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From: Terry S. Singeltary Sr. (216-119-144-61.ipset24.wt.net)
Subject: Politics/Industry could spread CWD to West Virgina $$$
Date: December 24, 2004 at 1:55 pm PST

-------- Original Message --------
Subject: Politics/Industry could spread CWD to West Virgina $$$
Date: Fri, 24 Dec 2004 15:56:17 -0600
From: "Terry S. Singeltary Sr."
To: Bovine Spongiform Encephalopathy


December 24, 2004
State DNR lifts ban on new deer farms

By John McCoy
Staff writer

Over the objections of some wildlife biologists, West Virginias top
natural resources official has lifted a nine-month-old ban on new deer
farms.

In a Dec. 10 letter to a prospective deer farmers lawyer, Division of
Natural Resources Director Ed Hamrick reversed the DNRs moratorium on
the issuance of commercial game farm licenses for captive-deer facilities.

I will consider issuing temporary licenses on a case-by-case basis,
Hamrick wrote, and only after determining that the proposed new
facilities and the source animals to be housed in those facilities
constitute a minimal threat for spreading chronic wasting disease or
other transmissible diseases.


Chronic wasting disease is a brain disorder that kills deer, elk and
other antlered animals with symptoms similar to mad cow disease. CWD
occurs primarily in the Rocky Mountains, the upper Midwest and the
Canadian plains provinces. Its spread has been strongly linked to the
interstate transportation of infected captive animals.

Hamrick imposed the moratorium early in 2004 to prevent CWD-infected
deer from being brought into West Virginia. At the time, the state had
no safeguards against interstate importation, and only scant regulations
to govern deer farming.

Chronic wasting disease hasnt yet been detected in Mountain State deer,
but an animal-disease expert said thats no assurance that it doesnt exist.

Theres no way to test a live, healthy animal to detect the disease,
said John Fischer, director of the Georgia-based Southeastern
Cooperative Wildlife Disease Study. You only know its there after an
animal starts showing symptoms.

Fischer called the movement of captive animals the greatest risk factor
for CWD introduction in any area.

The original DNR ruling did three things to prevent deer from being
moved: It prohibited deer from being imported from other states; it
prohibited existing deer farms from moving deer from one in-state
facility to another; and it prohibited the licensing of any new deer farms.

A subsequent legislative ruling upheld the ban on interstate transport
and the licensing moratorium, but allowed deer farms within the state to
move animals from one facility to another.

The moratorium was designed to give us time to work up a set of
regulations to govern these facilities, Hamrick said Wednesday. Over
the course of the past year, we had several meetings with deer farmers
and their representatives, and we were able to develop those regulations.

Hamrick said that in his opinion, the regulations provided enough
safeguards to allow him to lift the ban on new facilities.

It was my decision to send the letter and complete the process, he said.

In making that decision, however, Hamrick apparently overruled at least
some of his deer biologists.

Paul Johansen, the DNRs assistant wildlife chief, said he clearly
articulated his and some of his staffs objections to Hamrick before
the decision was made.

The captive-deer industry has a problem with illegal activity,
Johansen said. Some facility owners are moving infected animals as we
speak. Are those animals coming into West Virginia? I dont know. But
every new facility increases the chance that it could happen.

According to DNR records, 54 licensed captive-deer farms operate within
the states borders. Most of them are small, noncommercial facilities in
which landowners keep deer as pets. Johansen said fewer than half of
them are considered active businesses.

Most of the commercial ventures raise breeder stock for other
facilities, or sell their deer to shooting preserves, he said.

Recent increases in the breeder-stock business have led to additional
demands for deer-farm licenses. Hamricks recent ruling clears the way
for new facilities to open.

The difference is that we now have [DNR] regulations in place that will
govern the opening of those facilities, Hamrick said. And after the
U.S. Department of Agriculture issues its regulations, all facilities
will be forced to meet those requirements.

Johansen, however, said hed prefer that Hamrick wait for the USDA
regulations to be finalized before issuing any new licenses.

We should be extraordinarily cautious and conservative about issuing
any licenses for new facilities, Johansen said. We elevate our risk of
exposing our wild deer population to chronic wasting disease every time
we allow a captive deer to be moved.

The bottom line is that we do not know whether we already have CWD
behind fences in West Virginia right now. We pray to God we dont, but
we dont know. And with a million wild deer out there and a
quarter-billion-dollar deer-hunting industry at stake, we cant afford
to take a chance.

