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From: TSS ()
Subject: NEW YORK DEC AND DAM ANNOUNCE Second CWD Public Informational Meeting Announced Saturday, April 9, 2005, at 1 p.m
Date: April 7, 2005 at 9:11 am PST

-------- Original Message --------
Subject: Second CWD Public Informational Meeting Announced Saturday, April 9, 2005, at 1 p.m
Date: Thu, 07 Apr 2005 10:09:55 -0500
From: "Terry S. Singeltary Sr."
To: Bovine Spongiform Encephalopathy , fwinfo@gw.dec.state.ny.us, fwwildlf@gw.dec.state.ny.us, rwnp@gw.dec.state.ny.us, jessica.chittenden@agmkt.state.ny.us, dthorne@thejournal.canwest.com


For Release: Wednesday, April 6, 2005
Contact: Michael Fraser (518) 402-8000 or Jessica Chittenden (518) 457-3136


Media Advisory


Second CWD Public Informational Meeting Announced

The New York State Department of Environmental Conservation (DEC) and
Department of Agriculture and Markets (DAM) today announced that a
public meeting will be held on Saturday, April 9, 2005, at 1 p.m. to
inform the public of efforts being made in Oneida County in response to
the discovery of chronic wasting disease (CWD) in two captive deer herds
in Oneida County.

Saturday's meeting will be held at the Westmoreland Middle School,
located at 5176 Route 233 in the Town of Westmoreland. Directions to the
meeting are attached. Representatives from DEC and DAM will present
information on the discovery of CWD, provide details on the State's
response, and be available to answer questions from those in attendance.
Directions to the meeting are attached.

CWD is a transmissible disease that affects the brain and central
nervous system of certain deer and elk. There is no evidence that CWD is
linked to disease in humans or domestic livestock other than deer and elk.

In addition, DEC and DAM will hold a previously announced public meeting
on Friday, April 8, 2005, at 7 p.m. at the Oneida County Cornell
Cooperative Extension office, located at 121 Second Street in Oriskany.

Directions to Westmoreland Middle School:

From Rome: Go south on State Route 233. Cross the NYS Thruway and pass
through the 4 corners on Westmoreland. Middle School is a new building
which sits back away from the road on the left.

From Thruway, Exit 32: Turn right after exit then left on State Route
233 and (as above) pass through the 4 corners on Westmoreland. Middle
School is a new building which sits back away from the road on the left.

05-29a


http://www.dec.state.ny.us/website/press/pressrel/2005/200529a.html


Positive Cases of Chronic Wasting Disease

Found in New York State

------------------------------------------------------------------------

DEC and NYS Department of Agriculture & Markets have scheduled two
public meetings to provide information on chronic wasting disease. The
first meeting
will held
at the Oneida County Cornell Cooperative Extension Office on Friday,
April 8 at 7 p.m. and a second meeting

will be held at the Westmoreland Middle School on Saturday, April 9 at 1
p.m. in Oneida County.

Two positive cases of chronic wasting disease

(CWD) in New York State have been confirmed in white-tailed deer from
captive herds in Oneida County. CWD is a transmissible disease that
affects the brain and central nervous system of deer and elk. There is
no evidence that CWD is linked to disease in humans or domestic
livestock other than deer and elk. For additional information go to the
Department of Agriculture and Markets' press releases
.


Greetings New York,

CWD MEETING

I HOPE THIS MEETING STARTS OUT WITH THE TRUTH,
not the fabricated lies we are use to hearing.

SADLY, im afraid this meeting will consist of lies that CWD does not
transmit to humans (without any scientific proof or any transmission
studies to back there false statement up). IT would be much better
to just say that with what limited surveillance they have done with
human/CJD in relations to CWD transmission, they simply cannot
answer that question. THEN tell them of the transmission studies
that show CWD does transmit in the lab by innoculation,
CWD does transmit to primate, cattle and sheep. LIKE the lies
we hear about Scrapie, when we know it transmits to primates
by there NON-FORCED ORAL consumption of scrapie tainted
feed TO PRIMATE ;

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


PAGE 25

Transmission Studies

Mule deer transmissions of CWD were by intracerebral inoculation and
compared with natural cases resulted in a more rapidly
progressive clinical disease with repeated episodes of synocopy ending
in coma. One control animal became affected, it is believed through
contamination of inoculam (?saline). Further CWD transmissions were
carried out by Dick Marsh into ferret, mink and squirrel monkey.
Transmission occurred in all of these species with the shortest
incubation period in the ferret.

[hmmm, CWD transmission to squirrel monkey. are humans primates?TSS]

snip...

The occurrence of CWD must be viewed against the context of the
locations in which it occurred. It was an incidental and unwelcome
complication of the respective wildlife research programmes. Despite its
subsequent recognition as a new disease of cervids, therefore justifying
direct investigation, no specific research funding was forthcoming.
The USDA viewed it as a wildlife problem and consequently not their
province!

[figures...TSS]

snip...

VISIT TO USA - DR A E WRATHALL - INFO ON BSE AND SCRAPIE

1. Dr Clark lately of the Scrapie Research Unit, Mission Texas has
successfully transmitted ovine and caprine scrapie to cattle. The
experimental results have not been published but there are plans to do
this. This work was initiated in 1978. A summary of it is:-

better cut this short, you can read full text of part 2 here;

snip...

In Reply to: In Confidence - Perceptions of unconventional slow virus
diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells


http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

Adaptation of the bovine spongiform encephalopathy agent to primates
and comparison with Creutzfeldt- Jakob disease: Implications for
human health

THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*,
Virginie Nouvel*,

Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp [Dagger

] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique

Dormont*, and Jean-Philippe Deslys* et al, that The agent responsible
for French iatrogenic growth hormone-linked CJD taken as a control is
very different from vCJD but is similar to that found in one case of
sporadic CJD and one sheep scrapie isolate;

http://www.pnas.org/cgi/content/full/041490898v1

Characterization of two distinct prion strains
derived from bovine spongiform encephalopathy
transmissions to inbred mice

http://vir.sgmjournals.org/cgi/content/abstract/85/8/2471


CWD/TSEs & ENVIRONMENT CONTAMINATION

I believe it to be very irresponsible to dispose
of clinical/sub-clinial cases of CWD or any animal
with TSEs in landfills...

TSS

Aguzzi warns of CWD danger

The TSE family of diseases also includes chronic wasting disease (CWD)
in deer, a condition that has spread in the US in recent years (Nature
416, 569; 2002). Speaking at the Days of Molecular Medicine conference
in La Jolla in March, prion expert Adriano Aguzzi issued a strong
warning against underestimating this form of TSE.

"For more than a decade, the US has by-and-large considered mad cows
to be an exquisitely European problem. The perceived need to protect
US citizens from this alien threat has even prompted the deferral of
blood donors from Europe," he said. "Yet the threat-from-within
posed by CWD needs careful consideration, since the evidence that CWD
is less dangerous to humans than BSE is less-than-complete. Aguzzi
went on to point out that CWD is arguably the most mysterious of all
prion diseases.

"Its horizontal spread among the wild population is exceedingly
efficient, and appears to have reached a prevalence unprecedented even
by BSE in the UK at its peak. The pathogenesis of CWD, therefore,
deserves a vigorous research effort. Europeans also need to think
about this problem, and it would be timely and appropriate to increase
CWD surveillance in Europe too." Aguzzi has secured funding from the
National Institutes of Health to investigate CWD, and the effort will
be lead by Christina Sigurdson in his department at the University of
Zurich. KAREN BIRMINGHAM, LONDON

This quote from Dr. Gambetti is especially significant since he is the
rather cautious TSE researcher under contract with the Centers for Disease
Control to examine the brains of individuals who have died of CJD.
-----------------

Pierluigi Gambetti, director of the National Prion Disease Pathology
Surveillance Center at Case Western Reserve University in Cleveland,
said all deer should be tested for chronic wasting disease before any
processing is done.

"There is no way around it," he said. "Nobody should touch that meat
unless it has been tested."

http://www.ledger-enquirer.com/mld/...ion/3954298.htm


TSEs And The Environment

The LANCET
Volume 351, Number 9110 18 April 1998

BSE: the final resting place

How to dispose of dangerous waste is a question that has vexed the human
race for hundreds of years. The answer has usually been to get it out of
sight--burn it or bury it. In Periclean Athens, victims of the plague
were incinerated in funeral pyres; in 14th century Venice, a law
stipulated that Black Death corpses should be buried to a minimum depth
of 5 feet; and now, as the 20th century draws to a close, we are
challenged by everything from industrial mercury to the smouldering
reactors of decommissioned atomic submarines.

The Irish Department of Agriculture will convene an expert panel on
April 27-29 to discuss the disposal of tissues from animals with bovine
spongiform encephalopathy (BSE). Proper disposal of tissues from
infected cattle has implications for both human and animal safety.
Safety for human beings is an issue because there is now unassailable if
still indirect evidence that BSE causes infections in man in the form of
"new variant" Creutzfeld-Jakob disease (nvCJD).1-3 Safety for animals is
also an issue because BSE-affected cattle could possibly transmit
disease to species other than cattle, including sheep, the species that
was almost surely the unwitting source of the BSE epidemic.

The first matter to consider is the distribution of infectivity in the
bodies of infected animals. The brain (and more generally, the central
nervous system) is the primary target in all transmissible spongiform
encephalopathies (TSE), and it contains by far the highest concentration
of the infectious agent. In naturally occuring disease, infectivity may
reach levels of up to about one million lethal doses per gram of brain
tissue, whether the disease be kuru, CJD, scrapie, or BSE. The
infectious agent in BSE-infected cattle has so far been found only in
brain, spinal cord, cervical and thoracic dorsal root ganglia,
trigeminal ganglia, distal ileum, and bone marrow.4 However, the much
more widespread distribution of low levels of infectivity in human
beings with kuru or CJD, and in sheep and goats with scrapie, suggests
that caution is advisable in prematurely dismissing as harmless other
tissues of BSE-infected cattle.

A second consideration relates to the routes by which TSE infection can
occur. Decades of accumulated data, both natural and experimental, have
shown clearly that the most efficient method of infection is by direct
penetration of the central nervous system; penetration of peripheral
sites is less likely to transmit disease. Infection can also occur by
the oral route, and the ingestion of as little as 1 g of BSE brain
tissue can transmit disease to other cattle.5 Infection by the
respiratory route does not occur (an important consideration with
respect to incineration), and venereal infection either does not occur
or is too rare to be detected.

How can tissue infectivity be destroyed before disposal? The agents that
cause TSE have been known almost since their discovery to have awesome
resistance to methods that quickly and easily inactivate most other
pathogens. Irradiation, chemicals, and heat are the three commonest
inactivating techniques. Irradiation has proved entirely ineffective,
and only a handful of a long catalogue of chemicals have produced more
than modest reduction in infectivity. The most active of these are
concentrated solutions of sodium hypochlorite (bleach) or sodium
hydroxide (lye). As for heat, even though the agent shares with most
other pathogens the feature of being more effectively damaged by wet
heat than by dry heat, boiling has little effect, and steam heat under
pressure (autoclaving) at temperatures of 121ºC is not always
sterilising. To date, the most effective heat kill requires exposure of
infectious material to steam heat at 134ºC for 1 h in a porous-load
autoclave.6 Exposure to dry heat even at temperatures of up to 360ºC for
1 h may leave a small amount of residual infectivity.7 The standard
method of incineration, heating to about 1000ºC for at least several
seconds, has been assumed to achieve total sterilisation, but needs
experimental verification in the light of suggestions that rendered
tissue waste might find some useful purpose as a source of heating fuel.

Thus, TSE agents are very resistant to virtually every imaginable method
of inactivation, and those methods found to be most effective may, in
one test or another, fail to sterilise. It seems that even when most
infectious particles succumb to an inactivating process, there may
remain a small subpopulation of particles that exhibit an extraordinary
capacity to withstand inactivation, and that, with appropriate testing,
will be found to retain the ability to transmit disease. Also, almost
all available inactivation data have come from research studies done
under carefully controlled laboratory conditions, and it is always
difficult to translate these conditions to the world of commerce. Even
when the data are applied in the commercial process, the repetitive
nature of the process requires vigilance in quality control and
inspection to ensure adherence to its regulations.

The final issue that must be addressed is the "lifespan" of the
infectious agent after disposal if it has been only incompletely
inactivated beforehand. Given the extraordinary resistance of the agent
to decontamination measures, the epidemiological and experimental
evidence indicating that TSE agents may endure in nature for a long time
should come as no surprise. The first real clue to this possibility came
from the Icelandic observation that healthy sheep contracted scrapie
when they grazed on pastures that had lain unused for 3 years after
having been grazed by scrapie-infected sheep.8

Support for this observation was obtained from an experiment in which
scrapie-infected brain material was mixed with soil, placed in a
container, and then allowed to "weather" in a semi-interred state for 3
years.9 A small amount of residual infectivity was detected in the
contaminated soil, and most of the infectivity remained in the topmost
layers of soil, where the tissue had originally been placed--in other
words, there had been no significant leaching of infectivity to deeper
soil layers.

It is therefore plausible for surface or subsurface disposal of
TSE-contaminated tissue or carcasses to result in long-lasting soil
infectivity. Uncovered landfills are a favourite feeding site for
seagulls, which could disperse the infectivity.10 Other animals might do
likewise, and if the landfill site were later used for herbivore
grazing, or tilled as arable land, the potential for disease
transmission might remain. A further question concerns the risk of
contamination of the surrounding water table, or even surface
waste-water channels, by effluents and discarded solid waste from
treatment plants.

A reasonable conclusion from existing data is that there is a potential
for human infection to result from environmental contamination by
BSE-infected tissue residues. The potential cannot be quantified because
of the huge number of uncertainties and assumptions that attend each
stage of the disposal process.

On the positive side, spongiform encephalopathy can be said to be not
easily transmissible. Although the level of infectivity to which
creatures are exposed is not known, it is probably very low, since sheep
that die from scrapie, cattle that die from BSE, and human beings who
die from nvCJD represent only a small proportion of their respective
exposed populations.

Whatever risk exists is therefore extremely small, but not zero, hence
all practical steps that might reduce the risk to the smallest
acceptable level must be considered. What is practical and what is
acceptable are concepts that will be hammered out on the anvil of
politics: scientific input, such as it is, already waits in the forge. A
fairly obvious recommendation, based on the science, would be that all
material that is actually or potentially contaminated by BSE, whether
whole carcasses, rendered solids, or waste effluents, should be exposed
to lye and thoroughly incinerated under strictly inspected conditions.
Another is that the residue is buried in landfills to a depth that would
minimise any subsequent animal or human exposure, in areas that would
not intersect with any potable water-table source. Certainly, it has
been, and will continue to be, necessary in many instances to accept
less than the ideal.

Paul Brown

Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, Bethesda, MD 20892, USA

1 Will RG, Ironside JW, Zeidler M, et al. A new variant of
Creutzfeldt-Jakob disease in the UK. Lancet 1996; 347: 921-25 [PubMed].

2 Bruce M, Will RG, Ironside JW, et al. Transmissions to mice indicate
that 'new variant' CJD is caused by the BSE agent. Nature 1997: 389:
498-501.

3 Collinge J, Sidle KCL, Heads J, Ironside J, Hill AF. Molecular
analysis of prion strain variation and the aetiology of 'new variant'
CJD. Nature 1996; 383: 685-90 [PubMed].

4 Wells GAH, Hawkins SAC, Green RB, et al. Preliminary observations on
the pathogenesis of experimental bovine spongiform encephalopathy (BSE):
an update. Vet Rec 1998; 142: 103-06 [PubMed].

5 Collee JG, Bradley R. BSE: a decade on--part 2. Lancet 1997; 349:
715-21 [PubMed].

6 Taylor DM. Exposure to, and inactivation of, the unconventional agents
that cause transmissible degenerative encephalopathies. In: Baker HF,
Ridley RM, eds. Methods in molecular medicine: prion diseases. Totawa
NJ: Humana Press, 1996: 105-18.

7 Brown P, Liberski PP, Wolff A, Gajdusek DC. Resistance of scrapie
infectivity to steam autoclaving after formaldehyde fixation and limited
survival after ashing at 360°C: practical and theoretical implications,
J Infect Dis 1990; 161: 467-72 [PubMed].

8 Palsson PA. Rida (scrapie) in Iceland and its epidemiology. In:
Prusiner SB, Hadlow WJ, eds. Slow transmissible diseases of the nervous
system, vol I. New York: Academic Press, 1979: 357-66.

9 Brown P, Gajdusek DC. Survival of scrapie virus after 3 years'
interment. Lancet 1991; 337; 269-70.

10 Scrimgoeur EM, Brown P, Monaghan P. Disposal of rendered specified
offal. Vet Rec 1996; 139: 219-20 [PubMed].

http://www.thelancet.com/newlancet/sub/issues/vol351no9110/body.commentary1146.html


snip...

88. Natural decay: Infectivity persists for a long time in the
environment. A study by Palsson in 1979 showed how scrapie was
contracted by healthy sheep, after they had grazed on
land which had previously been grazed by scrapie-infected sheep, even
though the land had lain fallow for three years before the healthy sheep
were introduced. Brown also quoted an early experiment of his own
(1991), where he had buried scrapie-infected hamster brain and found
that he could still detect substantial infectivity three years later
near where the material had been placed. 89. Potential environmental
routes of infection: Brown discusses the various possible
scenarios, including surface or subsurface deposits of TSE-contaminated
material, which would lead to a build-up of long-lasting infectivity.
Birds feeding on animal remains (such as gulls visiting landfill sites)
could disperse infectivity. Other animals could become vectors if they
later grazed on contaminated land. "A further question concerns
the risk of contamination of the surrounding water table or even surface
water channels, by effluents and discarded solid wastes from treatment
plants. A reasonable conclusion is that there is a potential for human
infection to result from environmental contamination by BSE-infected
tissue residues. The potential cannot be quantified because of the huge
numbers of uncertainties and assumptions that attend each stage of the
disposal process". These comments, from a long established authority on
TSEs, closely echo my own statements which were based on a recent
examination of all the evidence. 90. Susceptibility: It is likely that
transmissibility of the disease to humans in vivo is probably low,
because sheep that die from scrapie and cattle that die from BSE are
probably a small fraction of the exposed population. However, no
definitive data are available.

91. Recommendations for disposal procedures: Brown recommends that
material which is actually or potentially contaminated by BSE should be:
1) exposed to caustic soda; 2) thoroughly incinerated under carefully
inspected conditions; and 3) that any residue should be buried in
landfill, to a depth which would minimise any subsequent animal or
human exposure, in areas that would not intersect with any potable
water-table source.

