#########How to dispose of deer with CWD?
By Lesley Rogers Barrett
MADISON -- Putting deer that might have chronic wasting disease in Dane
County's landfill seems to be the best option to dispose of the
thousands of carcasses expected this year, state officials told a task
force Monday.
But the 11-member task force, which met for the first time Monday, isn't
so sure. Many members urged incinerating the dead deer, and even
creation of a state-built incinerator.
"We can put a man on the moon; I don't know why we can't build an
incinerator in two to four months," said Sup. Vern Wendt, Mazomanie.
Department of Natural Resources officials said area incinerators don't
have the capacity to take the large number of deer expected to be killed
this fall, and there isn't enough time to build one.
So far, 18 area deer have tested positive for chronic wasting disease, a
fatal brain disease in deer and elk. The DNR wants to kill all the deer
in a 361-square-mile area in Dane, Iowa and Sauk counties.
Landfills are a safe solution to disposing of the deer, said Steve
Miller, administrator of the DNR's Land Division.
"I need options quick," Miller said. "What do you then want the
department to do to control CDW in your county? We have to do something."
The task force, which is comprised of county officials and area
residents, will make a recommendation next month on the disposal of
deer. They will seek assurance from the state that it will pay for any
future problems with the Rodefeld landfill east of Madison.
This spring, 500 deer were killed, tested for the disease and disposed
of in the county landfill. County Executive Kathleen Falk has since
directed the landfill to stop taking the deer until more information is
available.
Midwest Crematorium Services in Poynette is taking the roughly 1,500
deer expected to be killed during summer hunting. But that's too costly
to continue, said Joe Brusca, DNR waste specialist.
The fall hunting season would cost the DNR about $2 million to
incinerate or $45,000 to put in a landfill, Brusca said.
Jerry Mandhi, solid waste manager for the landfill, said that although
there hasn't been any proof the diseased deer can cause problems, he's
worried about the reputation of the landfill.
"My concern is from a public relations standpoint," Mandhi said. "Can
the DNR make me feel good and the people who live around the landfill
and who work at the landfill?"
Lesley Rogers Barrett is
a county reporter for the
Wisconsin State Journal.
http://baraboo.scwn.com/display/inn_news/news1.txt
Greetings List Members,
trying to get these folks to understand the seriousness of this
whole ordeal, is like trying to wake the dead. seems they will
have to learn the hard way, from what Miller is wanting $
he seems to insist on repeating what happened in the UK,
and elsewhere around the Globe. hell, will not matter anyway,
if they continue to refuse to test cows in sufficient numbers
to find. the plan to harvest/test 15,000 deer this fall, as i said,
will surpass the measley 12,000 head of cattle they tested
for TSEs/BSE since the inception of the surveillance in 1986.
that's correct, only 12,000 some odd cattle testing in USA for
TSE in some 15 years of surveillance, to 2001...TSS
> Landfills are a safe solution to disposing of the deer, said Steve
> Miller, administrator of the DNR's Land Division.
To,
wsjopine@madison.com
nsaylor@madison.com
national@madison.com
TO MRS. KATHLEEN FALK AND Mr. Gary Johnson,
TSEs and GROUND/WATER CONTAMINATION
INFECTIVITY REMAINING AFTER ASHING TO 600* CELSIUS
INFECTIVITY AFTER BURIAL FOR 3 YEARS
Falk: Any risk with dumping deer?
SNIPPED...
especially the possibility of dumping more than 2 million pounds of deer
carcasses in a county landfill.
"I have two goals," Falk said, "to protect public health and to protect
our deer herd."
"Do we need to worry about the carcasses leaking through the membrane of
the landfill?" Falk asked. "Or our groundwater becoming contaminated?"
Brett Hulsey, one of the County Board supervisors who will introduce the
task force resolution, said dealing with the disease will require some
tough choices - chief among them deciding whether to allow the disposal
of possibly diseased deer in the Dane County Landfill.