To contact staff writer John McCoy, use e-mail or call 348-1231.


http://wvgazette.com/section/News/2004122320

http://wvgazette.com/section/News/2004122320?pt=10

Greetings,

> Hamrick said that in his opinion, the regulations provided enough
> safeguards to allow him to lift the ban on new facilities.
>

i would love to see these safeguards.

ARE they going to now test all these farmed animals for
CWD/TSE before moving, if so, please tell me about this
new test?

HOW are they going to prevent sub-clinical CWD/TSE from passing
from one animal to another?

HOW are they going to prevent exposure to the environment from
the many proven routes of the CWD/TSE agent i.e. pastures/soil,
fence posts, bedding, etc.?

HOW can you have one state CWD/TSE regulations different from
other states, then transport between states, and expect to keep the
agent out from moving with the deer/elk and keep from contaminating
any transport vehicles from potential sub-clinical CWD/TSE animals?

WITH bone headed decisions made like Division of Natural Resources
Director Ed Hamrick just made about CWD, who needs Terrorists
to release biological agents into our environment, US officials like this do
a fine job by themselves...

and dumb gets dumber, while the agent continues to spread...

Research


Environmental Sources of Prion Transmission in Mule Deer

Michael W. Miller,*Comments
Elizabeth S.
Williams, N. Thompson Hobbs,! and Lisa L. Wolfe*
*Colorado Division of Wildlife, Fort Collins, Colorado, USA; University
of Wyoming, Laramie, Wyoming, USA; and !Colorado State University, Fort
Collins, Colorado, USA

Suggested citation for this article: Miller MW, Williams ES, Hobbs
NT, Wolfe LL. Environmental sources of prion transmission in mule
deer. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date
cited]. Available from:
http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm

snip...


Discussions ;

Prions cannot be directly demonstrated in excreta or soil. However, CWD
infectionspecific protease-resistant prion protein (PrPCWD) accumulates
in gut-associated lymphoid tissues (e.g., tonsils, Peyer patches, and
mesenteric lymph nodes) of infected mule deer (11,17
,22
), which
implicates alimentary shedding of the CWD agent in both feces and saliva
(10 ,11,17
). Because PrPCWD
becomes progressively abundant in nervous system and lymphoid tissues
through the disease course (11
), carcasses of
deer succumbing to CWD also likely harbor considerable infectivity and
thus serve as foci of infection. We could not determine the precise
mechanism for CWD transmission in excreta-contaminated paddocks, but
foraging and soil consumption seemed most plausible. Deer did not
actively consume decomposed carcass remains, but they did forage in the
immediate vicinity of carcass sites where a likely nutrient flush (23
) produced lush
vegetation (Figure
).

Our findings show that environmental sources of infectivity may
contribute to CWD epidemics and illustrate the potential complexity of
such epidemics in natural populations. The relative importance of
different routes of infection from the environment cannot be discerned
from our experiment, but each could play a role in sustaining natural
epidemics. Although confinement likely exaggerated transmission
probabilities, conditions simulated by this experiment do arise in the
wild. Mule deer live in established home ranges and show strong fidelity
to historic home ranges (24-26
). As a result of
such behavior, encounters with contaminated environments will occur more
frequently than if deer movements were random. Feces and carcass remains
are routinely encountered on native ranges, thus representing natural
opportunities for exposure. Social behavior of deer, particularly their
tendency to concentrate and become sedentary on their winter range, also
may increase the probability of coming into contact with sources of
infection in their environment.

The ability of the CWD agent to persist in contaminated environments for
>2 years may further increase the probability of transmission and
protract epidemic dynamics (8
). Because
infectivity in contaminated paddocks could not be measured, neither the
initial levels nor degradation rate of the CWD agent in the environment
was estimable. However, the observed persistence of the CWD agent was
comparable to that of the scrapie agent, which persisted in paddocks for
?1 to 3 years after removal of naturally infected sheep (7
). Similarities
between the CWD and scrapie agents suggest that environmental
persistence may be a common trait of prions. Whether persistence of the
BSE prion in contaminated feed production facilities or in environments
where cattle reside contributed to BSE cases in the United Kingdom after
feed bans were enacted (27
) remains
uncertain but merits further consideration.