92. This review and recommendations from Brown have particular
importance. Brown is one of the world's foremost authorities on TSEs and
is a senior researcher in the US National Institutes of Health (NIH). It
is notable that such a respected authority is forthright in
acknowledging the existence of potential risks, and in identifying the
appropriate measures necessary to safeguard public health.
Paper by SM Cousens, L Linsell, PG Smith, Dr M Chandrakumar, JW
Wilesmith, RSG Knight, M Zeidler, G Stewart, RG Will, "Geographical
distribution of variant CJD in the UK (excluding Northern Ireland)".
Lancet 353:18-21, 2 nd January 1999 93. The above paper {Appendix 41
(02/01/99)} (J/L/353/18) examined the possibility that patients with
vCJD (variant CJD) might live closer to rendering factories than would
be expected by chance. All 26 cases of vCJD in the UK with onset up to
31 st August 1998 were studied. The incubation period of vCJD is not
known but by analogy with other human TSEs could lie within the range
5-25 years. If vCJD had arisen by exposure to rendering products, such
exposure might plausibly have occurred 8-10 years before the
onset of symptoms. The authors were able to obtain the addresses of all
rendering plants in the UK which were in production in 1988. For each
case of vCJD, the distance from the place of residence on 1st January
1998 to the nearest rendering plant was calculated

snip...

http://www.bseinquiry.gov.uk/files/ws/s019b.pdf

Infectivity surviving ashing to 600*C is (in my opinion) degradable but
infective.
based on Bown & Gajdusek, (1991), landfill and burial may be assumed to
have a reduction factor of 98% (i.e. a factor of 50) over 3 years.
CJD-infected brain-tissue remained infectious after storing at
room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is
known to remain viable after at least 30 months of desiccation (Wilson
et al, 1950). and pastures that had been grazed by scrapie-infected
sheep still appeared to be contaminated with scrapie agent three years
after they were last occupied by sheep (Palsson, 1979).

http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf

PAUL BROWN SCRAPIE SOIL TEST

http://www.bseinquiry.gov.uk/files/sc/seac07/tab03.pdf

Some unofficial information from a source on the inside looking out -

Confidential!!!!

As early as 1992-3 there had been long studies conducted on small
pastures containing scrapie infected sheep at the sheep research station
associated with the Neuropathogenesis Unit in Edinburgh, Scotland.
Whether these are documented...I don't know. But personal recounts both
heard and recorded in a daily journal indicate that leaving the pastures
free and replacing the topsoil completely at least 2 feet of thickness
each year for SEVEN years....and then when very clean (proven scrapie
free) sheep were placed on these small pastures.... the new sheep also
broke out with scrapie and passed it to offspring. I am not sure that TSE
contaminated ground could ever be free of the agent!!
A very frightening revelation!!!

----------

You can take that with however many grains of salt you wish, and
we can debate these issues all day long, but the bottom line,
this is not rocket-science, all one has to do is some
experiments and case studies. But for the life of me,
I don't know what they are waiting on?

Kind regards,

Terry S. Singeltary Sr.
Bacliff, Texas USA

More here:

http://www.bseinquiry.gov.uk/files/ws/s018.pdf

INCINERATION TEMPS

Requirements include:

a. after burning to the range of 800 to 1000*C to eliminate smell;

well heck, this is just typical public relations fear factor control.
do you actually think they would spend the extra costs for fuel,
for such extreme heat, just to eliminate smell, when they spread
manure all over your veg's. i think not. what they really meant were
any _TSE agents_.

b. Gas scrubbing to eliminate smoke -- though steam may be omitted;

c. Stacks to be fitted with grit arreaters;

snip...

1.2 Visual Imact

It is considered that the requirement for any carcase incinerator
disign would be to ensure that the operations relating to the reception,
storage and decepitation of diseased carcasses must not be publicly
visible and that any part of a carcase could not be removed or
interfered with by animals or birds.

full text;

http://www.bseinquiry.gov.uk/files/yb/1989/04/03006001.pdf

New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template
of replication

Paul Brown*, [dagger ] , Edward H. Rau [Dagger ] , Bruce K. Johnson*,
Alfred E. Bacote*, Clarence J. Gibbs Jr.*, and D. Carleton Gajdusek§

* Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, and [Dagger ] Environmental
Protection Branch, Division of Safety, Office of Research Services,
National Institutes of Health, Bethesda, MD 20892; and § Institut Alfred
Fessard, Centre National de la Recherche Scientifique, 91198 Gif sur
Yvette, France

Contributed by D. Carleton Gajdusek, December 22, 1999

Abstract
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References

One-gram samples from a pool of crude brain tissue from hamsters
infected with the 263K strain of hamster-adapted scrapie agent were
placed in covered quartz-glass crucibles and exposed for either 5 or 15
min to dry heat at temperatures ranging from 150°C to 1,000°C. Residual
infectivity in the treated samples was assayed by the intracerebral
inoculation of dilution series into healthy weanling hamsters, which
were observed for 10 months; disease transmissions were verified by
Western blot testing for proteinase-resistant protein in brains from
clinically positive hamsters. Unheated control tissue contained 9.9
log10LD50/g tissue; after exposure to 150°C, titers equaled or exceeded
6 log10LD50/g, and after exposure to 300°C, titers equaled or exceeded 4
log10LD50/g. Exposure to 600°C completely ashed the brain samples,
which, when reconstituted with saline to their original weights,
transmitted disease to 5 of 35 inoculated hamsters. No transmissions
occurred after exposure to 1,000°C. These results suggest that an
inorganic molecular template with a decomposition point near 600°C is
capable of nucleating the biological replication of the scrapie agent.

transmissible spongiform encephalopathy | scrapie | prion | medical
waste | incineration

Introduction
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References

The infectious agents responsible for transmissible spongiform
encephalopathy (TSE) are notoriously resistant to most physical and
chemical methods used for inactivating pathogens, including heat. It has
long been recognized, for example, that boiling is ineffective and that
higher temperatures are most efficient when combined with steam under
pressure (i.e., autoclaving). As a means of decontamination, dry heat is
used only at the extremely high temperatures achieved during
incineration, usually in excess of 600°C. It has been assumed, without
proof, that incineration totally inactivates the agents of TSE, whether
of human or animal origin. It also has been assumed that the replication
of these agents is a strictly biological process (1), although the
notion of a "virus" nucleant of an inorganic molecular cast of the
infectious [beta ] -pleated peptide also has been advanced (2). In this
paper, we address these issues by means of dry heat inactivation studies.

snip...

GUTTING DEER/ELK AND THOSE THIN GLOVES;

Distribution of prion protein in the ileal Peyer's patch of scrapie-free
lambs and lambs naturally and experimentally exposed to the scrapie agent

Ragna Heggeb'z1, Charles McL. Press1, Gjermund Gunnes1, Kai Inge Lie1,
Michael A. Tranulis2, Martha Ulvund3, Martin H. Groschup4 and Thor
Landsverk1

Department of Morphology, Genetics and Aquatic Biology1 and Department
of Biochemistry, Physiology and Nutrition2, Norwegian School of
Veterinary Science, PO Box 8146 Dep., N-0033, Oslo, Norway
Department of Sheep and Goat Research, Norwegian School of Veterinary
Science, Kyrkjevegen 332/334, 4300 Sandnes, Norway3
Federal Research Centre for Virus Diseases of Animals, Paul-Ehrlich-Str.
28, 72076 TÃbingen, Germany4

Author for correspondence: Charles Press. Fax +47 22964764. e-mail
Charles.Press@veths.no

A sensitive immunohistochemical procedure was used to investigate the
presence of prion protein (PrP) in the ileal Peyer?s patch of
PrP-genotyped lambs, including scrapie-free lambs and lambs naturally
and experimentally exposed to the scrapie agent. The tyramide signal
amplification system was used to enhance the sensitivity of conventional
immunohistochemical procedures to show that PrP was widely distributed
in the enteric nervous plexus supplying the gut wall. In scrapie-free
lambs, PrP was also detected in scattered cells in the lamina propria
and in the dome and interfollicular areas of the Peyer?s patch. In the
follicles, staining for PrP was mainly confined to the capsule and cells
associated with vascular structures in the light central zone. In lambs
naturally exposed to the scrapie agent, staining was prominent in the
dome and neck region of the follicles and was also found to be
associated with the follicle-associated epithelium. Similar observations
were made in lambs that had received a single oral dose of
scrapie-infected brain material from sheep with a homologous and
heterologous PrP genotype 1 and 5 weeks previously. These studies show
that the ileal Peyer?s patch in young sheep may be an important site of
uptake of the scrapie agent and that the biology of this major
gut-associated lymphoid tissue may influence the susceptibility to oral
infection in sheep. Furthermore, these studies suggest that homology or
heterology between PrP genotypes or the presence of PrP genotypes seldom
associated with disease does not impede uptake of PrP.
======================================================

BSE, KURU, DENTAL AND ___CUT ABRASIONS___ from gutting a deer
perhaps;

snip...

Since there was a suggestion that kuru had been transmitted
through the gums and/or gum abrasions...

snip...

http://www.bseinquiry.gov.uk/files/yb/1989/04/17005001.pdf

[PDF]BSE INQUIRY Statement of behalf of the Environment Agency ...
File Format: PDF/Adobe Acrobat - View as HTML
... his Statement of March 1998 to the BSE Inquiry ... systems subject
to regular or intermittent
contamination by rapid movement of recharge water ...
www.bse.org.uk/files/ws/s490.pdf

http://www.bseinquiry.gov.uk/files/ws/s490.pdf

BSE INQUIRY

Statement of behalf of the Environment Agency
Concerning Thruxted Mill
By
Mr C. P. Young
Principal Hydrogeologist, Soil Waste and Groundwater Group
WRc plc; Medmenham, Bucks

http://www.bseinquiry.gov.uk/files/ws/s490.pdf

Very important to those hunters looking for healthy
deer/elk to eat...TSS

MRC-43-00 [ ] [Text only version of this site] [Print this page]
Issued: Monday, 28 August 2000
NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH
FINDINGS RELEVANT TO CJD AND BSE

A team of researchers led by Professor John Collinge at the Medical
Research Council Prion Unit1 report today in the Proceedings of the
National Academy of Sciences, on new evidence for the existence of a
'sub-clinical' form of BSE in mice which was unknown until now.

The scientists took a closer look at what is known as the 'species
barrier' - the main protective factor which limits the ability of
prions2 to jump from one species to infect another. They found the mice
had a 'sub-clinical' form of disease where they carried high levels of
infectivity but did not develop the clinical disease during their normal
lifespan. The idea that individuals can carry a disease and show no
clinical symptoms is not new. It is commonly seen in conventional
infectious diseases.

Researchers tried to infect laboratory mice with hamster prions3 called
Sc237 and found that the mice showed no apparent signs of disease.
However, on closer inspection they found that the mice had high levels
of mouse prions in their brains. This was surprising because it has
always been assumed that hamster prions could not cause the disease in
mice, even when injected directly into the brain.

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

The height of the species barrier varies widely between different
combinations of animals and also varies with the type or strain of
prions. While some barriers are quite small (for instance BSE easily
infects mice), other combinations of strain and species show a seemingly
impenetrable barrier. Traditionally, the particular barrier studied here
was assumed to be robust.

Professor John Collinge said: "These results have a number of important
implications. They suggest that we should re-think how we measure
species barriers in the laboratory, and that we should not assume that
just because one species appears resistant to a strain of prions they
have been exposed to, that they do not silently carry the infection.
This research raises the possibility, which has been mentioned before,
that apparently healthy cattle could harbour, but never show signs of, BSE.

"This is a timely and unexpected result, increasing what we know about
prion disease. These new findings have important implications for those
researching prion disease, those responsible for preventing infected
material getting into the food chain and for those considering how best
to safeguard health and reduce the risk that theoretically, prion
disease could be contracted through medical and surgical procedures."

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

FOR FURTHER INFORMATION CONTACT THE MRC PRESS OFFICE ON 020 7637 6011
(OFFICE HOURS) OR 07818 428297 OR 0385 774357 (OUT-OF-OFFICE-HOURS) OR
PROFESSOR JOHN COLLINGE ON 020 7594 3760. PLEASE NOTE THAT OWING TO
TRAVEL COMMITMENTS PROFESSOR COLLINGE WILL ONLY BE AVAILABLE UNTIL 16.30
ON FRIDAY 25 AUGUST AND CONTACTABLE AGAIN ON MONDAY 28 AUGUST VIA THE
MRC PRESS OFFICE. DR ANDREW HILL (A CO-AUTHOR ON THE PAPER) FROM THE
DEPARTMENT OF PATHOLOGY AT THE UNIVERSITY OF MELBOURNE WILL BE AVAILABLE
ON 00 61 3 8344 3995 (DURING OFFICE HOURS) OR 00 61 3 9443 0009
(OUT-OF-OFFICE HOURS). PLEASE NOTE THAT AUSTRALIA IS TEN HOURS AHEAD OF
UK TIME.

NOTES FOR EDITORS

Professor Collinge is a consultant neurologist and Director of the newly
formed MRC Prion Unit based at The Imperial College School of Medicine
at St Mary's Hospital. He is also a member of the UK Government's
Spongiform Encephalopathy Advisory Committee (SEAC). The MRC prion unit
is was set up in 1999, and its work includes molecular genetic studies
of human prion disease and transgenic modelling of human prion diseases.

Prions are unique infectious agents that cause fatal brain diseases such
as Creutzfeldt-Jakob disease (CJD) in humans and scrapie and BSE (mad
cow disease) in animals. In some circumstances prions from one species
of animals can infect another and it is clear that BSE has done this to
cause the disease variant CJD in the UK and France. It remains unclear
how large an epidemic of variant CJD will occur over the years ahead.

The strain of prion used here to infect the mice is the Sc237 strain
(also known as 263K) which infects hamsters, and until now was assumed
not to infect mice.

This research was funded by the Medical Research Council and Wellcome
Trust.

The Medical Research Council (MRC) is a national organisation funded by
the UK tax-payer. Its business is medical research aimed at improving
human health; everyone stands to benefit from the outputs. The research
it supports and the scientists it trains meet the needs of the health
services, the pharmaceutical and other health-related industries and the
academic world. MRC has funded work which has led to some of the most
significant discoveries and achievements in medicine in the UK. About
half of the MRC's expenditure of £345 million is invested in over 50 of
its Institutes and Units, where it employs its own research staff. The
remaining half goes in the form of grant support and training awards to
individuals and teams in universities and medical schools.

The Wellcome Trust is the world's largest medical research charity with
a spend of some £600 million in the current financial year 1999/2000.
The Wellcome Trust supports more than 5,000 researchers, at 400
locations, in 42 different countries to promote and foster research with
the aim of improving human and animal health. As well as funding major
initiatives in the public understanding of science, the Wellcome Trust
is the country's leading supporter of research into the history of
medicine.

©2002 Medical Research Council
Data Protection policy | Contact the MRC
=========================================

Subject: OPINION ON THE USE OF BURIAL FOR DEALING WITH ANIMAL CARCASSES
AND OTHER ANIMAL MATERIALS THAT MIGHT CONTAIN BSE/TSE
Date: Wed, 22 Jan 2003 14:58:53 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy

C:\WINNT\Profiles\bredagi.000\Desktop\Burial_OPINION_0301_OPINION_FINAL.doc
EUROPEAN COMMISSION
HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL
Directorate C - Scientific Opinions
C1 - Follow-up and dissemination of scientific opinions
OPINION ON
THE USE OF BURIAL FOR DEALING WITH ANIMAL
CARCASSES AND OTHER ANIMAL MATERIALS THAT
MIGHT CONTAIN BSE/TSE
ADOPTED BY THE
SCIENTIFIC STEERING COMMITTEE
MEETING OF 16-17 JANUARY 2003
1
OPINION
On 17 May 2002, the Scientific Steering Committee (SSC) was invited by
Commission Services to advice on the examples of conditions under which
safe burial of potentially TSE-infected (animal) materials can be
achieved. The details of the SSC's evaluation are provided in the
attached report. The SSC concludes as follows:
(1) The term "burial" includes a diversity of disposal conditions.
Although burial is widely used for disposal of waste the degradation
process essential for BSE/TSE infectivity reduction is very difficult to
control. The extent to which such an infectivity reduction can occur as
a consequence of burial is poorly characterised.
It would appear to be a slow process in various circumstances.
(2) A number of concerns have been identified including potential for
groundwater contamination, dispersal/transmission by
birds/animals/insects, accidental uncovering by man.
(3) In the absence of any new data the SSC confirms its previous opinion
that animal material which could possibly be contaminated with BSE/TSEs,
burial poses a risk except under highly controlled conditions (e.g.,
controlled landfill). The SSC reiterates the consideration made in its
opinion of 24-25 June 1999 on "Fallen Stock"1. The limited capacity for
destruction of animal wastes in certain countries or regions in the
first place justifies the installation of the required facilities; it
should not be used as a justification for unsafe disposal practices such
as burial. However, the SSC recognises that for certain situations or
places or for certain diseases (including animals killed and recycled or
disposed of as a measure to control notifiable diseases), the available
rendering or incinerator or disposal capacity within a region or country
could be a limiting factor in the control of a disease. Thus if hundreds
or even millions of animals need to be rendered after killing or if the
transport of a material to a rendering or disposal plant proved to be
impractical, an appropriate case by case risk assessment2 should be
carried out before deciding upon the most appropriate way of disposal.
In principle, the risk is expected to be the lower for small
incinerators3 as compared to burial. As such decisions in practice may
have to be taken at very short notice, risk management scenarios
according to various possible risks should be prepared in advance to
allow for a rapid decision when the need arises.

1 Scientific Opinion on The risks of non conventional transmissible
agents, conventional infectious agents or other hazards such as toxic
substances entering the human food or animal feed chains via raw
material from fallen stock and dead animals (including also: ruminants,
pigs, poultry, fish, wild/exotic/zoo animals, fur animals, cats,
laboratory animals and fish) or via condemned materials.
Adopted By the Scientific Steering Committee at its meeting of 24-25
June 1999. (and re-edited at its meeting of 22-23 July 1999).
2 See also the relevant sections and footnotes on risk assessment in the
report accompanying the SSC opinion of 24-25 June 1999.
3 See SSC opinion of 16-17 January 2003 on the use of small incinerators
for BSE risk reduction.
2

THE USE OF BURIAL FOR DEALING WITH CARCASSES AND OTHER MATERIALS THAT
MIGHT CONTAIN BSE/TSE
REPORT

1. MANDATE

On 17 May 2002, the Scientific Steering Committee (SSC) was invited by
Commission Services to advice on the examples of conditions under which
safe burial of potentially TSE-infected animal materials can be
achieved. The SSC appointed Prof.J.Bridges as rapporteur. His report was
discussed and amended by the TSE/BSE ad hoc Group at its meeting of 9
January 2003 and by the SSC at its meeting of 16-17 January 2003.

2. GENERAL CONSIDERATIONS

"Burial" covers a range of disposal situations ranging from the practice
of burying animals on farms and other premises in a relatively shallow
trench (with or without treatment such as lining) to deep disposal to a
lined and professionally managed landfill site (SSC 2001).
Buried organic material is normally decomposed by microbial and chemical
processes. However this is not a process amenable to control measures.
As noted by the SSC "Opinion on Fallen Stock" (SSC 25th June 1999) there
is little reliable information on the extent and rate of infectivity
reduction of BSE/TSEs following burial. An old paper by Brown and
Gajdusek 1991 assumed a reduction of 98% over 3 years. However it is
noted that the rate of degradation of materials following burial can
vary very considerably between sites. This is not surprising because the
degradation process is strongly influenced by factors such as water
content of the site, temperature inside the site, nature of adsorptive
"material" present etc. The previous SSC opinion noted that BSE/TSEs
appear to be resistant to degradation when stored at room temperature
over several years. It also raised concerns that mites could serve as a
vector and/or reservoir for the infected scrapie material.
Burial sites may have a thriving animal population. Uncovering of risk
material that is not deeply buried is therefore possible.
The SSC in its opinion of 28th-29th June 2001 set out a framework for
assessing the risk from different waste disposal processes. These
criteria may be applied to
burial as follows:

(1) Characterisation of the risk materials involved.

