidence of disease (89%) in a
cohort of deer in which maternal transmission was improbable. Our
results indicate that horizontal transmission is likely to be important
in sustaining CWD epidemics.

Although prion diseases have emerged worldwide as a threat to human and
animal health, they are incompletely understood. Of those recognized so
far in mammalian species (including humans), only scrapie and CWD behave
as contagious diseases; however, their control is impeded by a lack of
basic knowledge about the transmission of the infective prion agent.
Horizontal transmission apparently drives scrapie epidemics in sheep3


http://www.vegsource.com/talk/madcow/messages/1089.html

TSS

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TSS




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