Indirect transmission and environmental persistence of prions will
complicate efforts to control CWD and perhaps other animal prion
diseases. Historically, control strategies for animal prion diseases
have focused on infected live animals as the primary source of
infection. Although live deer and elk represent the most plausible
mechanism for geographic spread of CWD, our data show that environmental
sources could contribute to maintaining and prolonging local epidemics,
even when all infected animals are eliminated. Moreover, the efficacy of
various culling strategies as control measures depends in part on the
rates at which the CWD agent is added to and lost from the environment.
Consequently, these dynamics and their implications for disease
management need to be more completely understood.

http://www.cdc.gov/ncidod/eid/vol10no6/04-0010.htm


Chronic Wasting Disease and Potential Transmission to Humans

Ermias D. Belay,*Comments
Ryan A.
Maddox,* Elizabeth S. Williams, Michael W. Miller,! Pierluigi
Gambetti,§ and Lawrence B. Schonberger*
*Centers for Disease Control and Prevention, Atlanta, Georgia, USA;
University of Wyoming, Laramie, Wyoming, USA; !Colorado Division of
Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve
University, Cleveland, Ohio, USA

Suggested citation for this article: Belay ED, Maddox RA, Williams
ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease
and potential transmission to humans. Emerg Infect Dis [serial on
the Internet]. 2004 Jun [date cited]. Available from:
http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm

snip...


Conclusions

The lack of evidence of a link between CWD transmission and unusual
cases of CJD, despite several epidemiologic investigations, and the
absence of an increase in CJD incidence in Colorado and Wyoming suggest
that the risk, if any, of transmission of CWD to humans is low. Although
the in vitro studies indicating inefficient conversion of human prion
protein by CWD-associated prions raise the possibility of low-level
transmission of CWD to humans, no human cases of prion disease with
strong evidence of a link with CWD have been identified. However, the
transmission of BSE to humans and the resulting vCJD indicate that,
provided sufficient exposure, the species barrier may not completely
protect humans from animal prion diseases. Because CWD has occurred in a
limited geographic area for decades, an adequate number of people may
not have been exposed to the CWD agent to result in a clinically
recognizable human disease. The level and frequency of human exposure to
the CWD agent may increase with the spread of CWD in the United States.
Because the number of studies seeking evidence for CWD transmission to
humans is limited, more epidemiologic and laboratory studies should be
conducted to monitor the possibility of such transmissions. Studies
involving transgenic mice expressing human and cervid prion protein are
in progress to further assess the potential for the CWD agent to cause
human disease. Epidemiologic studies have also been initiated to
identify human cases of prion disease among persons with an increased
risk for exposure to potentially CWD-infected deer or elk meat (47
). If such cases
are identified, laboratory data showing similarities of the etiologic
agent to that of the CWD agent would strengthen the conclusion for a
causal link. Surveillance for human prion diseases, particularly in
areas where CWD has been detected, remains important to effectively
monitor the possible transmission of CWD to humans. Because of the long
incubation period associated with prion diseases, convincing negative
results from epidemiologic and experimental laboratory studies would
likely require years of follow-up. In the meantime, to minimize the risk
for exposure to the CWD agent, hunters should consult with their state
wildlife agencies to identify areas where CWD occurs and continue to
follow advice provided by public health and wildlife agencies. Hunters
should avoid eating meat from deer and elk that look sick or test
positive for CWD. They should wear gloves when field-dressing carcasses,
bone-out the meat from the animal, and minimize handling of brain and
spinal cord tissues. As a precaution, hunters should avoid eating deer
and elk tissues known to harbor the CWD agent (e.g., brain, spinal cord,
eyes, spleen, tonsils, lymph nodes) from areas where CWD has been
identified.

http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm


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

http://www.nature.com/cgi-taf/dynapage.taf?file=/nm/journal/v8/n5/index.html

Prof. Dr. Adriano Aguzzi

http://www.unizh.ch/pathol/neuropathologie/ptn_aag_cv.html

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

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.


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


and CWD has transmitted to 5 cows and one sheep ;

-------- Original Message --------
Subject: Re: CWD TO CATTLE by inoculation (ok,is it three or four OR NOW
FIVE???)
Date: Mon, 23 Jun 2003 12:36:59 -0500
From: "Janice M. Miller"
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L


I am happy to provide an update on the experimental inoculation of
cattle and sheep with CWD. These are ongoing experiments and updates
are normally provided via presentations at meetings. Dr. Hamir has
prepared a poster of the following information that will be displayed at
4 upcoming meetings this summer and fall.