Unlike many other waste disposal options there are no technical or
economic factors that would limit the nature of the material that can be
disposed of by burial. Moreover in many cases the location of burial
sites is uncertain. The potential for transmission of BSE/TSEs for SRM
that is buried near the surface is also poorly characterised.3

(2) Risk reduction.

The extent to which the infectivity is reduced is likely to vary
substantially according to the nature of the site depth of burial
whether pre-treatment by burning or through the addition of lime is used
etc. There appears to be no scientific basis at present for the
prediction of the rate of loss of infectivity. In the absence of such
data, as a worst case, it has to be assumed that over a three-five year
period the loss of infectivity may be slight. In principle on a
well-managed fully contained landfill the risks from infective material
can approach zero. However this requires rigorous management over many
years. This is difficult to guarantee.

(3) Degree to Which the Risks can be Contained

The principal concerns are:

* Prevention of access to the SRM by animals that could result in the
transmission (directly or indirectly) of the BSE/TSE.

* Penetration of prions into the leachate/groundwater. It is noted that
on some landfill sites leachate is sprayed into the air to facilitate
oxidation of some organic components. Such a practice could in principle
lead to dispersal of BSE/TSEs. It is also noted that it is not uncommon
for landfill sites to be re-engineered to increase their stability, gas
and leachate flow and/or total capacity. If this re-engineering involved
an area where previous burial of BSE/TSE contaminated material had taken
place and additional risk could accrue. The possibility of contaminated
material being dug up in shallow and unmarked burial sites on farms etc
constitutes a considerably greater risk.

3. FURTHER INVESTIGATIONS

Research is needed on specific aspects of the behaviour of prion like
molecules in controlled landfills i.e.:

* Potential for adsorption to other material present in the waste that
might limit their mobility.

* Principal factors influencing rates of degradation.

* Effectiveness of encasement in cement in controlling/reducing the risk.

4. CONCLUSION

In the absence of new evidence the opinion of the SSC "Opinion on Fallen
Stock" (SSC 25th June 1999) must be endorsed strongly that land burial
of all animals and material derived from them for which there is a
possibility that they could incorporate BSE/TSEs poses a significant
risk. Only in exceptional circumstances where there could be a
considerable delay in implementing a safe means of disposal
should burial of such materials be considered. Guidelines should be made
available to aid on burial site selection.

http://europa.eu.int/comm/food/fs/sc/ssc/out309_en.pdf

C:\WINNT\Profiles\bredagi.000\Desktop\Burning_OPINION_0301_OPINION_FINAL.doc


EUROPEAN COMMISSION
HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL
Directorate C - Scientific Opinions
C1 - Follow-up and dissemination of scientific opinions

OPINION ON

OPEN BURNING OF POTENTIALLY TSE-INFECTED ANIMAL
MATERIALS

ADOPTED BY THE
SCIENTIFIC STEERING COMMITTEE
AT ITS MEETING OF 16-17 JANUARY 2003

2
OPINION

On 17 May 2002, the Scientific Steering Committee (SSC) was invited by
Commission Services to advice on the examples of conditions under which
safe burning of potentially TSE-infected (animal) materials can be
achieved. The details of the SSC's evaluation are provided in the
attached report. The SSC concludes as follows:

(1) "Burning" covers a wide variety of combustion conditions. This
opinion is concerned with the process of open burning e.g. bonfires.

(2) There are serious concerns regarding the use of open burning for the
destruction of pathogen contaminated animal waste, particularly for
waste which may be contaminated with relatively heat stable pathogens.
Issues include: the potentially very high variability of the pathogen
inactivation, the nature of the gaseous and particulate emissions, and
the risks from the residual ash.

(3) The SSC recommends that open burning is only considered for pathogen
destruction under exceptional circumstances following a specific risk
assessment. In the case of animal waste possibly contaminated with
BSE/TSE in view of the uncertainty of the risk open burning should be
considered a risk. Suitable monitoring methods for TSE contamination of
both air and ash are needed. Protocols for safe burning in emergency
situations need to be established. The SSC reiterates the consideration
made in its opinion of 24-25 June 1999 on "Fallen Stock"1. The limited
capacity for destruction of animal wastes in certain countries or
regions in the first place justifies the installation of the required
facilities; it should not be used as a justification for unsafe disposal
practices such as burial. However, the SSC recognises that for certain
situations or places or for certain diseases (including animals
killed and recycled or disposed of as a measure to control notifiable
diseases), the available rendering or incinerator or disposal capacity
within a region or country could be a limiting factor in the control of
a disease. Thus if hundreds or even millions of animals need to be
rendered after killing or if the transport of a material to a rendering
or disposal plant proved to be impractical, an appropriate case by case
risk assessment2 should be carried out before deciding upon the most
appropriate way of disposal. In principle, the risk is expected to be
the lower for small incinerators3 as compared to open burning. As
such decisions in practice may have to be taken at very short notice,
risk management scenarios according to various possible risks should be
prepared in advance to allow for a rapid decision when the need arises.
1 Scientific Opinion on The risks of non conventional transmissible
agents, conventional infectious agents or other hazards such as toxic
substances entering the human food or animal feed chains via raw
material from fallen stock and dead animals (including also: ruminants,
pigs, poultry, fish, wild/exotic/zoo animals, fur animals, cats,
laboratory animals and fish) or via condemned materials.
Adopted By the Scientific Steering Committee at its meeting of 24-25
June 1999. (and re-edited at its meeting of 22-23 July 1999).
2 See also the relevant sections and footnotes on risk assessment in the
report accompanying the SSC opinion of 24-25 June 1999.
3 See SSC opinion of 16-17 January 2003 on the use of small incinerators
for BSE risk reduction.
3

OPEN BURNING OF POTENTIALLY TSE-INFECTED ANIMAL MATERIALS
REPORT

1. MANDATE

On 17 May 2002, the Scientific Steering Committee (SSC) was invited by
Commission Services to advice on the examples of conditions under which
safe burning of potentially TSE-infected animal materials can be
achieved. The SSC appointed Prof.J.Bridges as rapporteur. His report was
discussed and amended by the TSE/BSE ad hoc Group at its meeting of 9
January 2003 and by the SSC at its meeting of 16-17 January 2003.

2. GENERAL CONSIDERATIONS

Burning is a combustion process to which a range of control measures may
be applied to contain emissions and to ensure the completeness of the
degradation process for organic matter. Depending on the source (waste)
material the burning process may or may not require addition of other
energy sources. Incineration/pyrolysis are contained combustion
processes are contained combustion processes and therefore have the
potential for a high level of control.
(However see opinion on small incinerators). At the other end of the
control spectrum is open burning; such as bonfires.
Typically combustion of animal waste requires the addition of a high
calorific fuel in order to initiate (and for some materials to sustain)
the process. It is recognised that open burning of animal waste is a
very cheap and convenient method of disposal. However uncontained
burning has a number of problems in terms of the potential risks involved:

(1) In the open burning situation a range of temperatures will be
encountered. It is difficult therefore to ensure complete combustion of
the animal waste. If the waste is contaminated with pathogens there will
remain considerable uncertainty as to the degree of their inactivation.

(2) Gaseous and particulate emissions to the atmosphere will occur and
consequently worker and public exposure is likely. There is very little
data to indicate whether or not some pathogens could be dispersed to air
as a consequence of open burning.

(3) The supporting/secondary fuel may be a source of contamination
itself. For example in the recent foot and mouth disease outbreak in the
UK timbers were used at some sites that were heavily contaminated with
pentachlorophenol.

(4) The residual ash must be considered to be a risk source. Its safe
disposal needs to be assured (see opinion on small incinerators) to
prevent human and animal contact and protect from groundwater
contamination. While careful selection of burning sites can reduce the
risks open burning should only be considered in emergency situations.
For each such emergency situation a specific risk assessment should be
conducted which must include the risk 4 from the pathogen of immediate
concern but also other pathogens that might be present.

3. RISK ASSESSMENT OF OPEN BURNING FOR BSE

The SSC, at its meeting of 28th-29th June 2001, recommended "a framework
for the assessment of the risk from different options for the safe
disposal or use of meat and bone meal (MBM) and other products which
might be contaminated with TSEs and other materials. Applying the
framework to the practice of open burning, the following conclusions can
be drawn:

3.1. Nature of the materials handled
Potentially a wide variety of materials can be used provided suitable
secondary fuel is available. The burning process is very simple in
principle and difficult in practice to regulate effectively.

3.2. Risk reduction due to open burning There is no reliable data to
indicate the extent of risk reduction that could be achieved by open
burning. It is reasonable however to assume that overall it
will be rather less effective in reducing the infectivity of BSE/TSE
than wellconducted incineration. Moreover the reproducibility of the
risk reduction is likely to be very variable even at a single location.

3.3. Airborne emissions and residue ash The composition of airborne
emissions and residue ash is rarely monitored. From a risk assessment
viewpoint particular attention needs to be given to the potential for
the airborne dispersal of relatively heat stable pathogens as a
consequence of open burning. In the absence of reliable data both
airborne emissions and residual ash must be considered to constitute a
significant risk if animal waste that might be contaminated with TSEs is
being burnt.

4. FURTHER INVESTIGATION

Research is needed particularly on:
* The potential for airborne dispersal of relatively heat stable pathogens.
* Methodologies to improve the efficacy of the combustion process to
ensure the inactivation of pathogen contaminated animal waste.

5. CONCLUSION

Open burning potentially represents a significant risk where the animal
waste has the possibility of being contaminated with BSEs/TSEs. Suitable
monitoring methods for TSE contamination of both air and ash are needed.
Protocols for safe burning in emergency situations need to be established.

http://europa.eu.int/comm/food/fs/sc/ssc/out310_en.pdf

C:\WINNT\Profiles\bredagi.000\Desktop\Incinerator_OPINION_0301_FINAL.doc

EUROPEAN COMMISSION
HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL

Directorate C - Scientific Opinions
C1 - Follow-up and dissemination of scientific opinions
OPINION ON

THE USE OF SMALL INCINERATORS FOR BSE RISK REDUCTION

SCIENTIFIC STEERING COMMITTEE
MEETING OF 16-17 JANUARY 2003

2
OPINION
On 17 May 2002, the Scientific Steering Committee (SSC) was invited by
Commission Services to (i) evaluate a risk assessment1 prepared for the
UK's Spongiform Encephalopathy Advisory Committee (SEAC), on the
potential risk arising from the use of small incinerators to dispose of
specified risk materials and (ii) to advise on the safety
with regard to TSE risks of the use of such small incinerators.

The details of the SSC's evaluation are provided in the attached report.
The SSC concludes as follows:

(i) The SSC, at its meeting of 28th -29th June 2001, recommended "a
framework for the assessment of the risk from different options for the
safe disposal or use of meat and bone meal (MBM) and other products
which might be contaminated with TSEs and other materials." This
framework comprised five components:

(1) Identification and characterisation of the risk materials involved,
the possible means for their transmission and potential at risk groups.

(2) The risk reduction achieved by the particular process.

(3) The degree to which the risks can be contained under both normal and
emergency operating conditions. This inevitably includes consideration
of the effectiveness of control measures.

(4) Identification of interdependent processes for example transport,
storage, loading of any TSE related risk materials.

(5) The intended end-use of the products for example disposal, recycling
etc. The risk assessment prepared for SEAC focuses on the risks involved
steps 1 and 2 in respect of BSE/TSEs only and is based on a visit to 10
incinerators out of a total of 263 in the UK of which 60% had after
burners. The risk assessment is also using a number of assumptions and
data that may be valid for certain incinerator types under certain
conditions, but are not necessarily applicable either for all types of
materials to be disposed of, or to the whole range of types of small
incinerators in use the EU and the UK.

(ii) Small incinerators are widely used to meet the needs of local
communities. These incinerators vary greatly in their design, nature of
use and performance characteristics and the quality of their management.
As a consequence of this variability there are many uncertainties in
identifying risks posed by small incinerators that are used to treat SRM
materials and each type should eventually receive its own assessment.
Also, general operating and control criteria should be established for

1 DNV Consulting (Det Norske Veritas), 2001. Risk assessment of SRM
incinerators. Prepared for the UK Ministry of Agriculture, Fisheries and
Food. Revision 2 of the Draft report, February 2001. 24
pages. 3

Potential risk sources arising from the incineration process include:
gaseous emissions and residual ash. Research is currently ongoing
mimicking incineration of TSE-infected brain tissue to assess the
infectivity clearance level under various scenarios2. However, there are
no final reported measurements that enable the risk to be assessed from
either the emissions or the ash from small incinerators. It has
been argued that the protein content of the ash is a reasonable
surrogate measure of the degree of risk deduction caused by the
incineration process. This assumption is questionable in view of the
resistance to heat of prions as compared to other proteins. Protein
measurements in ash are however probably a useful general
measure of the overall efficiency and reproducibility of the
incineration process. Results in the aforementioned report1 indicate a
large degree of variability in performance among the small incinerators
in the UK that have been evaluated. It is anticipated that small
incinerators, used by other Member States will also show a
considerable variation in performance. In evaluating the risk of small
incinerators, consideration should be given to the risk of potential
contamination of the ash and of the gaseous emissions.
In the absence of generally accepted and enforced performance standards
for small incinerators handling SRMs each such facility therefore needs
to be the subject of a specific risk assessment. The SSC considers that
the standards set up by the new Waste Incinerator Directive (2000/76/EC)
and in its opinion of June 1999 on waste disposal should serve as
guidance. In the absence of reliable data on the possible residual
infectivity of the ash, it should be disposed of, i.e., in controlled
landfills as described in the SSC opinion of June 1999 on safe disposal
of waste. The SSC finally wishes to emphasise the need for suitable
monitoring methods in order that risks can be assessed readily for
individual types of small incinerators.
2 P.Brown, pers.comm., December 2002. Publication in progress.4

THE USE OF SMALL INCINERATORS FOR BSE RISK REDUCTION
REPORT

1. MANDATE

On 17 May 2002, the Scientific Steering Committee (SSC) was invited by
Commission Services to (i) evaluate a risk assessment3 prepared for the
UK's Spongiform Encephalopathy Advisory Committee (SEAC), on the
potential risk arising from the use of small incinerators to dispose of
specified risk materials and (ii) to advise on the safety with regard to
TSE risks of the use of such small incinerators.

The SSC appointed Prof. J. Bridges as rapporteur. His report was discussed
and amended by the TSE/BSE ad hoc Group at its meeting of 9 January 2003
and by the SSC at its meeting of 16-17 January 2003.

2. CURRENT LEGISLATIVE FRAMEWORK

Until 2000, small incinerators were exempt from the emission limits set
by the EC for MSW and hazardous waste incinerators with throughputs
greater than 50 kg/hour. An "incineration plant" is defined by the new
Incineration of Waste Directive (2000/76/EC) as "any stationary or
mobile technical equipment dedicated to the thermal treatment of waste
with or without recovery of the combustion heat generated". This
definition would appear to exclude open burning of waste. The
new Directive, which must be transposed into the legislation of each
Member State by December 2002, replaces a range of previous directives
on incineration. It applies to all new incinerator installations from
December 28th 2002 and all existing installations from December 28th
2005. The principal aim of the Directive is to prevent and/or limit
negative environmental effects due to emissions into air, soil,
surface and ground water and the resulting risks to human health from
the incineration and co-incineration of waste. It covers many aspects
from a requirement for afterburners to airborne emission limits and
criteria for the composition of residual ash. Previous EC legislation
has exempted small incinerators (i.e. those operating at less than 50 kg
per hour). The Waste Incinerator Directive (WID) (2000) allows such
small incinerators to be exempt from licensing at the national level
however they will still be subjected to the same onerous
requirements of the WID as larger incinerators.

In the UK it is proposed that in future incinerators dealing with
non-hazardous waste but with a throughput of less than 1 tonne per hour
will be regulated by local authorities whereas those with a larger
throughput will be regulated by the national authority. It is possible
that different regulatory mechanisms may result in differences in the
rigour with which the new standards are enforced. The position
on the disposal of animal waste is complicated. Animal carcass
incineration use not covered by the WID and therefore the existing
regulatory framework (90/66/EEC which covers animal and public health
requirements to ensure destruction of pathogens) will continue to be
applied. A new Animal By-Products Regulation

3 DNV Consulting (Det Norske Veritas), 2001. Risk assessment of SRM
incinerators. Prepared for the UK Ministry of Agriculture, Fisheries and
Food. Revision 2 of the Draft report, February 2001. 24
pages.
5

(ABPR) will apply in Member States during the first part of 2003. The
relationship to WID has been included in the ABPR. It is important that
it does not result in less strict standards being applied for animal
carcass incineration. In contrast to whole carcasses WID will apply to
the burning of meat and bone meal, tallow or other material (even if
they burn animal carcasses too). Additional specific directives will
continue to apply to waste that could be contaminated with BSE/TSEs.
(96/449/EC)

3. CURRENT USE OF SMALL INCINERATORS TO DISPOSE OF ANIMAL WASTE
Small incinerators are used for a variety of purposes and in a range of
locations among Member States. Many are located alongside small
abattoirs, knackers, hunt kennels, or laboratories. Thus they meet the
needs of relatively small communities. Across Member States these small
incinerators include a variety of designs and operating conditions (as
indicated above in principle they will probably be required
to meet specific standards for emissions and for the composition of the
residual ash by December 28th 2005).
In the UK there are indications (see DNV Report 2001) that a
considerable quantity of SRM which would have previously been sent for
rendering is now being incinerated directly in small incinerators. Thus
evaluation of the risks from such incinerators is of increasing importance.

4. RISK ASSESSMENT FOR SMALL INCINERATORS

The SSC, at its meeting of 28th -29th June 2001, recommended "a
framework for the assessment of the risk from different options for the
safe disposal or use of meat and bone meal (MBM) and other products
which might be contaminated with TSEs and other materials.
This framework comprised five components:

(1) Identification and characterisation of the risk materials involved,
the possible means for their transmission and potential at risk groups.

(2) The risk reduction achieved by the particular process.

(3) The degree to which the risks can be contained under both normal and
emergency operating conditions. This inevitably includes consideration
of the effectiveness of control measures.

(4) Identification of interdependent processes for example transport,
storage, loading of any TSE related risk materials.

(5) The intended end-use of the products for example disposal, recycling
etc. Recently a report has been prepared by DNV consulting (2001) for
the UK Ministry of Agriculture, Fisheries and Food (now known as DEFRA)
that assesses the risks from small incinerators in the UK that receive
SRMs. This report focuses on the risks involved steps 1 and 2 in respect
of BSE/TSEs only. 10 incinerators out of a total of 263 in the UK were
visited of which 60% had after burners.

(1) Nature of the materials handled.

The DNV report 2001 starts with the assumption that "the materials
incinerated at small abattoirs will be mainly SRM and bones from animals
that are fit for human consumption. It may also include material from
animals failed by meat inspectors. The likelihood of there being an animal
6 with significant BSE infectivity is very small and certainly much less
than for the fallen stock handled by hunt kennels and knackers4. For
this reason the study has concentrated on the latter type of operation".
The Report notes that "the material handled by both knacker and hunt
kennels is highly variable and difficult to characterise". In terms of
input the key factors to consider are:

* The number of adult bovines processed and the proportion of these
carcasses that are likely to be infected.

* The extent of infectivity (in terms of human oral Infectious Units)
that may occur (average and worst case).