Gary Johnson, public health manager for Dane County, said the problem is
that prions are very hard to destroy and have been shown to linger for
years. He said England's experience with mad cow disease, a similar
prion disease that did pass to humans and killed more than 100 people,
should be an example. Just as with CWD here in the states, Johnson said,
people were told mad cow disease wasn't a human health threat.
indent"People were saying the same thing," Johnson said, "and taking
more comfort from that than they should have. We don't want to be too
confident about this given that what we don't know may come back to hurt
us later."
SNIP...
http://www.wisconsinstatejournal.com/local/25318.html
==============================================
Greetings,
i must say, from the gab, i'm impressed. but it's only talk, and
that my friends needs to be backed up with action. don't let the
industry and there backers in office manipulate science,
for _their_ best interest$
now, as most know, TSEs are extremely hard to destroy.
the concerns for public health that you pointed out
are very valid. these carcasses must be destroyed by
incinerations of extreme heat, to exceed 1000* Celsius.
you can bury tainted TSE materials and the infectivity
be there years later. you will taint the water tables.
instead of me trying to explain this, i send you these
studies. i hope someone reads them, and makes the correct
decissions...TSS;
LANCET
Volume 351, Number 9110 18 April 1998
[Previous] [Next]
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.bse.org.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 info. 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 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!!!
xxxxxxxxxxx
you can take that with however many grains of salt you wish, and
we can debate these issues all day long, but 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.bse.org.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.bse.org.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 Heggebø1, 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 Tübingen, 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.bse.org.uk/files/yb/1989/04/17005001.pdf
USA/CWD 'ROUND-UP'
Wildlife official frets over restocking of elk ranch
By Todd Hartman, News Staff Writer
June 11, 2002
BURLINGTON -- A Colorado elk rancher's restocking of his herd despite
concerns about chronic wasting disease could put the industry at risk, a
top state wildlife official said Monday.
Colorado Wildlife Commission Chairman Rick Enstrom said he was perplexed
by Trophy Mountain Elk Ranch operator Mark Mitchell's apparent disregard
for the hazards of CWD and for government rules.
The Colorado Division of Wildlife discovered to its dismay last week
that Mitchell had restocked his elk ranch with more than 300 animals
just months after the federal government paid him as much as $570,000 to
kill his previous herd of 200 elk to contain the spread of CWD.
Mitchell said he restocked with the permission of the Colorado
Department of Agriculture, which regulates elk ranches. But Division of
Wildlife officials said they were supposed to participate in discussions
on how or whether Mitchell could bring new elk onto his ranch just
outside Cowdrey.
The government's concern is based on evidence that the infectious agent
behind CWD, called a prion, can survive in the soil apparently for
years. Since Mitchell had three infected elk on his land last fall,
wildlife officials worry that the always fatal disease may still be
present on part of his roughly 3,000-acre spread.
Particularly galling, Enstrom added, is the fact that the division is
spending about $300,000 to add fencing to Mitchell's ranch, to help keep
migrating wildlife separated from his captive elk.
Mitchell said last week that the Division of Wildlife has no
jurisdiction over him. Waiting for its permission would have put him out
of business, he said.
Enstrom said wildlife and agriculture officials have to work together
when elk ranching and CWD intersect.
"The state of Colorado needs this mess fixed," he said.
The Colorado Wildlife Commission, which sets policy for the division, on
Monday considered several new actions to address CWD. Commissioners
approved:
* Definitions for parts of the state affected by CWD. Areas where
the disease festers for long periods and where there's little hope of
eradicating it will be termed "established areas."
"Discovery area" denotes a previously uninfected area where CWD is found.
"Elimination area" denotes a place where division biologists employ
large-scale culling to wipe out the disease.
* Rules preventing hunters who kill a deer or elk within
northeastern Colorado's endemic area to transport the carcass outside of
the region unless certain parts of the body, including brain tissue and
spinal column, are left behind.
* Giving the director discretion to allow division biologists to
kill hundreds of deer, or more, if CWD is found in a previously
uninfected area.
Contact Todd Hartman at (303) 892-5048 or hartmant@RockyMountainNews.com.
http://www.rockymountainnews.com/drmn/state/article/0,1299,DRMN_21_1201392,00.html
TSS
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