Experimental Transmission of Chronic Wasting Disease (CWD) to Cattle
and Sheep
Progress report - June 23, 2003

Experimental Transmission to Cattle

Background:
In 1997, 13 calves were inoculated intracerebrally with brain
suspension from mule deer naturally affected with CWD. During the first
3 years, 3 animals were euthanized 23, 24, and 28 months after
inoculation because of weight loss (2) or sudden death (1). Although
microscopic examination of the brains did not show classical lesions of
transmissible spongiform encephalopathy (TSE), a specific TSE marker
protein, PrPres, was detected by immunohistochemistry (IHC) and western
blot. Detailed information on these animals has been published
previously (A Hamir et al., J Vet Diagn Invest 13: 91-96, 2001).

Update:
During the 3rd, 4th and 6th years of observation, 7 additional animals
have been euthanized due to a variety of health concerns (primarily
chronic joint and foot problems). IHC and western blot results indicate
that 2 of these animals, necropsied 59 and 63 months after inoculation,
were positive for PrPres. One animal (# 1746) had not been eating well
for approximately 1 week prior to being found recumbent. At necropsy,
significant gross lesions consisted of an oblique fracture of L1
vertebral arch with extension into the body, and moderate multifocal
hemorrhagic ulceration in the abomasum. Microscopic examination of
brain revealed a few isolated neurons with single or multiple vacuoles,
but neither neuronal degeneration nor gliosis was observed. IHC
revealed the presence of PrPres in sections from several areas of the
brain. The other PrPres positive animal (#1742) was euthanized after
being found in lateral recumbency with a body temperature of 104.6 F.
It had not shown prior clinical signs except for some decreased appetite
for 2 days. Necropsy revealed only moderate hepatitis and a small renal
infarct due to intravascular thrombosis.

Summary of findings on all necropsied animals to date:

Ear tag Date of Survival Disease Clinical
Histo- IHC WB
no. necropsy period course signs
pathology
_____________________________________________________________________
1745 8/18/99 23m 2m +
± + +
1768 9/22/99 24m 3m +
± + +
1744 1/29/00 28m 3d ±
- + +
1749 5/20/01 44m NA -
- - -
1748 6/27/01 45m NA -
- - -
1743 8/21/02 59m NA -
- - -
1741 8/22/02 59m NA -
- - -
1746 8/27/02 59m 7d ±
± + +
1765 11/27/02 62m 1d ±
± - -
1742 12/28/02 63m 2d ±
- + +
NT = not tested; IHC = immunohistochemistry for PrPres; SAF = scrapie
associated fibrils; NA = not applicable; WB = Western blot
(Prionics-Check); + = lesions or antigen present; - = lesions or
antigen absent; ± = signs/lesions equivocal; i/c = intracerebral; m =
months; d = days.

Summary:
After 5.75 years of observation we have 5 CWD transmissions to cattle
from a group of 13 inoculates. These animals, which were necropsied 23,
24, 28, 59, and 63 months after inoculation, did not show the clinical
signs or histopathologic lesions typical of a TSE, but PrPres was
detected in brain samples by both immunohistochemistry and western blot.
Five other animals necropsied during the 4th, 5th and 6th years of
observation have not shown evidence of PrPres and the remaining 3 cattle
are apparently healthy. Note that this study involved direct
intracerebral inoculation of cattle with the CWD agent, which is an
unnatural route of exposure. Likely, it would be more difficult to
infect cattle by the oral route. Cattle have been inoculated orally at
the University of Wyoming with the same inoculum used in this
experiment, and 5.75 years into the study the animals remain healthy
(personal communication, Dr. Beth Williams).

Experimental Transmission of CWD to sheep

Eight Suffolk sheep from the NADC scrapie-free flock were inoculated
intracerebrally with the CWD brain suspension used to inoculate cattle.
PRNP genotyping showed that 4 of the sheep were QQ at codon 171 and the
other four were QR. Two of the QQ sheep were euthanized during the 3rd
year of observation. At necropsy one of these animals had a urethral
obstruction and PrPres was not detected in brain or lymphoid tissues.
The other sheep, necropsied 35 months after inoculation, showed clinical
signs and histopathologic lesions that were indistinguishable from
scrapie. IHC tests showed typical PrPres accumulations in brain,
tonsil, and some lymph nodes. The 2 remaining QQ sheep and all 4 QR
sheep are apparently healthy 47 months after inoculation.

Summary:
After 4 years of observation we have 1 transmission of CWD to a 171 QQ
sheep. This animal, which was necropsied 35 months after inoculation,
showed clinical signs and histopathologic lesions that were
indistinguishable from scrapie. Another QQ sheep that was necropsied
during the 3rd year showed no evidence of prion disease and all
remaining sheep (2 QQ and 4 QR) are apparently healthy.


TSS





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