In the DNV (2001) risk assessment only the BSE risk from processing
bovine SRMs was considered. For quantitative risk assessment purposes
the mean value of the oral ID50 for cattle was taken as 0.1 gram. A
range of values was taken to cover uncertainty in the inter-species
barrier from 104 to 1 (as recommended by the SSC 2000). In order to
assess the likelihood that a particular carcass could be infected, UK
and Swiss monitoring data was used. An incidence rate based on Prionics
test findings of between 0.013 and 0.0025 was calculated. The DNV Report
notes that prevalence rates are progressively reducing from these
1998/99 figures. Finally the report concludes that the SRM from an
infected bovine could contribute 700 Infectious Units.

(2) Risk reduction due to incineration

Once a carcass/SRM has been introduced into a small incinerator there
are two main sources for the potential release of BSE infectivity

(a) Airborne emissions
(b) Residual ash

There is no direct data on the TSE levels that may occur in those two
media. The SSC however is aware of currently ongoing heat studies
mimicking various incineration conditions and scenarios and aiming at
assessing the TSE clearance efficacy of these processes (P.Brown,
pers.comm., 16.01.03) on both the residual ash and the trapped emission
gases. In the absence of final data from such experiments for individual
(small) incinerator types, the DNV Report (2001) assumes that
measurement of the total protein content of ash is a relevant surrogate
for BSE/TSE material. Protein content is a useful indicator of the
general performance of an incinerator. However it is much more
problematic whether it is also a valid marker for possible BSE/TSE
contamination as it known that BSE/TSE are relatively heat resistant as
compared to other proteins. Failure to detect certain amino acids
present in prions is encouraging but the sensitivity limits
for amino acids are relatively poor for reassurance purposes. Equally
important, the data provided in the DNV report shows moderate split sample
4 It may be mentioned that this assumption may be valid for the UK as a
whole, but note necessarily for all other Member States. 7
variation but often substantial inter sampling variation (up to 600
fold). This indicates a wide span of performance standards among the
small SRM incinerators in the UK and most likely across the whole of the
EU. Typically performance was substantially poorer than is the case for
larger incinerators. Unburned material is not uncommonly noted in the
ash from small incinerators. If the reduction in protein content due to
incineration is accepted as a valid indicator, typical infectivity
reduction can be calculated to be of the order of 1600 (DNV Report
2001). Incinerators are known to emit particulate matter from their
stacks. Larger incinerators have much higher stacks to facilitate
disposal of emissions, they also have gas cleaning equipment to minimise
the emission of particulate matter, metals and acidic gases. Small
incinerators generally do not have any gas cleaning equipment. It can be
speculated (as in the DNV Report 2001) that unburned materials (and
therefore potentially infections is much less likely to be emitted in
the form of particulate matter than burnt material.
Nonetheless there is no data to support this assumption.

(3) Other considerations.

(a) Disposal of ash.

In the case of small incinerators ash is often dispersed of locally to a
trench, which is typically neither lined, nor is the residue buried
deeply. In contrast for larger incinerators in the UK ash is normally
disposed of to a contained landfill. The risk from disposal to a trench
is difficult to gauge in the absence of reliable data on the possible
infectivity of the ash.

(b) Management factors.

Almost inevitably the level of expertise available for the management
of small incinerators is highly variable because few such facilities can
afford to employ specialists in incineration. This is also likely to be
often the case for the inspectors as well. While such considerations
cannot formally be taken into account in a risk assessment, they are
not the less relevant factors that need to be considered in assessing
the risk from a particular plant.

(c) Benchmarking.

The DNV 2001 risk assessment relies greatly on the assumption that
BSE/TSE contaminated material is very unlikely to be processed.
The Report seeks to compare the risks from a small incinerator with
that from large SRM incinerators which the author had assessed
previously (DNV, 1997). It identifies that the risk is four-five -fold
less from a typical small incinerator because the scale of activities is
much lower. However it is noted that the amount of experimental
data to back this conclusion is extremely limited and does not take
into account either risks from the residual ash or any consequences of
a substantially lower stack height limiting the dilution of the emitted
particulate and gaseous matter. 8

5. FURTHER INVESTIGATIONS

In view of the uncertainty regarding the risks due to BSE/TSE
contamination of the fly and bottom ash and airborne emissions it is
recommended that further research is conducted to identify the residual
risks (along with attendant uncertainties) from the burial of ash
(without further treatment,) in uncontained sites. It is essential that
suitable monitoring methods are developed.

6. LITERATURE

EC (European Commission), 1999. Opinion on The risks of non conventional
transmissible agents, conventional infectious agents or other hazards
such as toxic substances entering the human food or animal feed chains
via raw material from fallen stock and dead animals (including also:
ruminants, pigs, poultry, fish, wild/exotic/zoo animals, fur animals,
cats, laboratory animals and fish) or via condemned materials. Adopted
By the Scientific Steering Committee at its meeting of 24-25 June 1999
and re-edited at its meeting of 22-23 July 1999. DNV Consulting (Det
Norske Veritas), 1997. Risks from disposing of BSE infected cattle in
animal carcass incinerators. Report prepared for the UK Environment
Agency. DNV Consulting (Det Norske Veritas), 2001. Risk assessment of
SRM incinerators. Prepared for the UK Ministry of Agriculture, Fisheries
and Food. Revision 2 of the Draft report, February 2001. 24 pages.
SEAC (Spongiform Encephalopathy Advisory Committee, UK), 2001. Public
summary of the SEAC meeting of 25 April 2001.

http://europa.eu.int/comm/food/fs/sc/ssc/out311_en.pdf

The BSE Inquiry / Statement No 19D
Dr Alan Colchester
Issued 27/01/2000
STATEMENT BY DR A C F COLCHESTER IN RESPONSE TO
WS493 DATED 09/08/99 BY PAUL GALE
1. WS493 by Dr Paul Gale discusses the infectivity and environmental
behaviour of
the BSE agent, and makes comments on WS18 and WS19.
2. The present statement responds to some of the points made in WS493.
3. In paragraphs 13, 14, and 15 of WS493, Dr Gale reviews recent
evidence relevant
to the debate about possible minimum or median infective dose of
BSE-infected
cattle tissue to humans after oral ingestion. Evidence from experiments by
Raymond et al 1997 [J/N/388/285] is reviewed. That research contributes
to our
gradually increasing understanding of factors affecting prion infection,
but many
aspects are still not understood. One of the apparent implications of
the Raymond
et al paper is quoted by Dr Gale [WS493 para 15], viz. that sheep
scrapie is
inherently as transmissible to humans as BSE. One could draw three
conclusions
from this. The first possible conclusion (this is the interpretation
chosen by Dr
Gale) is that because scrapie is not known to cause human illness, so
the risk of
BSE causing a human illness is therefore very small. A second, alternative
conclusion is that scrapie may indeed turn out to be transmissible to
man, although
this has never been demonstrated. Considering the strength of the
evidence that
BSE is indeed the cause of variant CJD, the second interpretation is
arguably the
more plausible of the two. A third possible conclusion is that the
information
provided by Raymond et als experiments about transmissibility to man of
BSE, or
of scrapie, or both, have to be interpreted with caution.
2
4. These points underline the fundamental fact that our understanding of
these
processes is still very limited. We have no direct evidence to enable us
to quantify
the human oral infective dose of BSE-infected bovine material. The
Government
naturally has to draw heavily on the advice of expert scientific
committees when
making decisions about such matters as the regulation of rendering.
However, even
for an expert scientific committee, uncertainty derived from shortage of
data is
difficult if not impossible to quantify. Conventional risk assessments are
notoriously bad at coping with such uncertainty. The consensus view of a
committee does not necessarily provide even coverage of the true
spectrum of
possibilities. When there is a serious shortage of experimental data,
ten opinions
about the same single source of experimental data may be no more
valuable than
one. In such circumstances, Government decision making needs to be
guided much
more by issues of principle, for example the relative prioritisation of
business and
health interests.
5. In paragraphs 18, 19 and 20 [WS493], Dr Gale discusses the expected
binding of
prion protein to the particulates. He states (paragraph 18) that prion
molecules,
which are about 4nm in size, could only pass through 400nm filters if
solubilised in
highly concentrated detergent which would not occur in a natural aquatic
environment. In my view, we should keep an open mind about the possible
physico-chemical state of the prion protein in the water-based products of
rendering. As I proposed in WS19 paragraphs 21 and 25, rendering may
paradoxically increase the total available infectivity. The cooking
processes
involved in rendering are likely to generate an emulsion of lipid
droplets to which
the lipid-soluble moiety of the prion protein would attach (Planning
Inquiry APP
J2210/A/96/2687; Proof of Evidence by ACF Colchester, Jan 1997, pages 3 and
15), leaving the hydrophilic moiety orientated outwards, effectively
stabilising the
droplet in solution. This concept was developed by John Williams [WS
18]. Thus,
the amphipathic prion protein molecule would itself act as a detergent.
6. In paragraph 20 [WS493], Dr Gale refers to my definition of
amphipathic as
slightly misleading. He has slightly misinterpreted my definition, and I
believe I
have clarified this in the above paragraph.
3
7. At the end of paragraph 20 [WS493] Dr Gale asserts any prions become an
integral part of the meat and bone meal formed during rendering. As I
have argued
in WS19, this has not been demonstrated experimentally, and in my view
Dr Gale
has not justified his assertion. Later, in paragraph 25, he repeats one
of the
conclusions from one of Taylors 1995 experiments: the rendering
process itself
eliminates 98% of BSE infectivity. Again, these were difficult and limited
experiments carried out on pilot-scale equipment and without assaying
all the output
products [WS19 paras 21-28]. The type of rendering processes simulated
were not
necessarily the same as those in use in real life rendering.
8. Gales paragraphs 29 to 43 [WS493] cover issues concerning the potential
minimum size of infective particles. He refers to WS19, in which I
summarised
two possible scenarios (paragraph 37). These are clarified below.
9. In Scenario 1, infective particles cannot be split i.e. they are
undilutable. In these
circumstances, ingestion by an individual of a minute mass of material
carrying the
infective particle (e.g. a soil particle, a droplet of water etc.) could
transmit the
entire infective dose. The risk assessment would need to estimate the
probability
that a specific individual might ingest such a particle - and thereby
acquire a
significant chance of infection. Risk assessment should also estimate the
probability that the action of releasing a certain number of infective
particles
would cause any individual(s) to develop the disease. This should be
extended to
a probability distribution giving the probabilities that the actions of
releasing a
certain number of infective particles would cause different numbers of
individuals
to develop the disease (one probability for each number of individuals).
10. In my Scenario 2, components of infective particles were so small
that they were
highly dilutable. In such circumstances, minute sub-fractions of
infective doses
might reach a much larger number of individuals. If cumulative dosing
were not
possible, this would not imply any risk to those individuals. On the
other hand, if
cumulative dosing were possible, then the probability that a specific
individual
4
might accumulate one total infective dose from multiple ingestions of
minute subdoses
would need to be calculated. I agreed that Scenario 2 should indeed be
evaluated, to cover one of the possibilities. The risk assessments
carried out for
the Environment Agency mainly focused on Scenario 2, and used
assumptions of
dilutibility and even mixing within very large volumes of water or soil.
It was
calculated that it would be necessary to consume impossibly large
volumes of the
water or soil before accumulating an infective dose. For example, Young
et al in
WRc Report CO4268, published in Jan 97 as EA14 at the Public Planning
Inquiry,
estimated that 8.3 litres of contaminated soil from the discharge zone
would have to
be consumed to transmit one human oral infection dose. (This was based
on a socalled
worst case situation  see below). It seems inconceivable that any human
would ever ingest 8.3 litres of soil. However, under scenario 1, local
aggregations
of one or more infectious doses could certainly be ingested as a result of
contamination of e.g. hands by trivial amounts of soil. As an aside, I
do not accept
that Youngs so-called worst case assumptions for the above example were
really
worst case. One of the assumptions was a species barrier. In fact, it
assumed a
species barrier of 1000 which is certainly not worst case. Professor
Almond
considered that a species barrier of 1 would be a reasonable worst-case
assumption and this would have implied a human oral infectious dose
could be
carried in 8.3ml of soil  a volume which might easily be ingested. For
scenario 2
(as for scenario 1), the probability that the action of releasing a
certain dose of
infectivity would cause any individual(s) to develop the disease should
also be
calculated. This second probability may be quite different in the different
scenarios.
11. To recap, I argued that the risk assessments should fully evaluate
both scenarios. In
addition, the risk assessments should not only calculate the probability
of a specific
individual acquiring infection, but the probability that the action of
discharging
infective material would lead to one or more infections. I do not
think Dr Gales
responses [WS493] have answered these points.
5
12. In my discussions about the potential risks associated with
rendering, and the whole
approach to its regulation, I have repeatedly stressed that there is a
spectrum of
possible risks, associated with various environmental pathways and various
possible portals of entry into the body. Once again, the Environment
Agency has
focused specifically on the issue of the possibility of transmission by
the water
supply. I regard the water supply pathway as representing only a very
small risk,
but one which is very hard to quantify and one which would potentially
affect a
large number of people. The debate about water supply should not detract
attention
from the existence of several other potential pathways which need to be
considered
and evaluated.
Issued on behalf of the witness by:
The BSE Inquiry Press Office
6th Floor Hercules House
Hercules Road
London SE1 7DU
Fax: 0171 803 0893
Website: http://www.bse.org.uk
email: inquiry@bse.org.uk

http://www.bseinquiry.gov.uk/files/ws/s019d.pdf


The BSE Inquiry / Statement No 19C
Dr Alan Colchester
Issued 27/01/2000
STATEMENT BY DR A C F COLCHESTER IN RESPONSE TO
WS490 DATED 09/08/99 BY MR C P YOUNG
1. Statement WS490 by Mr C. P. Young, Principal Hydrogeologist, Soil
Waste and
Ground Water Group, WRc, Medmenham, Bucks, concerned geological and
hydrogeological factors which may control the movement and attenuation
of BSE
infectivity in water in the environment, and referred to specific points
raised in
WS18 and WS19 of March 1998.
2. WS490 referred particularly to the potential impact of the discharges
from Thruxted
Mill on the ground water, particularly because of its proximity to
drinking water
extraction bore holes. However, it did not consider the other risks
arising from
material delivered to or discharged from this factory.
3. In paragraph 18 [WS490], Mr Young described his conclusions about the
probable
rate of flow of water through the unsaturated zone. This would be slow,
with the
result that it would take from a few to several tens of years for
material to travel
from the surface to the water table. It is likely that such slow
transmission applies
at many parts of the discharge zone around Thruxted Mill. This is true
whether or
not there are also locations where transit through to the water table is
faster. It is
therefore clear that some of the material discharged many years ago may
only now
be beginning to reach the aquifer. This is one of several reasons why
the past
history of discharges at Thruxted Mill continues to be important.
4. Mr Young gave a very clear review of the potential behaviour of water
and
dissolved or particulate materials when soaking through a medium such as
chalk
2
which may contain variable numbers of large fissures. The presence of
significant
numbers of fissures, or the use of a borehole or old well for discharge
purposes,
would provide a rapid route to the water table through which a variety of
particulate substances could pass. Mr Young referred to the absence of
persuasive
evidence of rapid movement via fissures of water and dissolved or
particulate
materials from the surface to the water table at Thruxted Mill [WS490
para 20].
In my view, it should be borne in mind that absence of persuasive
evidence is not
persuasive evidence of absence. The physical existence of potential routes
allowing rapid transit is one type of evidence; evidence from water
samples (tested
for conventional pathogens, ionic substances etc) is another.
5. My Young also provided a clear review of the potential mechanisms of
removal of
particulate matter from liquid passing through intact chalk [WS490] (ie.
not through
large fissures or boreholes). He discussed the potential for filtration and
adsorption of particles carrying BSE prions. In my view, the problem
about this is
that prions can exist in several physico-chemical forms. The range of
types of
particles which might exist in the inputs and outputs of a rendering
factory and
which might carry BSE prions is simply not known with confidence. In
particular,
the rendering process itself will alter the properties of lipid and
protein particles.
We do not know enough to quantify the possibility that particles may
exist in a form
that could pass through the chalk matrix. We certainly know that, in
laboratory
conditions, preparations of infective material are often passed through a
microporous filter, with pore sizes of less that 0.5 micron. This does
not generally
attenuate prion infectivity but does remove most other pathogens.
6. In paragraph 26, final bullet point, Mr Young referred to pore sizes
used in the
laboratory of 500 micrometers [WS490] (one micrometer is one millionth
of a
metre or one micron). I presume this is a typographical error, because
he should
have referred to nanometers (a nanometer is one thousand millionth of a
meter).
7. Considering what is now known about the potential infectivity of
rendering factory
output, there would seem to be an overwhelming case for its
classification as toxic
waste. However, in the historical context, rendering factory outputs
appear to have
3
been classified with strong organic and biodegradable effluents. The
Environment Agency emphasise the consistency of their approach, as if
this were to
be commended, an attitude which seems dangerously inflexible in the
light of the
new information about the risks to human health of the products of
rendering.
Within the historically accepted class of strong organic and biodegradable
effluents, the categorisation should clearly be low nutrient/ industrial
effluent
(Policy and Practice for the Protection of Groundwater, National Rivers
Authority,
1992). When the discharge area is near a water supply borehole, the
ground above
is graded into three Source Protection Zones: the Inner Protection Zone
(based on
a 50 day travel time from any point below the water table to the
source); the Outer
Protection Zone (400 days); and the Source Catchment Zone (the remaining
catchment area of the ground water source). The approach to regulation of
discharge, according to the type of effluent and the travel times to the
water
extraction point, is shown as a matrix (table) on page 36 of the NRA
booklet
(Appendix 1 [YB92/00.00/10.1]). Appendix 1 shows that there is an important
threshold between the Outer Protection Zone and the Source Catchment Zone,
because, in the former (areas closer then 400 days transit time to the
water supply
extraction point), discharges of low nutrient content or industrial
effluent should be
automatically prohibited.
8. In paragraph 21 of WS490, Mr Young referred to Thruxted Mills
location as being
in an area in which time for flow in a saturated zone to the boreholes
is about 400
days, or greater. In the light of the historical importance of this 400
day threshold,
I examined the situation of Thruxted Mill in relation to the 400 day
transit time to
the nearest borehole (Godmersham). Maps included in the Environment
Agencys
studies confirm that the Mill in fact must lie extremely close to that
threshold. Two
such maps are reproduced here for ease of comparison: Appendix 2 is p
16, fig 2.3
(Hydrogeological features of the area around Thruxted Mill), from C.P.
Young et
al Assessment of the Potential Impact of Past and Present Disposal of
Effluent
from Thruxted Mill on Ground Water Quality, March 1997 [M70 Tab 9].
Appendix 3 is fig 1 (Location map) from WS490 itself. The 400 day
threshold
line has clearly been drawn freehand (compare the two maps in the
Appendices),
and indeed small differences in drawing could lead to the Mill lying
inside or
4
outside the Outer Protection Zone. The transit time from Thruxted Mill
to the
aquifer in the saturated zone appears only to have been estimated very
approximately. More accurate measurement might well indicate a shorter
transit
time. If this were to be the case, the Environment Agency should have
prohibited
discharge long ago, even assuming that no new, more stringent,
regulation was
applied to take account of the recent discovery of serious risks to
humans of BSEcontaminated
material. It is accepted that the NRA document is not prescriptive
and while it seeks to control activities within certain travel time
zones around
public water supply sources, it allows for individual site specific
assessment
(Canterbury Planning Inquiry, EA Proof of Evidence, section EA 1, Pages
7 & 8,
Groundwater Protection Policies). However, in the case of Thruxted Mill,
the
heightened concern about the safety of discharges should clearly have
led to a more,
rather than a less, stringent interpretation of the Policies.
9. In paragraph 22, Mr Young referred to the February 1997 Public
Planning Inquiry in
Canterbury [WS490]. Concerning the old well on the site of the Mill, he
says that
its potential impact on groundwater quality was not assessed. However,
as my
second statement to the BSE Inquiry [WS19B] showed, the EA were fully
informed
about the recent allegations of discharges into the well as early as
June 1996. The
EA have also admitted that the NRA/ EA had been fully aware of the
presence of
the well on the site for some years previously, and that the well had
only been
partially backfilled with sand in 1978, which would of course have
allowed its
continuing use as a discharge route. The EA were requested, at the
pre-Planning
Inquiry meeting in Canterbury in December 1996, to take full account of
the well,
although Counsel acting for the EA argued that it was irrelevant (cf
WS19B para
59). Furthermore, Mr Youngs report, which was dated March 1997 [M70 Tab
9],
contained extensive data obtained before the Planning Inquiry. It is
quite clear from
that report that many of the analyses contained in it must have been
completed well
before the publication date of the report, in other words well before
the Planning
Inquiry. In summary, while I agree that the potential impact on
groundwater
quality of the well was not assessed in the context of the Planning
Inquiry, the
relevant data and analyses were available at the time of the Inquiry. In
my opinion,
5
these data should have been discussed at the Planning Inquiry, and my
reasons were
made very clear before and during that Inquiry itself.
10. In paragraph 24 [WS490], Mr Young refers to readings quoted by the
EA showing
that the rate of fall of the water level in the well during late 1996
was low. This
implied that the well had become blinded. However, the data about the
rate of
soaking away obtained in late 1996 do not provide any information about
the time
when the blinding may have taken place. In the risk assessments
referred to by
Young in his report dated March 1997 [M79 Tab 9] it was assumed that the
rate of
leakage from the well had smoothly reduced from 1988 to 1996. This is
complete
speculation. The arbitrary assumption of a gradual reduction over many
years
generated predictions which appeared to contradict one of the
allegations by a
former contractor who worked on the site (who had stated that he had
seen flexible
hoses dragged to the top of the well and effluent being discharged
through them).
These apparent contradictions were used by the EA and by solicitors
acting for
Canterbury Mills Ltd to argue that the former contractors evidence was
unreliable.
In my view, exactly the opposite conclusions were more logical. That is,
the
possibility that the blinding was a recent event was not only plausible
a priori, but
such an interpretation was supported by the observations alleged by the
former
contractor of the use of the well as a route of discharge.
11. In paragraph 26 [WS490], final bullet point, Mr Young refers to the
precautionary
principle. He quotes PPG 23, where the precautionary principle is set
out. PPG
23 requires that the precautionary principal should be applied when
there is
perceived to be an unacceptable risk, even if it cannot be scientifically
quantified. Youngs argument is circular. He merely states that because
the EA, or
the scientific consultants acting for the EA, did not themselves
perceive there to be
an unacceptable risk, the precautionary principle automatically did not
apply. Any
serious debate about this issue should address the question of how to
define an
unacceptable risk which cannot be scientifically quantified.
12. Once again, the Environment Agency has focused specifically on the
issue of the
possibility of transmission by the water supply. I regard the water
supply pathway
6
as representing only a very small risk, but one which is very hard to
quantify and
one which would potentially affect a large number of people. The debate
about
water supply should not divert attention from the existence of several
other
potential pathways which need to be considered and evaluated. In my
discussions
about the potential risks associated with rendering, and the whole
approach to its
regulation, I have repeatedly stressed that there is a spectrum of
possible risks,
associated with various environmental pathways and various possible
portals of
entry into the body. In my opinion, the recent statements by the
Environment Agency
and its contractors have not invalidated the very strong case to support
the view that
the precautionary principle should be applied to the disposal of liquid
effluent and
sludge from rendering factories. In particular, it should be applied to
the proposed
new subsoil drainage method, as well as to the existing discharge method
in use at
Thruxted Mill.
Issued on behalf of the witness by:
The BSE Inquiry Press Office
6th Floor Hercules House
Hercules Road
London SE1 7DU
Fax: 0171 803 0893
Website: http://www.bse.org.uk
email: inquiry@bse.org.uk

http://www.bseinquiry.gov.uk/files/ws/s019c.pdf

Rendering practices and inactivation of transmissible spongiform ...

File Format: PDF/Adobe Acrobat
... The UK BSE Inquiry. concluded that the disease was bovine derived
(1) but the
Horn ... recombinant prion protein in water, lipid and lipid-water ...
www.oie.int/eng/publicat/rt/2201/19.%20Taylor.pdf -

http://www.oie.int/eng/publicat/rt/2201/19.%20Taylor.pdf

Health Stream Article- Issue 10 June 1998


Water supplies at risk from BSE?

A leading neurologist has warned the British Government's Inquiry into
BSE (bovine spongioform encephalopathy or "mad cow disease") that
drinking water supplies may be at risk of contamination. Dr Alan
Colchester from Guy's Hospital in London gave evidence that the practice
of allowing the spreading of sludge and liquid effluent from carcass
rendering plants onto land could allow the infectious agent to enter
underground aquifiers. The infectious agent of BSE is believed to be an
extremely stable protein molecule (prion) which Dr Colchester believes
may be able to survive the rendering process.

Dr Colchester is one of over 100 scientists and 300 civil servants
expected to testify before the Inquiry which began in March this year.
The terms of reference of the enquiry are "to establish and review the
history of the emergence and identification of BSE and nvCJD (new
variant Creutzfeld-Jakob Disease) in the United Kingdom, and of the
action taken in response to it up to 20th March 1996; to reach
conclusions on the adequacy of that response, taking into account the
state of knowledge at the time".

The proceedings of the Inquiry have been made available on a World Wide
Web site including detailed submissions by witnesses, descriptions of
the roles of key people, and a chronology of events
(http://www.bse.org.uk). The scientific evidence now appears conclusive
that the 26 cases of nvCJD diagnosed in the UK since 1995 represent a
distinct and new form of the disease, and that the characteristics of
the nvCJD agent in animal infection experiments closely match those of
the BSE agent.

However the possibility of transmission of BSE via water supplies would
appear to be remote if the assumptions used in a recent paper by Gale et
al. are accurate (1). The authors assessed the risks associated with a
rendering plant processing BSE infected cattle and disposing of
carcasses in the catchment of a chalk aquifier. The exercise was
difficult because specific data on several aspects are lacking - there
is no dose-reponse data for humans, no information on the behaviour of
the BSE prion in water, no information on the effectiveness of barriers
that may reduce movement of the prion into water, and limited data on
the decay of infectivity in the environment.

To overcome these problems, the authors assessed the available data on
the BSE agent and extrapolated using a series of worst case assumptions.

Infectivity to humans
Infectivity is expressed as the 50% infectious dose (ID50) - the dose
which would infect 50% of exposed individuals. Animal experiments have
shown that infectivity is concentrated in the brain and spinal column of
cattle, and a partial barrier to transmission exists between species so
that about 1000 times the dose is needed to consitute an ID50 in a
different species.

Infectivity via oral or gastric exposure is reduced about 100,000 fold
compared to the intracerebral and intraperitoneal routes. Mice
experiments have shown an oral ID50 of 6.3 g for BSE infected cattle
brain, and the human ID50 is likely to be similar. For risk assessment,
it is assumed the oral ID50 in humans is 1g, and each infected cow
contains 1000 infectious doses (in the brain and spinal tissue). It is
estimated that the oral ID50 in humans is equivalent to about 1013 prion
molecules.

BSE in the aquatic environment
The BSE prion protein is known to contain both hydrophobic and
hydrophilic regions, and to be associated with cell membranes. It binds
strongly to surfaces and is unlikely to exist in free solution in
aqueous media. The authors conclude that as cattle carcasses decay the
BSE agent would be released from cell membranes but would immediately
bind to other particles.

While aggregates of BSE prion have been observed in some infected
animals the maximum number of molecules in an aggregate is about 10 5
molecules, or about 108 fold less than the estimated human ID50.
Therefore such aggregates are not likely to pose an infection risk and
significant net dilution is likely to occur in aqueous environments.

Risks from ingestion
As the considerations above show that it would not be possible to ingest
an entire infectious dose in a single esposure (eg a glass of water),
the risks associated with small fractions of an ID50 were considered.
Using the conventional linear low dose extrapolation commonly applied to
microbial infections, it is calculated that ingestion of 108 prion
molecules (the largest aggregate observed in infected animals) would
correspond to a risk of 0.5 x 10-5, or 1 infection per 200 million
people ingesting this dose.

The authors also discuss experimental evidence that a threshold may
exist for infection - this would have the effect of further reducing the
risk.

Environmental input of BSE
The sources of BSE input are described and it is noted that rendering is
known to destroy 98% of infectivity. Residual infectivity has been
demonstrated for MBM (meat and bone meal) but not tallow (fats).

Environmental barriers
The prion protein is resistent to proteolysis and heat degradation, but
there is evidence that infectivity declines in buried carcasses. There
are no data on the effect of conventional water chlorination on the BSE
prion, but given the molecule's resistance to other chemical treatments
it is unlikely that chlorination would reduce infectivity.

Quantitative risk assessment
The above considerations are factored into a risk assessment with the
following assumptions:

* the rendering plant processes 2000 BSE infected carcasses per week.
* all infectivity is associated with MBM particles
* effluent is treated by dissolved air flotation and sand filtration
before discharge to chalk substrata, 80 m above an aquifier.

By modelling the removal of suspended solids (and attached BSE prion) it
is concluded that only 0.004 human oral ID50 would be discharged from
the plant each day.

It is assumed that the discharge from the plant would take at least 2
years to reach the aquifier layer and that infectivity would decline by
93% in this time. No allowance was made for removal of the BSE prion by
filtration or binding to the chalk, although the authors believe this
would be a major effect. A dilution factor of 83-fold is assumed for the
borehole fed by the aquifier (ratio of plant discharge volume to water
extraction volume).

On this basis the estimated concentration in the extracted water would
be 3.0 x 10-11 of a human ID50 per litre of water. Assuming that
consumers drink up to 2 litres of water per day, the daily risk of
infection would be less than 10-10. An individual would require 45
million years of exposure to reach a cumulative exposure of one ID50.
The application of worst case assumptions at each step means that even
this risk estimate may be grossly over inflated.

The authors note that for quantitative risk assessment to be of
practical use, there must be confidence that the outcome has a
reasonable degree of accuracy. In this case the many unknowns in the
data and the adoption of extreme worst case assumptions means that this
is not the case. However the systematic consideration of each step in
the process illustrate that even if some assumptions are incorrect (eg
if there is no species barrier) the risk of transmission of BSE by
drinking water is still remote.

While the incidence of diagnosed new cases of BSE in cattle in the UK
and other European countries appears to be declining, researchers in
Switzerland have found evidence that many cattle may be infected without
displaying symptoms. A report in the 13th June issue of New Scientist
described the development of a sensitive test to detect the abnormal
protein which causes BSE.

Application of this test to brain tissue samples from 1761 apparently
healthy cows slaughtered because they came from herds where cases of BSE
had occurred, found 8 which tested positive. This suggests that BSE
infection is present at a rate of 4.5 per 1,000 cows, yet the rate of
symptomatic BSE in Switzerland is 100 times less than this. The Swiss
government will now test cows from herds where BSE has not been
reported, to determine whether they too may be infected.

(1) Gale P, Young R, Stanfield G and Oakes D. Development of a risk
assessment for BSE in the aquatic environment. J Applied Microbiology
(1998) 84 p467-477.

http://www.waterquality.crc.org.au/hsarch/HS10c.htm

More than 90 burial sites were used to dispose of all the cattle
slaughtered due to foot and mouth disease. The burials included cattle
over five years old, which should have been incinerated under the
governments own BSE regulations. The government has now ordered the
carcasses to be dug up to protect water supplies from infection with the
BSE agenta rather belated attempt because most body fluids will have
leaked out after two months.

http://www.wsws.org/articles/2001/jul2001/bse-j06.shtml
http://www.wsws.org/correspo/1998/july1998/bse-j23.shtml


THE CITY OF NEW YORK
DEPARTMENT OF HEALTH AND MENTAL HYGIENE
Michael R. Bloomberg Thomas R. Frieden, M.D., M.P.H.
Mayor Commissioner
_______________________________________________________________
nyc.gov/health
2004 Health Update #5: Surveillance for Transmissible Spongiform
Encephalopathies,
including the Classic and Variant Forms of Creutzfeld-Jakob Disease, in
New York City

snip...

Chronic Wasting Disease in Elk and Deer in the United States
The importance of having strong prion disease surveillance in the United
States has been further
underlined by recent reports that chronic wasting disease (CWD), an
endemic prion disease affecting elk
and deer which is found in an increasing number of states in the Midwest
and Southwest, may be
transmitted to humans generating a new prion disease. The World Health
Organization (WHO) and the
CDC agree that there currently is insufficient evidence to establish a
link between human disease and
handling or consuming CWD-infected deer. Although no human cases of CWD
have been identified,
laboratory research suggests that it is theoretically possible; however
it is believed that the risk to humans
is low.
Requirements for Reporting CJD and other TSEs to the New York City DOHMH:
Given the increasing public concern about vCJD and the possibility of
new forms of TSEs, the DOHMH
has implemented enhanced surveillance for all suspect or confirmed cases
of TSE. The New York City
Health Code Section 11.03 was amended as of July 28, 2001, to include
reporting of any form of CJD and
other TSEs as soon as these are diagnosed or suspected. We encourage
providers to request laboratory
testing for the 14-3-3 protein and/or brain biopsy or autopsy on suspect
cases as well as to report both
suspected or confirmed cases of CJD or other TSEs. When you report a
suspect case to us, we will work
closely with you to determine if the patient meets criteria for either
the classic or variant form of CJD
(See Attachment 1Diagnostic Criteria for CJD and Attachment 2
Diagnostic Criteria on variant CJD
in the United States) and help arrange laboratory testing.
For suspect or confirmed cases of classic or vCJD, or other TSEs among
New York City residents, please
contact the Bureau of Communicable Disease during normal business hours:

snip...

full text ;

http://www.nyc.gov/html/doh/pdf/cd/04md05.pdf

-------- Original Message --------
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of
Material From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr."
To: fdadockets@oc.fda.gov

Greetings FDA,

i would kindly like to comment on;

Docket 03D-0186

FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal
Feed; Availability

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

1. MY first point is the failure of the partial ruminant-to-ruminant feed
ban of 8/4/97. this partial and voluntary feed ban of some ruminant
materials being fed back to cattle is terribly flawed. without the
_total_ and _mandatory_ ban of all ruminant materials being fed
back to ruminants including cattle, sheep, goat, deer, elk and mink,
chickens, fish (all farmed animals for human/animal consumption),
this half ass measure will fail terribly, as in the past decades...

2. WHAT about sub-clinical TSE in deer and elk? with the recent
findings of deer fawns being infected with CWD, how many could
possibly be sub-clinically infected. until we have a rapid TSE test to
assure us that all deer/elk are free of disease (clinical and sub-clinical),
we must ban not only documented CWD infected deer/elk, but healthy
ones as well. it this is not done, they system will fail...

3. WE must ban not only CNS (SRMs specified risk materials),
but ALL tissues. recent new and old findings support infectivity
in the rump or ass muscle. wether it be low or high, accumulation
will play a crucial role in TSEs.

4. THERE are and have been for some time many TSEs in the
USA. TME in mink, Scrapie in Sheep and Goats, and unidentified
TSE in USA cattle. all this has been proven, but the TSE in USA
cattle has been totally ignored for decades. i will document this
data below in my references.

5. UNTIL we ban all ruminant by-products from being fed back
to ALL ruminants, until we rapid TSE test (not only deer/elk) but
cattle in sufficient numbers to find (1 million rapid TSE test in
USA cattle annually for 5 years), any partial measures such as the
ones proposed while ignoring sub-clinical TSEs and not rapid TSE
testing cattle, not closing down feed mills that continue to violate the
FDA's BSE feed regulation (21 CFR 589.2000) and not making
freely available those violations, will only continue to spread these
TSE mad cow agents in the USA. I am curious what we will
call a phenotype in a species that is mixed with who knows
how many strains of scrapie, who knows what strain or how many
strains of TSE in USA cattle, and the CWD in deer and elk (no
telling how many strains there), but all of this has been rendered
for animal feeds in the USA for decades. it will get interesting once
someone starts looking in all species, including humans here in the
USA, but this has yet to happen...

6. IT is paramount that CJD be made reportable in every state
(especially ''sporadic'' cjd), and that a CJD Questionnaire must
be issued to every family of a victim of TSE. only checking death
certificates will not be sufficient. this has been proven as well
(see below HISTORY OF CJD -- CJD QUESTIONNAIRE)

7. WE must learn from our past mistakes, not continue to make
the same mistakes...

REFERENCES

Six white-tailed deer fawns test positive for CWD

MADISON -- Six fawns in the area of south central Wisconsin where
chronic wasting disease has been found in white-tailed deer have tested
positive for the disease, according to Department of Natural Resources
wildlife health officials. These are the youngest wild white-tailed deer
detected with chronic wasting disease (CWD) to date.

Approximately 4,200 fawns, defined as deer under 1 year of age, were
sampled from the eradication zone over the last year. The majority of
fawns sampled were between the ages of 5 to 9 months, though some were
as young as 1 month. Two of the six fawns with CWD detected were 5 to 6
months old. All six of the positive fawns were taken from the core area
of the CWD eradication zone where the highest numbers of positive deer
have been identified.

snip...

http://www.dnr.state.wi.us/org/caer/ce/news/on/2003/on20030513.htm#art4

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

Issued: Monday, 28 August 2000
NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH
FINDINGS RELEVANT TO CJD AND BSE

A team of researchers led by Professor John Collinge at the Medical
Research Council Prion Unit1 report today in the Proceedings of the
National Academy of Sciences, on new evidence for the existence of a
'sub-clinical' form of BSE in mice which was unknown until now.

The scientists took a closer look at what is known as the 'species
barrier' - the main protective factor which limits the ability of
prions2 to jump from one species to infect another. They found the mice
had a 'sub-clinical' form of disease where they carried high levels of
infectivity but did not develop the clinical disease during their normal
lifespan. The idea that individuals can carry a disease and show no
clinical symptoms is not new. It is commonly seen in conventional
infectious diseases.

Researchers tried to infect laboratory mice with hamster prions3 called
Sc237 and found that the mice showed no apparent signs of disease.
However, on closer inspection they found that the mice had high levels
of mouse prions in their brains. This was surprising because it has
always been assumed that hamster prions could not cause the disease in
mice, even when injected directly into the brain.

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

The height of the species barrier varies widely between different
combinations of animals and also varies with the type or strain of
prions. While some barriers are quite small (for instance BSE easily
infects mice), other combinations of strain and species show a seemingly
impenetrable barrier. Traditionally, the particular barrier studied here
was assumed to be robust.

Professor John Collinge said: "These results have a number of important
implications. They suggest that we should re-think how we measure
species barriers in the laboratory, and that we should not assume that
just because one species appears resistant to a strain of prions they
have been exposed to, that they do not silently carry the infection.
This research raises the possibility, which has been mentioned before,
that apparently healthy cattle could harbour, but never show signs of, BSE.

"This is a timely and unexpected result, increasing what we know about
prion disease. These new findings have important implications for those
researching prion disease, those responsible for preventing infected
material getting into the food chain and for those considering how best
to safeguard health and reduce the risk that theoretically, prion
disease could be contracted through medical and surgical procedures."

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

FOR FURTHER INFORMATION CONTACT THE MRC PRESS OFFICE ON 020 7637 6011
(OFFICE HOURS) OR 07818 428297 OR 0385 774357 (OUT-OF-OFFICE-HOURS) OR
PROFESSOR JOHN COLLINGE ON 020 7594 3760. PLEASE NOTE THAT OWING TO
TRAVEL COMMITMENTS PROFESSOR COLLINGE WILL ONLY BE AVAILABLE UNTIL 16.30
ON FRIDAY 25 AUGUST AND CONTACTABLE AGAIN ON MONDAY 28 AUGUST VIA THE
MRC PRESS OFFICE. DR ANDREW HILL (A CO-AUTHOR ON THE PAPER) FROM THE
DEPARTMENT OF PATHOLOGY AT THE UNIVERSITY OF MELBOURNE WILL BE AVAILABLE
ON 00 61 3 8344 3995 (DURING OFFICE HOURS) OR 00 61 3 9443 0009
(OUT-OF-OFFICE HOURS). PLEASE NOTE THAT AUSTRALIA IS TEN HOURS AHEAD OF
UK TIME.

NOTES FOR EDITORS

Professor Collinge is a consultant neurologist and Director of the newly
formed MRC Prion Unit based at The Imperial College School of Medicine
at St Mary's Hospital. He is also a member of the UK Government's
Spongiform Encephalopathy Advisory Committee (SEAC). The MRC prion unit
is was set up in 1999, and its work includes molecular genetic studies
of human prion disease and transgenic modelling of human prion diseases.

Prions are unique infectious agents that cause fatal brain diseases such
as Creutzfeldt-Jakob disease (CJD) in humans and scrapie and BSE (mad
cow disease) in animals. In some circumstances prions from one species
of animals can infect another and it is clear that BSE has done this to
cause the disease variant CJD in the UK and France. It remains unclear
how large an epidemic of variant CJD will occur over the years ahead.

The strain of prion used here to infect the mice is the Sc237 strain
(also known as 263K) which infects hamsters, and until now was assumed
not to infect mice.

This research was funded by the Medical Research Council and Wellcome Trust.

The Medical Research Council (MRC) is a national organisation funded by
the UK tax-payer. Its business is medical research aimed at improving
human health; everyone stands to benefit from the outputs. The research
it supports and the scientists it trains meet the needs of the health
services, the pharmaceutical and other health-related industries and the
academic world. MRC has funded work which has led to some of the most
significant discoveries and achievements in medicine in the UK. About
half of the MRC's expenditure of £345 million is invested in over 50 of
its Institutes and Units, where it employs its own research staff. The
remaining half goes in the form of grant support and training awards to
individuals and teams in universities and medical schools.

The Wellcome Trust is the world's largest medical research charity with
a spend of some £600 million in the current financial year 1999/2000.
The Wellcome Trust supports more than 5,000 researchers, at 400
locations, in 42 different countries to promote and foster research with
the aim of improving human and animal health. As well as funding major
initiatives in the public understanding of science, the Wellcome Trust
is the country's leading supporter of research into the history of medicine.

©2002 Medical Research Council
Data Protection policy | Contact the MRC

http://www.mrc.ac.uk/index/public_interest/public-press_office/public-press_releases_2000/public-mrc-43-00.htm

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

Oral transmission and early lymphoid tropism of chronic wasting disease
PrPres in mule deer fawns (Odocoileus hemionus )
Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3,
Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1

Department of Pathology, College of Veterinary Medicine and Biomedical
Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1
Department of Veterinary Sciences, University of Wyoming, 1174 Snowy
Range Road, University of Wyoming, Laramie, WY 82070, USA 2
Colorado Division of Wildlife, Wildlife Research Center, 317 West
Prospect Road, Fort Collins, CO 80526-2097, USA3
Colorado State University Veterinary Diagnostic Laboratory, 300 West
Drake Road, Fort Collins, CO 80523-1671, USA4
Animal Disease Research Unit, Agricultural Research Service, US
Department of Agriculture, 337 Bustad Hall, Washington State University,
Pullman, WA 99164-7030, USA5

Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail
ehoover@lamar.colostate.edu

Mule deer fawns (Odocoileus hemionus) were inoculated orally with a
brain homogenate prepared from mule deer with naturally occurring
chronic wasting disease (CWD), a prion-induced transmissible spongiform
encephalopathy. Fawns were necropsied and examined for PrP res, the
abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days
post-inoculation (p.i.) using an immunohistochemistry assay modified to
enhance sensitivity. PrPres was detected in alimentary-tract-associated
lymphoid tissues (one or more of the following: retropharyngeal lymph
node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42
days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No
PrPres staining was detected in lymphoid tissue of three control fawns
receiving a control brain inoculum, nor was PrPres detectable in neural
tissue of any fawn. PrPres-specific staining was markedly enhanced by
sequential tissue treatment with formic acid, proteinase K and hydrated
autoclaving prior to immunohistochemical staining with monoclonal
antibody F89/160.1.5. These results indicate that CWD PrP res can be
detected in lymphoid tissues draining the alimentary tract within a few
weeks after oral exposure to infectious prions and may reflect the
initial pathway of CWD infection in deer. The rapid infection of deer
fawns following exposure by the most plausible natural route is
consistent with the efficient horizontal transmission of CWD in nature
and enables accelerated studies of transmission and pathogenesis in the
native species.

snip...

These results indicate that mule deer fawns develop detectable PrP res
after oral exposure to an inoculum containing CWD prions. In the
earliest post-exposure period, CWD PrPres was traced to the lymphoid
tissues draining the oral and intestinal mucosa (i.e. the
retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and
ileocaecal lymph nodes), which probably received the highest initial
exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie
agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum
and spleen in a 10-month-old naturally infected lamb by mouse bioassay.
Eight of nine sheep had infectivity in the retropharyngeal lymph node.
He concluded that the tissue distribution suggested primary infection
via the gastrointestinal tract. The tissue distribution of PrPres in the
early stages of infection in the fawns is strikingly similar to that
seen in naturally infected sheep with scrapie. These findings support
oral exposure as a natural route of CWD infection in deer and support
oral inoculation as a reasonable exposure route for experimental studies
of CWD.

snip...

http://vir.sgmjournals.org/cgi/content/full/80/10/2757
===================================

now, just what is in that deer feed? _ANIMAL PROTEIN_

Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 -0700
From: "Terry S. Singeltary Sr."
Reply-To: BSE-L
To: BSE-L

8420-20.5% Antler Developer
For Deer and Game in the wild
Guaranteed Analysis Ingredients / Products Feeding Directions

snip...

_animal protein_

http://www.surefed.com/deer.htm

BODE'S GAME FEED SUPPLEMENT #400
A RATION FOR DEER
NET WEIGHT 50 POUNDS
22.6 KG.

snip...

_animal protein_

http://www.bodefeed.com/prod7.htm

Ingredients

Grain Products, Plant Protein Products, Processed Grain By-Products,
Forage Products, Roughage Products 15%, Molasses Products,
__Animal Protein Products__,
Monocalcium Phosphate, Dicalcium Pyosphate, Salt,
Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol
(source of Vitamin D3), Vitamin E Supplement, Vitamin B12 Supplement,
Riboflavin Supplement, Niacin Supplement, Calcium Panothenate, Choline
Chloride, Folic Acid, Menadione Soduim Bisulfite Complex, Pyridoxine
Hydorchloride, Thiamine Mononitrate, d-Biotin, Manganous Oxide, Zinc
Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried
Sacchoromyces Berevisiae Fermentation Solubles, Cellulose gum,
Artificial Flavors added.

http://www.bodefeed.com/prod6.htm
===================================

MORE ANIMAL PROTEIN PRODUCTS FOR DEER

Bode's #1 Game Pellets
A RATION FOR DEER
F3153

GUARANTEED ANALYSIS
Crude Protein (Min) 16%
Crude Fat (Min) 2.0%
Crude Fiber (Max) 19%
Calcium (Ca) (Min) 1.25%
Calcium (Ca) (Max) 1.75%
Phosphorus (P) (Min) 1.0%
Salt (Min) .30%
Salt (Max) .70%


Ingredients

Grain Products, Plant Protein Products, Processed Grain By-Products,
Forage Products, Roughage Products, 15% Molasses Products,
__Animal Protein Products__,
Monocalcium Phosphate, Dicalcium Phosphate, Salt,
Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol
(source of Vitamin D3) Vitamin E Supplement, Vitamin B12 Supplement,
Roboflavin Supplement, Niacin Supplement, Calcium Pantothenate, Choline
Chloride, Folic Acid, Menadione Sodium Bisulfite Complex, Pyridoxine
Hydrochloride, Thiamine Mononitrate, e - Biotin, Manganous Oxide, Zinc
Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried
Saccharyomyces Cerevisiae Fermentation Solubles, Cellulose gum,
Artificial Flavors added.

FEEDING DIRECTIONS
Feed as Creep Feed with Normal Diet

http://www.bodefeed.com/prod8.htm

INGREDIENTS

Grain Products, Roughage Products (not more than 35%), Processed Grain
By-Products, Plant Protein Products, Forage Products,
__Animal Protein Products__,
L-Lysine, Calcium Carbonate, Salt, Monocalcium/Dicalcium
Phosphate, Yeast Culture, Magnesium Oxide, Cobalt Carbonate, Basic
Copper Chloride, Manganese Sulfate, Manganous Oxide, Sodium Selenite,
Zinc Sulfate, Zinc Oxide, Sodium Selenite, Potassium Iodide,
Ethylenediamine Dihydriodide, Vitamin E Supplement, Vitamin A
Supplement, Vitamin D3 Supplement, Mineral Oil, Mold Inhibitor, Calcium
Lignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium Bisulfite
Complex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid,
Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate

DIRECTIONS FOR USE

Deer Builder Pellets is designed to be fed to deer under range
conditions or deer that require higher levels of protein. Feed to deer
during gestation, fawning, lactation, antler growth and pre-rut, all
phases which require a higher level of nutrition. Provide adequate
amounts of good quality roughage and fresh water at all times.

http://www.profilenutrition.com/Products/Specialty/deer_builder_pellets.html
===================================================

DEPARTMENT OF HEALTH & HUMAN SERVICES
PUBLIC HEALTH SERVICE
FOOD AND DRUG ADMINISTRATION

April 9, 2001 WARNING LETTER

01-PHI-12
CERTIFIED MAIL
RETURN RECEIPT REQUESTED

Brian J. Raymond, Owner
Sandy Lake Mills
26 Mill Street
P.O. Box 117
Sandy Lake, PA 16145
PHILADELPHIA DISTRICT

Tel: 215-597-4390

Dear Mr. Raymond:

Food and Drug Administration Investigator Gregory E. Beichner conducted
an inspection of your animal feed manufacturing operation, located in
Sandy Lake, Pennsylvania, on March 23,
2001, and determined that your firm manufactures animal feeds including
feeds containing prohibited materials. The inspection found significant
deviations from the requirements set forth in
Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins
Prohibited in Ruminant Feed. The regulation is intended to prevent the
establishment and amplification of Bovine Spongiform Encephalopathy
(BSE) . Such deviations cause products being manufactured at this
facility to be misbranded within the meaning of Section 403(f), of the
Federal Food, Drug, and Cosmetic
Act (the Act).

Our investigation found failure to label your
swine feed with the required cautionary statement "Do Not Feed to cattle
or other Ruminants" The FDA suggests that the statement be
distinguished
by different type-size or color or other means of highlighting the
statement so that it is easily noticed by a purchaser.

In addition, we note that you are using approximately 140 pounds of
cracked corn to flush your mixer used in the manufacture of animal
feeds containing prohibited material. This
flushed material is fed to wild game including deer, a ruminant animal.
Feed material which may potentially contain prohibited material should
not be fed to ruminant animals which may become part of the food chain.

The above is not intended to be an all-inclusive list of deviations from
the regulations. As a manufacturer of materials intended for animal
feed use, you are responsible for assuring that your overall operation
and the products you manufacture and distribute are in compliance with
the law. We have enclosed a copy of FDA's Small Entity Compliance Guide
to assist you with complying with the regulation... blah, blah, blah...

http://www.fda.gov/foi/warning_letters/g1115d.pdf
==================================

-------- Original Message --------
Subject: ON THE ORIGIN OF MINK TME MARSH/HANSON (Scrapie in USA sheep,
to TSE in USA cattle, or BOTH)
Date: Thu, 15 May 2003 15:23:46 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de

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

ABSTRACT--studies on mink susceptibility to sources of scrapie
from the United States, but not from the United Kingdom, indicate that
transmissible mink encephalopathy (TME) most likely originates from
mink fed scrapie-infected sheep or goat tissues.
Experiments further suggest that the shortest natural route of infection is
via bite wounds inflicted by littermates rather than by the oral route
per se.
Other studies, on the biologic characterization of TME agent from Sawyer
County, Wisconsin, indicate that this particular source of TME is composed
of a mixture of subpopulations which include a hamster pathogen and a
mink-monkey pathogen...

snip...

with so many disease features in common, it would seem a simple matter
to demonstrate that TME results from feeding scrapie-infected tissue to
mink.
BUT such has not been the case. Epizootiologic studies of the 14 worldwide
occurrences of TME have revealed probably exposure to scrapie in only one
instance, a 1965 incidence in Finland in which the affected farm was the
only
one in the area feeding sheep heads (Kangas, personal communication).
Experimentally, mink have been found to be susceptible to some sources of
scrapie and the disease produces was indistinguishable from TME (6)...

snip...

The purpose of these present studies was to attempt to explain differences
between field and experimental observations, and to further characterize
the
biologic properties of the Sawyer County, Wisconsin, isolate of TME.
Our results indicate that mink are more susceptible to sources of scrapie
present in the UNITED STATES that those found in the UK, and that
BITE WOUNDS from littermates may represent a significant route of
natural exposure...

snip...

This Nubian X Toggenburg buck was naturally infected via exposure to
scrapie-contaminated pasture at Mission, TEXAS; the pasture being
previously occupied by a flock of scrapie-affected Suffolk sheep. At 6
months
of age, animal B-834 was removed from exposure and placed in a pen where
he subsequently developed signs of scrapie at 40 months of age...

snip...

Therefore, it should be expected that the pathology of natural TME will vary
depending on the source of scrapie to which mink are exposed.
Johannsen and Hartung have reported an incidence of TME occuring
in East Germany in 1967 in which affected mink had diffuse cerebral
''edema'' and widespread lesions in the spinal cord (10)...

snip...

Even though B-834 produced short incubation periods when inoculated
intracerebrally, exposure by the oral route was ineffective during an
observation period of two years. Thus, we once again seem to have a
conflict between field and experimental data. However, Gajdusek
has suggested that the main route of entry for these transmissible agents
is not the oral route per se, but rather via breaks or abrasions of skin and
mucosal surfaces (11).

full text;

http://www.bseinquiry.gov.uk/files/mb/m08/tab016.pdf

years later Marsh finds out;

Part of the Proceedings of an International Roundtable on Bovine
Spongiform Encephalopathy, Bethesda, Maryland, USA, June 27-28, 1989.

The possibility of infection with BSE in the United States, as defined
by studies on the disease in Great Britain, is judged to be low on the
basis of the following: (1) meat and bonemeals imported into the United
States from Great Britain between 1980 and 1988 were used mainly in
poultry, not ruminant feed; (2) the Scrapie Eradication Program had
reduced the prevalence of scrapie in the United States compared with
that in Great Britain; and (3) little, if any, rendered animal products
are used for protein supplements in cattle feed in the United States.
However, there is some evidence that there may already be a scrapie-like
disease in cattle in the United States. This evidence comes from
epidemiologic studies on an incident of transmissible mink
encephalopathy (TME) in Stetsonville, Wis, in 1985. This mink farmer
used no commercially available animal by-product mixtures in his feed,
but instead slaughtered all animals going into the mink diet, which
included mostly (>95%) "downer" dairy cows, a few horses, but never
sheep. To examine the possibility that cattle may have been the source
of this incident of TME, two 6-week-old Holstein bull calves were
inoculated intracerebrally with mink brain from the affected farm. The
bulls developed neurologic disease 18 and 19 months after inoculation.
Both brains had spongiform degeneration at necropsy and both were
transmissible back to mink by either intracerebral (incubation period of
4 months) or oral (incubation period of 7 months) inoculation
Whereas TME has been thought to be caused by feeding scrapie-infected
sheep to mink, this theory has no conclusive evidence. Experimental oral
inoculation of mink with several different sources of sheep scrapie has
never been successful, and an incubation period of less than 12 months
has never (sic) produced by intracerebral inoculation. Transmissible
mink encephalopathy can develop naturally by infection with incubation
periods of less than 12 months.
There is reason to believe that scrapie has not been transmitted in the
United States from sheep to cattle by rendered protein concentrates as
it was in Great Britain. However, some circumstantial evidence exists
that cattle may be a source of some TME infections. It is recommended
that we increase our surveillance for a BSE-like disease in American
cattle by encouraging state diagnostic laboratories to formalin-fix
specimens of midbrain and brain stem from bovine brains submitted for
rabies testing. If results of these tests are negative, these fixed
tissues can then be examined for evidence of spongiform degeneration of
the gray matter.

Letter to the Editor, Journal of the American Veterinary Medical
Association, August 15, 1990
In my article, "Bovine spongiform encephalopathy in the United States"
(JAVMA, May 15, 1990, p 1677), I stated that "little, if any, rendered
animal products are used for protein supplements in cattle feed in the
United States." I have since learned that this is incorrect, because of
the recent trend of using less assimilated "by-pass" proteins in cattle
feed. A large amount of meat-and-bone meal is being fed to American
cattle, and this change in feeding practice has greatly increased the
risk of bovine spongiform encephalopathy (BSE) developing in the United
States.
Epidemiologic studies on BSE in Great Britain have indicated that the
disease originated in cattle by exposure to the heat-resistant
transmissible agent in compounded feed containing rendered animal
protein. The most likely source of infection was assumed to be
meat-and-bone meal prepared from scrapie-infected sheep, but it is also
possible that a heretofore unrecognized scrapie-like infection of cattle
could have been spread in the same manner.
Because of concern for the possible development of BSE in the United
States, the American rendering industry discontinued the processing of
fallen and sick sheep last December. In my opinion, this was a prudent
policy, but one that will not prevent the possible transmission of BSE
from cattle to cattle. As emphasized in my article, there is some
evidence that BSE-like infection may already exist in American cattle.
The current practice of feeding meat-and-bone meal to cattle solidifies
the most important means to perpetuate and amplify the disease cycle.
In Great Britain, BSE has produced a great economic and emotional
burden. We must take all reasonable measures to prevent BSE from
developing in the United States. Therefore, the practice of using animal
protein in cattle feed should be discontinued as soon as possible.
Waiting until the first case of BSE is diagnosed in the United States
will certainly be "closing the barn door after the horse is gone." With
a disease having a 3- to 6-year incubation period, thousands of animals
would be exposed before we recognize the problem and, if that happens,
we would be in for a decade of turmoil.
R. F. Marsh, DVM, PhD
Madison, Wis

To be published in the Proceedings of the
Fourth International Scientific Congress in
Fur Animal Production. Toronto, Canada,
August 21-28, 1988

Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle

_ - R.F. Marsh* and G.R. Hartsough

"Department of Veterinary Science, University of Wisconsin-Madison, Madison,
Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville,
Wisconsin 53092

ABSTRACT
Epidemiologic investigation of a new incidence of
transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin
suggests that the disease may have resulted from feeding infected
cattle to mink. This observation is supported by the transmission of
a TME-like disease to experimentally inoculated cattle, and by the
recent report of a new bovine spongiform encephalopathy in
England.

INTRODUCTION

Transmissible mink encephalopathy (TME) was first reported in 1965
by Hartsough and Burger who demonstrated that the disease was
transmissible with a long incubation period, and that affected mink
had a spongiform encephalopathy similar to that found in scrapie-affecied
sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965).
Because of the similarity between TME and scrapie, and the subsequent
finding that the two transmissible agents were indistinguishable
(Marsh and Hanson, 1969), it was concluded that TME most likely resulted
from feeding mink scrapie-infecied sheep.
The experimental transmission of sheep scrapie to mink (Hanson et al.,
1971) confirmed the close association of TME and scrapie, but at the
same time provided evidence that they may be different. Epidemiologic
studies on previous incidences of TME indicated that the incubation periods
in field cases were between six months and one year in length (Harxsough
and Burger, 1965). Experimentally, scrapie could not be transmitted to mink
in less than one year.
To investigate the possibility that TME may be caused by a (particular
strain of scrapie which might be highly pathogenic for mink, 21 different
strains of the scrapie agent, including their sheep or goat sources, were
inoculated into a total of 61 mink. Only one mink developed a progressive
neurologic disease after an incubation period of 22 mon..s (Marsh and Hanson,
1979). These results indicated that TME was either caused by a strain of
sheep scrapie not yet tested, or was due to exposure to a scrapie-like
agent from an unidentified source.

OBSERVATIONS AND RESULTS

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 formal 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.

Experimental Transmission. The clinical diagnosis of TME was confirmed by
histopaihologic examination and by experimental transmission to mink
after incubation periods of four months. To investigate the possible involvement
of cattle in this disease cycle, two six-week old castrated Holstein bull calves
were inoculated intracerebrally with a brain suspension from affected mink.
Each developed a fatal spongiform encephalopathy after incubation periods of
18 and 19 months.

DISCUSSION

These findings suggest that TME may result from feeding mink infected
cattle and we have alerted bovine practitioners that there may exist an
as yet unrecognized scrapie-like disease of cattle in the United States
(Marsh and Hartsough, 1986). A new bovine spongiform encephalopathy has
recently been reported in England (Wells et al., 1987), and investigators
are presently studying its transmissibility and possible relationship to
scrapie. Because this new bovine disease in England is characterized by
behavioral changes, hyperexcitability, and agressiveness, it is very
likely it would be confused with rabies in the United Stales and not be
diagnosed. Presently, brains from cattle in the United States which are
suspected of rabies infection are only tested with anti-rabies virus antibody
and are not examined histopathologically for lesions of spongiform
encephalopathy. We are presently pursuing additional studies to further
examine the possible involvement of cattle in the epidemiology of TME.
One of these is the backpassage of our experimental bovine encephalopathy
to mink. Because (here are as yet no agent-specific proteins or nucleic
acids identified for these transmissible neuropathogens, one means of
distinguishing them is by animal passage and selection of the biotype
which grows best in a particular host. This procedure has been used to
separate hamster-adapted and mink-udapted TME agents (Marsh and Hanson,
1979). The intracerebral backpassage of the experimental bovine agent
resulted in incubations of only four months indicating no de-adaptation
of the Stetsonville agent for mink after bovine passage. Mink fed infected
bovine brain remain normal after six months. It will be essential to
demonstrate oral transmission from bovine to mink if this proposed
epidemiologic association is to be confirmed.

ACKNOWLEDGEMENTS
These studies were supported by the College of Agricultural and Life
Sciences, University of Wisconsin-Madison and by a grant (85-CRCR-1-1812)
from the United States Department of Agriculture. The authors also wish
to acknowledge the help and encouragement of Robert Hanson who died during
the course of these investigations.

REFERENCES
Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II.
Experimental and natural transmission. J. Infec. Dis. 115:393-399.
Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L.
and Gustatson, D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861.
Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I.
Epizoociologic and clinical observations. 3. Infec. Dis. 115:387-392.
Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the
transmissible mink encephalopathy agent. 3. ViroL 3:176-180.
Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink
encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible
diseases of the nervous system. Vol. 1, Academic Press, New York, pp
451-460.
Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in
cattle?
Proceedings of the Seventh Annual Western Conference for Food Animal
Veterinary Medicine. University of Arizona, pp 20.
Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D.,
Jeffrey, M., Dawson, M. and Bradley, R. 1987. A novel progressive spongiform
encephalopathy in cattle. Vet. Rec. 121:419-420.

http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf

Is there a Scrapie-like disease in cattle in USA

http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf


SEWING THE SEEDS OF CWD THROUGH ANIMAL PROTEIN?

http://www.tx-outdoors.com/hunting_issues/_disc11/00000084.htm

re-vCJD/blood and meeting of Feb. 20, 2003

http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.pdf

Subject: SCRAPIE 'USA' ANNUAL REPORT (105 __newly__ infected flocks
2002) & CWD IN USA Date: Tue, 10 Dec 2002 08:17:17 -0600 From: "Terry S.
Singeltary Sr." To: flounder@wt.net Date: Mon, 9 Dec
2002 21:21:10 -0600 Reply-To: Bovine Spongiform Encephalopathy Sender:
Bovine Spongiform Encephalopathy From: "Terry S. Singeltary Sr."
Subject: SCRAPIE 'USA' ANNUAL REPORT (105 newly
infected flocks 2002) & CWD IN USA As of September 30, 2002, there were
45 scrapie infected and source flocks (figure 3). There were 105 newly
infected flocks, reported in FY2002 (figure 4). In addition, 379 scrapie
cases were confirmed and reported by the National Veterinary Services
Laboratories (NVSL) in FY 2002 (figure 5) and (figure 6). Five cases of
scrapie in goats were reported in FY 2002 (figure 7), the last of which
was confirmed in August 2002. New infected and source flocks numbers and
the number of these flocks released in FY 2002 are depicted in chart 4.
One hundred (100) flocks which is 67 percent of the scrapie infected and
source flocks present in FY 2002 were released or put on clean-up plans
in FY2002. Slaughter Surveillance Slaughter Surveillance is currently in
Phase II which is intended to determine the prevalence of scrapie in the
US culled sheep population. Through September 2002 samples from 3,269
sheep were submitted to NVSL for testing. Samples from a total of 6,795
sheep have been submitted since the beginning of Phase II on April 1,
2002. Surveillance regions are depicted in (figure 8). Scrapie Testing
During FY 2002 11,751 animals have been tested for scrapie which
includes: 2,711 regular necropsy cases, 1,343 third eyelid biopsies for
the test validation project, 546 third eyelid biopsies for the
regulatory program, and approximately 7,151 animals for Phase I & II of
SOSS (chart 5). Laboratory testing has been taking 10 - 11 days on
average with a range of 3 - 34 days. Ear Tag Orders During FY 2002 9.9
million plastic and 6.0 million metal tags were distributed by APHIS
(chart 6).
http://www.aphis.usda.gov/vs/nahps/scrapie/annual_report/annual-report.html
NEW SCRAPIE INFECTED AND SOURCE FLOCKS
http://www.aphis.usda.gov/vs/nahps/scrapie/annual_report/figure04.gif
DISTRIBUTION OF CHRONIC WASTING DISEASE THROUGHOUT THE STATES (as of
Oct. 2002) http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html
CWD USA surveillance http://www.aphis.usda.gov/vs/nahps/cwd/cwd-state.html

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease
in the United States [FULL TEXT] Date: February 22, 2003 at 7:38 am PST
plus TSS rebuttal and submission to Neurology

http://www.vegsource.com/talk/madcow/messages/9912538.html

or short version;

http://www.neurology.org/cgi/eletters/60/2/176#535

TSS

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############

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


USA 8/4/97 RUMINANT-TO-RUMINANT FEED BAN that never was...

'ANIMAL PROTEIN' SEARCH 9/9/02
==============================

Darling International, Inc.
5/07/02
Seattle District Office Animal Proteins Prohibited in Ruminant
Feed/Misbranded [PDF]
[HTML] All American Feed & Tractor
4/01/02
Seattle District Office Animal Proteins Prohibited in Ruminant
Feed/Adulterated [PDF]
[HTML] Tyson Foods
2/12/02
Seattle District Office Animal Proteins Prohibited in Ruminant
Feed/Misbranded [PDF]
[HTML] The Feed Bucket
12/11/01
Atlanta District Office Animal Proteins Prohibited in Ruminant
Feed/Adulterated/Misbranded [PDF]
[HTML] Finlayson Ag Center
11/08/01
Minneapolis District Office Animal Proteins Prohibited in Ruminant
Feed/Adulterated [PDF]
[HTML] Dixon Feeds, Inc.
10/24/01
Seattle District Office Animal Proteins Prohibited in Ruminant
Feed/Adulterated [PDF]
[HTML] Buckeye Feed Mills, Inc.
9/20/01
Cincinnati District Office Animal Proteins Prohibited in Ruminant
Feed/Adulterated/Misbranded [PDF]
[HTML] Wilcox Farms, Inc.
9/14/01
Seattle District Office Animal Proteins Prohibited in Ruminant Feed [PDF]
[HTML]

http://www.accessdata.fda.gov/scripts/wlcfm/full_text.cfm?full_text=animal+protein&Search=Search

now, compare search on 8/8/01...tss
===================================

'ANIMAL PROTEIN' SEARCH 8/8/01
==============================

Date: Tue, 28 Aug 2001 11:13:43 -0700
Reply-To: BSE-L
Sender: Bovine Spongiform Encephalopathy BSE-L
From: "Terry S. Singeltary Sr."
Subject: MAD COW FEED BAN WARNING LETTERS U.S.A. AUGUST 8, 2001

DEPARTMENT OF HEALTH AND HUMAN SERVICES

Food and Drug Administration

Seattle District Pacific Region 22201 23rd Drive SE Bothell, WA 98021-4421

Telephone: 426-486-8788 FAX: 426-483-4996

August 8, 2001

VIA CERTIFIED MAIL RETURN RECEIPT REQUESTED

In reply refer to Warning Letter SEA 01-75

William W. Himmelspach, Owner 22195 S.W. 78th Tualatin, Oregon 97062

WARNING LETTER

Dear Mr. Himmelspach:

An investigation at your animal feed manufacturing operation located at
22195 S.W. 78th Tualatin, Oregon 97062, conducted by a Food and Drug
Administration investigator on July 12, 2001, 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 adulterated
within the meaning of Section 402(a)(2)(C), and 402(a)(4) of the Federal
Food, Drug and Cosmetic Act (the Act).

Our investigation found a failure to separate the receipt, processing,
and storage of the product containing prohibited material from
non-prohibited material; failure to establish a written system,
including clean-out and flushing procedures, to avoid commingling and
cross-contamination of common equipment; and failure to maintain records
sufficient to track the materials throughout the receipt, processing,
and distribution of your products.

In addition, our investigation found a failure to label your products
with the required cautionary, statement "Do Not Feed to Cattle or Other
Ruminants," Your pig feeds, containing prohibited materials, were not
labeled with the cautionary statement, and you reuse poly-tote bags for
ruminant feed and pig feed, where the bags could become contaminated
with prohibited material. The FDA suggests 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.

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

William W. Himmelspach Tualatin, Oregon Re: Warning Letter SEA 01-75 Page 2

your overall operation and the products you manufacture and distribute
are in compliance with the law. We have enclosed a copy of the FDA's
Small Entity Compliance Guide to assist you with complying with the
regulation.

You should take prompt action to correct these violations, and you
should establish a system whereby such violations do not recur. Failure
to promptly correct these violations may result in regulatory action
without further notice, such as seizure and/or injunction.

You should notify this office in writing within 15 working days of
receipt of this letter, of the steps you have taken to bring your firm
into compliance with the law. Your response should include an
explanation of each step being taken to correct the violations, and
prevent their recurrence. If corrective action cannot be completed in 15
working days, state the reason for the delay and the date by which the
corrections will be completed. Include copies of any available
documentation demonstrating that corrections have been made.

Your reply should be directed to the Food and Drug Administration,
Attention: Bruce Williamson, Compliance Officer. If you have any
questions please contact Mr. Williamson at (425) 483-4976.

Sincerely,

Charles M. Breen District Director

Enclosure; Form FDA 483 Small Entity Compliance Guide

http://www.fda.gov/foi/warning_letters/g1619d.pdf

Warning Letters Index - Search Form Results Company Name Date Issued
Issuing Office

Subject

File Adrian Elevator, Inc. 5/03/01 Minneapolis District Office Animal
Proteins Prohibited in Ruminant Feed

View File Alaska Garden and Pet Supply, Inc. 4/27/01 Seattle District
Office Animal Proteins Prohibited in Ruminant Feed

View File Bryan Enterprises 2/20/01 Cincinnati District Office Feed
Mill/Animal Proteins Prohibited in Ruminant Feed/Adulterated

View File Carrollton Farmers Exchange 7/12/01 Cincinnati District Office
Animal Proteins Prohibited in Ruminant Feed

View File Centerburg Mill and General Store, Inc 3/23/01 Cincinnati
District Office Animal Proteins Prohibited in Ruminant Feed

View File Centerburg Mill and General Store, Inc. 5/23/01 Cincinnati
District Office Animal Proteins Prohibited in Ruminant Feed

View File Central Ohio Farmers Cooperative, Inc. 5/24/01 Cincinnati
District Office Animal Protein Prohibited in Ruminant Feed

View File Champaign Landmark, Inc. 3/05/01 Cincinnati District Office
Animal Proteins Prohibited in Ruminant Feed/Misbranded

View File Countryline Co-Op, Inc. 5/14/01 Cincinnati District Office
Animal Proteins Prohibited in Ruminant Feed

View File Dorset Milling 4/16/01 Cincinnati District Office Animal
Proteins Prohibited in Ruminant Feed

View File Earl B. Olson Feed Mill 4/23/01 Minneapolis District Office
Animal Proteins Prohibited in Ruminant Feed

View File Faler Feed Store, Inc. 3/21/01 Cincinnati District Office
Animal Proteins Prohibited in Ruminant Feed

View File Farmers Mill & Elevator Company 3/30/01 Atlanta District
Office Animal Proteins Prohibited in Ruminant Feed

View File Farnam Companies, Inc. 7/20/01 Kansas City District Office
Animal Proteins Prohibited in Ruminant Feed/Adulterated

View File Greeley Elevator Company 4/04/01 Denver District Office Animal
Proteins Prohibited in Ruminant Feed

View File Hartville Elevator Company, Inc. 2/22/01 Cincinnati District
Office Feed Mill/Animal Proteins Prohibited in Ruminant Feed/Adulterated

View File Himmelspach, William W. 8/08/01 Seattle District Office Animal
Proteins Prohibited in Ruminant Feed

View File Integral Fish Foods, Inc. 6/12/01 Denver District Office
Animal Proteins Prohibited in Ruminant Feed

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District Office Animal Proteins Prohibited in Ruminant Feed/Feed Mill

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Requirements for Medicated Feeds/Animal Proteins Prohibited in Ruminant Feed

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Animal Proteins Prohibited in Ruminant Feed

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Prohibited in Ruminant Feed

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Prohibited in Ruminant Feed

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Proteins Prohibited in Ruminant Feed

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Animal Proteins Prohibited in Ruminant Feed

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Animal Proteins Prohibited in Ruminant Feed

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Office Animal Proteins Prohibited in Ruminant Feed

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Office Animal Proteins Prohibited in Ruminant Feed

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Proteins Prohibited in Ruminant Feed

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View File

http://63.75.126.221/scripts/wlcfm/resultswl.cfm

(TYPE IN 'ANIMAL PROTEIN')

In Reply to: Docket No. 01-068-1 Risk Reduction Strategies for Potential
BSE Pathways Involving Downer Cattle and Dead Stock of Cattle and Other
Species [TSS SUBMISSION] January 21, 2003

http://www.vegsource.com/talk/madcow/messages/9912358.html

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

Date: Sun, 13 Apr 2003 11:14:20 -0500
Reply-To: Bovine Spongiform Encephalopathy
Sender: Bovine Spongiform Encephalopathy
From: "Terry S. Singeltary Sr."
Subject: SCRAPIE AGENT IN MUSCLE - PATTISON I A (1990) & Prusiner et al
2001

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

Greetings List Members,

in response to;

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 Krüger & 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&titleabstract=prions+meat+tissue+mice&fulltext=prions+meat+tissue+mice&searchid=1024346978866_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&titleabstract=prions+meat+tissue+mice&fulltext=prions+meat+tissue+mice&searchid=1050249844061_1953&stored_search=&FIRSTINDEX=0&fdate=1/1/2002


Greetings,

seems they just will not accept that BSE and Scrapie can transmit to
primates and humans. how many times do we have to do the same studies
over and over again, before action is taken on all human/animal TSEs? if
they would have just listened. they were so wrong about BSE, how can
they be so right about Scrapie, especially since it too transmits to
primates...

COMMERCIAL IN CONFIDENCE NOT FOR PUBLICATION SUB COMMITTEE ON
BIOLOGICALS. COMMITTEE ON SAFETY OF MEDICINES

CSM/SEAR/88 10TH MEETING. BIOLS/88/6TH MEETING

This paper was discussed by the Biological Sub-Committee on 2 November
1988, when the following recommendations were made;

1. No immediate licensing action should be taken against oral products,
in which bovine material has been used.

2. All bovine materials should come from cattle from appropriately
certified healthy herds, which have not been given food supplements
containing material of animal origin. No brain or lymphoid tissue should
be used in parenteral products.'

3. Manufacturers of parenteral products should show that their
manufacturing processes are capable of eliminating scrapie-like agents.

4. All licences for new products from bovine materials should comply
with the above.

5. There should be an article in MAIL requesting manufacturers to
identify products in which bovine materials have been used. Bovine
albumin and foetal calf serum should come from appropriately certified
healthy herds.

6. The above should be drawn to the attention of the review/CDSM
sections along with the need to search for preparations containing
bovine material.

7. The above should be drawn to the attention of the ADR Section and
SEAR along with the need to search the ADR database for reactions to
bovine products.

REMARK.

1. The Licensing Authority's attention was drawn to the need to give
ongoing consideration to whether action was required on bovine insulin
and heparin products.

88/11.02/5.1

http://www.bseinquiry.gov.uk/files/yb/1988/11/02005001.pdf

Adaptation of the bovine spongiform encephalopathy agent to primates and
comparison with Creutzfeldt- Jakob disease: Implications for human health

snip...

We found that the BSE agent in nonhuman primates is similar to that
causing vCJD in humans and tends to evolve rapidly toward a
primate-adapted variant. Furthermore, we showed that the strain
responsible for iCJD is closely related to that of one patient with
sCJD, and, more unexpectedly, that these agents were similar to the
French scrapie strain studied (but different from the U.S. scrapie strain).

snip...

http://www.pnas.org/cgi/content/full/041490898v1

BSE Inquiry VACCINES & SUTURES

http://www.bseinquiry.gov.uk/files/yb/1989/02/14010001.pdf

http://www.bseinquiry.gov.uk/files/yb/1989/02/14011001.pdf

http://www.bseinquiry.gov.uk/files/yb/1990/01/10009001.pdf

http://www.bseinquiry.gov.uk/files/ws/s422.pdf

http://www.bseinquiry.gov.uk/files/yb/1989/07/03004001.pdf

1: J Infect Dis 1980 Aug;142(2):205-8 Related Articles, Links

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.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract


TSS

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html
############

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

-------- Original Message --------

Subject: HISTORY OF CJD -- CJD QUESTIONNAIRE
Date: Thu, 15 May 2003 10:59:54 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de

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

CJD QUESTIONNAIRE

http://www.bseinquiry.gov.uk/files/mb/m26/tab04.pdf

THE EPIDEMIOLOGY OF CJD
R.G. WILL 1984 (182 PAGES)

snip...

Table I: Synonyms for CJD

Creutzfeldt-Jakob Disease
Spastic Pseudosclerosis
Cortico-Striatal-spinal Degeneration
Brownell-Oppenheimer Syndrome
Jakob Type of Spastic Pseudosclerosis
with muscular atropy
Disseminated Encephalomyelopathy
Transmissible Virus Dementia
Subacute Spongiform Encephalopathy
Heidenhain's Syndrome
Jakob's Syndrome
Subacute Progressive Encephalopthy
with Bulbar Myoclonus
[and now vCJD...how many names are we going to name the same disease?
i call this disease ''nobelitice'' $$$ TSS]

snip...

Scrapie infected meat or sheep products are an obvious potential
environmental source of infection. Oral transmission of Scrapie
and TME in the laboratory is well established (Burger and Hartsourgh,
1965; Pattison et al., 1972) and more recently CJD has been transmitted
to primates by the oral consuption of brain, kidney or spleen
(Gibbs et al., 1980). TME is __thought__ to have been transmitted
to mink by the consumption of scrapie affected sheep carcases (Marsh
and Hanson, 1979) [but that theory has changed, please see url...TSS]

MARSH

To be published in the Proceedings of the
Fourth International Scientific Congress in
Fur Animal Production. Toronto, Canada,
August 21-28, 1988

Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle

_ - R.F. Marsh* and G.R. Hartsough

"Department of Veterinary Science, University of Wisconsin-Madison,
Madison, Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service,
Thiensville, Wisconsin 53092

ABSTRACT
Epidemiologic investigation of a new incidence of
transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin
suggests that the disease may have resulted from feeding infected
cattle to mink. This observation is supported by the transmission of
a TME-like disease to experimentally inoculated cattle, and by the
recent report of a new bovine spongiform encephalopathy in
England.

INTRODUCTION

Transmissible mink encephalopathy (TME) was first reported in 1965 by
Hartsough and Burger who demonstrated that the disease was transmissible
with a long incubation period, and that affected mink had a spongiform
encephalopathy similar to that found in scrapie-affecied sheep (Hartsough
and Burger, 1965; Burger and Hartsough, 1965). Because of the similarity
between TME and scrapie, and the subsequent finding that the two
transmissible agents were indistinguishable (Marsh and Hanson,
1969), it was concluded that TME most likely resulted from feeding
mink scrapie-infecied sheep.
The experimental transmission of sheep scrapie to mink (Hanson et al., 1971)
confirmed the close association of TME and scrapie, but at the same time
provided evidence that they may be different. Epidemiologic studies on
previous incidences of TME indicated that the incubation periods in field
cases were between six months and one year in length (Harxsough and Burger,
1965). Experimentally, scrapie could not be transmitted to mink in less than
one year.
To investigate the possibility that TME may be caused by a (particular
strain of scrapie which might be highly pathogenic for mink, 21 different
strains of the scrapie agent, including their sheep or goat sources, were
inoculated into a total of 61 mink. Only one mink developed a progressive
neurologic disease after an incubation period of 22 mon..s (Marsh and Hanson,
1979). These results indicated that TME was either caused by a strain of sheep
scrapie not yet tested, or was due to exposure to a scrapie-like agent
from an unidentified source.

OBSERVATIONS AND RESULTS

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 alt 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.

Experimental Transmission. The clinical diagnosis of TME was confirmed
by histopaihologic examination and by experimental transmission to mink
after incubation periods of four months. To investigate the possible
involvement of cattle in this disease cycle, two six-week old castrated
Holstein bull calves were inoculated intracerebrally with a brain suspension
from affected mink. Each developed a fatal spongiform encephalopathy after
incubation periods of 18 and 19 months.

DISCUSSION

These findings suggest that TME may result from feeding mink infected
cattle and we have alerted bovine practitioners that there may exist
an as yet unrecognized scrapie-like disease of cattle in the United States
(Marsh and Hartsough, 1986). A new bovine spongiform encephalopathy has
recently been reported in England (Wells et al., 1987), and investigators
are presently studying its transmissibility and possible relationship to
scrapie. Because this new bovine disease in England is characterized by
behavioral changes, hyperexcitability, and agressiveness, it is very
likely it would be confused with rabies in the United Stales and not be
diagnosed. Presently, brains from cattle in the United States which are
suspected of rabies infection are only tested with anti-rabies virus antibody
and are not examined histopathologically for lesions of spongiform
encephalopathy.
We are presently pursuing additional studies to further examine the possible
involvement of cattle in the epidemiology of TME. One of these is the
backpassage of our experimental bovine encephalopathy to mink. Because
(here are as yet no agent-specific proteins or nucleic acids identified
for these transmissible neuropathogens, one means of distinguishing them
is by animal passage and selection of the biotype which grows best in a
particular host. This procedure has been used to separate hamster-
adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The
intracerebral backpassage of the experimental bovine agent resulted in
incubations of only four months indicating no de-adaptation of the
Stetsonville agent for mink after bovine passage. Mink fed infected bovine
brain remain normal after six months. It will be essential to demonstrate
oral transmission fiom bovine to mink it this proposed epidemiologic
association is to be confirmed.

ACKNOWLEDGEMENTS
These studies were supported by the College of Agricultural and Life
Sciences, University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the
United States Department of Agriculture. The authors also wish to acknowledge
the help and encouragement of Robert Hanson who died during the course of these
investigations.

REFERENCES

Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II.
Experimental and
natural transmission. J. Infec. Dis. 115:393-399.
Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L.
and Gustatson,
D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861.
Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I.
Epizoociologic and
clinical observations. 3. Infec. Dis. 115:387-392.
Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the
transmissible mink encephalopathy agent. 3. ViroL 3:176-180.
Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink
encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible
diseases of the nervous system. Vol. 1, Academic Press, New York, pp
451-460.
Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in
cattle?
Proceedings of the Seventh Annual Western Conference for Food Animal
Veterinary
Medicine. University of Arizona, pp 20.
Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D.,
Jeffrey, M.,
Dawson, M. and Bradley, R. 1987. A novel progressive spongiform
encephalopathy
in cattle. Vet. Rec. 121:419-420.

http://www.bseinquiry.gov.uk/

Is there a Scrapie-like disease in cattle in USA

http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf

http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf

and kuru was almost certainly spread by ritual cannibalism (Alpers, 1979)...

snip...

the conclusion must be that there is no _firm_ evidence linking the
development of CJD to environmental exposure to the scrapie agent...

snip...

Localised areas with high incidence of CJD have been described in England,
Hungary, Czechoslovakia, ''U.S.A.'', and Italy, but in the absence of a
comparison with the national incidence, these ''CLUSTERS'' may well have been
discovered by chance...[hense, the reason USA still refuses to have _NO_ CJD
Questionnaire...TSS]

snip...

HOWEVER, detailed _questioning of patients, relatives and subsequent
investigation_ (which the USA still refused to do in 2003...TSS)
revealed some remarkable coincidences. (or where they that coincidental?tss)
One patient, a dentist, had for many years daily passed the residence of
another patient, the husband of a hairdresser who worked in the family home. The
dentist's wife used the hairdresser on occasions but the patient himself had never
entered the salon. Interestingly the dentist himself had possible contact with
other cases (vide infra) and a close acquaintance, another dentist, worked in a
small town in Essex in which two further cases of CJD had occurred. In a different
part of the country a district nurse who died of possible CJD may have
tended a patient dying of CJD seven years before she herself died of the condition.
The nurse's daughter lived in a nearby city within 30 yards of the house of another
patient. Detailed investigation of other cases revealed close proximity to other
cases but no definite contact. Intensive questioning of surviving relatives and
other witnesses was limited for FEAR OF CAUSING UNNECESSARY ALARM OR DISTRESS...

snip...

One patient who had previously worked on a farm died of CJD, but he had
workded with cattle, a species not known to be susceptible to natural
scrapie, and had no contact with sheep. [wrong they did know at this
time ...tss]

snip...

(Masters et al., 1979b) concluded that 'in familial clusters of CJD, the
virus is more likely to have gained access to the host through some form
of common environmental contamination than by vertical transmission'.

snip...

One reason for this was the _inaccuracy_ in coding of cases correctly
certified as CJD Coding is carried out by staff who are not medically
qualified and it is not surprising that coding errors occur in the
processing of large numbers of certificates. In 1982, 12,000 certificates
per week were processed at the office of population censuses and surveys
by 15 coders and 6 checkers (Alderson et al., 1983). The occurrence of
both inter- and intra-observer coding errors has been described
(Curb et al., 1983) and the _inaccuracies_ of BOTH certification and
coding discovered in this study _support_ the introduction of a more
accurate system of death certificates and a more detailed and specific
coding system...

snip...

http://www.bseinquiry.gov.uk/files/mb/m26/tab01.pdf

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease
in the United States (or lack of monitoring for CJD)
[FULL TEXT]

http://www.vegsource.com/talk/madcow/messages/9912538.html

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States
26 March 2003

http://www.neurology.org/cgi/eletters/60/2/176#535

TSS

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############

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

MAD COW: 1,479,034 ANALYSES CARRIED OUT, 97 CASES


(AGI) - Rome, Italy, May 12 - 265,321 anti-mad cow tests have been

carried out since the beginning of the year. So far, 1,479,034 tests

have been done in Italy to verify the presence of the so-called "mad

cow" disease (1,477,588 since the check was made compulsory). Another

1,347 samples were tested, and the outcome will be available within 48

hours. That's what the ministry of health communicated, stating that 97

cases of BSE were acknowledged (pre-clinical, two of which non

autochtonous).

A constant and punctual update of the test trend indicating how the

diseases comes about and is transmitted from one cow to another, what

are the consequences for humans is available on the website on BSE of

the ministry of health: www.sanita.it/bse. (AGI)

122055 MAG 03 COPYRIGHTS 2002-2003 AGI S.p.A.

http://www.agi.it/english/news.pl?doc=200305122055-0305-RT1-CRO-0-NF11&page=0&id=agionline-eng.oggitalia

Greetings,

> MAD COW: 1,479,034 ANALYSES CARRIED OUT, 97 CASES

let's see, the USA has now tested probably about 35,000 in some

14 years of surveillance, and have found no TSE in USA cows

(except for the data/discovery of Prof. R. Marsh that everyone

ignores), this is from some 100 million cattle in any given year

and some 37 million slaughtered every year. no wonder i cannot

get my mad cow feed ban warning letters through the FOIA.

considering the findings from Prof. Marsh, if i were the USDA/FDA, i would

refuse to rapid TSE test the USA bovine in such numbers as to

find as well $$$ if i were wanting to cover-up any TSEs in the USA

cattle...TSS
=============

As implied in the Inset 25, we must not _ASSUME_ that transmission
of BSE to other species will invariably present pathology typical
of a scrapie-like disease...

snip...

G A H WELLS 4 January 1991

http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
==========================================

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

https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000df08d?OpenDocument

Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL
IMPORTS FROM CANADA


https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9d?OpenDocument&AutoFramed


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

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

01N-0423 Substances Prohibited from use in animal food/Feed Ruminant

APE 5 National Renderers Association, Inc. Vol#: 2

APE 6 Animal Protein Producers Industry Vol#: 2

APE 7 Darling International Inc. Vol#: 2

EMC 1 Terry S. Singeltary Sr. Vol#: 3

http://www.fda.gov/ohrms/dockets/dailys/01/Oct01/101501/101501.htm

Send Post-Publication Peer Review to journal:


Re: 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

LANCET INFECTIOUS DISEASE JOURNAL


Volume 3, Number 8 01 August 2003


Newsdesk


Tracking spongiform encephalopathies in North America


Xavier Bosch

My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost

my mom to hvCJD (Heidenhain variant CJD) and have been searching for

answers ever since. What I have found is that we have not been told the

truth. CWD in deer and elk is a small portion of a much bigger problem.


49-year-old Singeltary is one of a number of people who have remained

largely unsatisfied after being told that a close relative died from a

rapidly progressive dementia compatible with spontaneous

Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of

documents on transmissible spongiform encephalopathies (TSE) and

realised that if Britons could get variant CJD from bovine spongiform

encephalopathy (BSE), Americans might get a similar disorder from

chronic wasting disease (CWD)the relative of mad cow disease seen among

deer and elk in the USA. Although his feverish search did not lead him

to the smoking gun linking CWD to a similar disease in North American

people, it did uncover a largely disappointing situation.


Singeltary was greatly demoralised at the few attempts to monitor the

occurrence of CJD and CWD in the USA. Only a few states have made CJD

reportable. Human and animal TSEs should be reportable nationwide and

internationally, he complained in a letter to the Journal of the

American Medical Association (JAMA 2003; 285: 733). I hope that the CDC

does not continue to expect us to still believe that the 85% plus of all

CJD cases which are sporadic are all spontaneous, without route or source.


Until recently, CWD was thought to be confined to the wild in a small

region in Colorado. But since early 2002, it has been reported in other

areas, including Wisconsin, South Dakota, and the Canadian province of

Saskatchewan. Indeed, the occurrence of CWD in states that were not

endemic previously increased concern about a widespread outbreak and

possible transmission to people and cattle.


To date, experimental studies have proven that the CWD agent can be

transmitted to cattle by intracerebral inoculation and that it can cross

the mucous membranes of the digestive tract to initiate infection in

lymphoid tissue before invasion of the central nervous system. Yet the

plausibility of CWD spreading to people has remained elusive.


Part of the problem seems to stem from the US surveillance system. CJD

is only reported in those areas known to be endemic foci of CWD.

Moreover, US authorities have been criticised for not having performed

enough prionic tests in farm deer and elk.


Although in November last year the US Food and Drug Administration

issued a directive to state public-health and agriculture officials

prohibiting material from CWD-positive animals from being used as an

ingredient in feed for any animal species, epidemiological control and

research in the USA has been quite different from the situation in the

UK and Europe regarding BSE.


Getting data on TSEs in the USA from the government is like pulling

teeth, Singeltary argues. You get it when they want you to have it,

and only what they want you to have.


Norman Foster, director of the Cognitive Disorders Clinic at the

University of Michigan (Ann Arbor, MI, USA), says that current

surveillance of prion disease in people in the USA is inadequate to

detect whether CWD is occurring in human beings; adding that, the

cases that we know about are reassuring, because they do not suggest the

appearance of a new variant of CJD in the USA or atypical features in

patients that might be exposed to CWD. However, until we establish a

system that identifies and analyses a high proportion of suspected prion

disease cases we will not know for sure. The USA should develop a

system modelled on that established in the UK, he points out.

Ali Samii, a neurologist at Seattle VA Medical Center who recently

reported the cases of three hunterstwo of whom were friendswho died

from pathologically confirmed CJD, says that at present there are

insufficient data to claim transmission of CWD into humans; adding that

[only] by asking [the questions of venison consumption and deer/elk

hunting] in every case can we collect suspect cases and look into the

plausibility of transmission further. Samii argues that by making both

doctors and hunters more aware of the possibility of prions spreading

through eating venison, doctors treating hunters with dementia can

consider a possible prion disease, and doctors treating CJD patients

will know to ask whether they ate venison.


CDC spokesman Ermias Belay says that the CDC will not be investigating

the [Samii] cases because there is no evidence that the men ate

CWD-infected meat. He notes that although the likelihood of CWD

jumping the species barrier to infect humans cannot be ruled out 100%

and that [we] cannot be 100% sure that CWD does not exist in humans&

the data seeking evidence of CWD transmission to humans have been very

limited.


http://infection.thelancet.com/journal/journal.isa


he complained in a letter to the Journal of the American Medical

Association (JAMA 2003; 285: 733). I hope that the CDC does not

continue to expect us to still believe that the 85% plus of all CJD

cases which are sporadic are all spontaneous, without route or source.<<<

actually, that quote was from a more recent article in the Journal of

Neurology (see below), not the JAMA article...

Full Text

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

BRITISH MEDICAL JOURNAL

SOMETHING TO CHEW ON

BMJ

http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2

BMJ

http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1

THE PATHOLOGICAL PROTEIN

BY Philip Yam

Yam Philip Yam News Editor Scientific American www.sciam.com
http://www.thepathologicalprotein.com/

IN light of Asante/Collinge et al findings 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;

-------- Original Message -------- Subject: re-BSE prions propagate as

either variant CJD-like or sporadic CJD Date: Thu, 28 Nov 2002 10:23:43

-0000 From: "Asante, Emmanuel A" To:
"'flounder@wt.net'"

Dear Terry,

I have been asked by Professor Collinge to respond to your request. I am

a Senior Scientist in the MRC Prion Unit and the lead author on the

paper. I have attached a pdf copy of the paper for your attention. Thank

you for your interest in the paper.

In respect of your first question, the simple answer is, yes. As you

will find in the paper, we have managed to associate the alternate

phenotype to type 2 PrPSc, the commonest sporadic CJD.

It is too early to be able to claim any further sub-classification in

respect of Heidenhain variant CJD or Vicky Rimmer's version. It will

take further studies, which are on-going, to establish if there are

sub-types to our initial finding which we are now reporting. The main

point of the paper is that, as well as leading to the expected new

variant CJD phenotype, BSE transmission to the 129-methionine genotype

can lead to an alternate phenotype which is indistinguishable from type

2 PrPSc.

I hope reading the paper will enlighten you more on the subject. If I

can be of any further assistance please to not hesitate to ask. Best wishes.

Emmanuel Asante

<> ____________________________________

Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial

College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG

Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email:

e.asante@ic.ac.uk (until 9/12/02)

New e-mail: e.asante@prion.ucl.ac.uk (active from now)

____________________________________

snip...

full text ;

http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm


AND the new findings of 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


Adaptation of the bovine spongiform encephalopathy agent to primates
and comparison with Creutzfeldt- Jakob disease: Implications for
human health

THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*,
Virginie Nouvel*,

Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp [Dagger

] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique

Dormont*, and Jean-Philippe Deslys* et al, that The agent responsible
for French iatrogenic growth hormone-linked CJD taken as a control is
very different from vCJD but is similar to that found in one case of
sporadic CJD and one sheep scrapie isolate;

http://www.pnas.org/cgi/content/full/041490898v1

Characterization of two distinct prion strains
derived from bovine spongiform encephalopathy
transmissions to inbred mice

http://vir.sgmjournals.org/cgi/content/abstract/85/8/2471


ALL animals for human/animal consumption must be tested for TSE.

ALL human TSEs must be made reportable Nationally and Internationally,

OF ALL AGES ... TSS

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
CJD WATCH






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