SEARCH VEGSOURCE:

 

 

Follow Ups | Post Followup | Back to Discussion Board | VegSource
See spam or
inappropriate posts?
Please let us know.
  




From: TSS ()
Subject: CWD UPDATE, CWD Found In Three Deer, Officials are probing if man's death linked to CWD, First study CWD on humans is announced
Date: November 23, 2005 at 6:35 am PST


Nov 23, 2005 7:04 am US/Central

CWD Found In Three Deer

(AP) Three deer killed in a buffer area surrounding the chronic wasting disease zone in Wisconsin have tested positive for the disease, state officials say.

The Department of Natural Resources said this week that the deer determined to have the fatal brain disease were in the herd reduction zone, which is outside the eradication zone where most of the deer infected with the disease have been found.

They included a 3-year-old doe shot between state Highway 26 and Lake Koshkonong in Jefferson County, a 3-year-old doe shot in Dane County east of Stoughton and a 2-year-old doe killed by a bow hunter west of Plain in Sauk County.

The DNR said it did not plan to take any immediate action in response to the test results and will wait until getting results from this fall's hunting season before deciding on future actions to stem the spread of the disease.

Chronic wasting disease was first confirmed in the state in February 2002.

The DNR has tried to control it by reducing the deer population in areas where concentrations of deer with the disease were found.


(© 2005 CBS Worldwide Inc. All Rights Reserved. This material may not be published, broadcast, rewritten, or redistributed. The Associated Press contributed to this report.)

http://wfrv.com/topstories/local_story_327080536.html

November 21, 2005 11:01 pm

Fifth wasting diseased deer confirmed

Mannix Porterfield
Register-Herald Reporter


A fifth deer infected with Chronic Wasting Disease has surfaced in Hampshire County, where hunters have gladly turned over harvested deer heads at check-in stations so more tests can be run.

Hampshire has become an enigma to game officials ever since a road-kill deer discovered a year ago tested positive for the neurological disorder.

This latest victim, a doe, was called to the attention of wildlife biologist Rich Rogers by a friend late last month. It was located about 7 1/2 miles away from the site of the first diseased animal, after he became concerned over the animal’s apparent disoriented behavior.

“He told me he found a deer sitting under a bush and it didn’t look right,” the Division of Natural Resources biologist said.

“It was not really skinny, but it was a 7 1/2-year-old doe. It couldn’t get up. It just wasn’t acting right.”

A brain sample was taken and came back positive.

Found Oct. 23, the doe was not far from the area where three subsequent deer infected with CWD were found once the DNR began killing them for its analytical mission, however, it was further east of the others, Rogers pointed out.

The area is known as Cold Stream, just southeast of Slanesville.

“Originally, we drew a 5-mile radius around the sample found on the highway, and got three more when we did the shooting,” he said.

The DNR killed 223 deer and sent samples of brain tissue on 186 of them, and from that number, three tested positive. Then came the fifth animal found with CWD, a disorder that always proves fatal to deer and elk, but so far, has not proven harmful to humans.

“We’re trying to define the range of this stuff, the distribution of it in the herd,” Rogers said.

“Then, we might have to make some management decisions next year on how to contain or control it, if that’s even possible.”

Game officials in Pennsylvania already have moved to block the potential introduction of any infected deer by banning all but the meat of animals taken while hunting in Hampshire County.

“There is what we call a ‘high risk parts ban’ on states with CWD positive animals,” said Dr. Elizabeth Santini, veterinary medical field officer for the Pennsylvania Department of Agriculture.

“That includes whole heads or spinal cords. Essentially, unless it’s just muscle — meat that has been deboned — or a clean skull cap, or hide, you can’t come into Pennsylvania with it. It’s so close to our borders. We have a vested interest in that.”

West Virginia wildlife authorities were taking brain tissue samples at nine check-in stations in Hampshire County in an effort to get a better handle on the possible spread of the disease.

Assistant chief Paul Johansen said hunters displayed “good cooperation” in letting the DNR have heads for testing. Ultimately, the DNR hopes to have 500 deer analyzed — including the 186 already tested.

Next Wednesday, two days after the buck season opens there, officials in Pennsylvania will be testing 100 deer killed by hunters, and ultimately will test some 5,000, the veterinary official said.

“The game commission is sending teams to the shops for processing,” Santini said.

“We’ll choose a certain number of heads that people don’t want to mount as trophies and bring them back to testing stations. Our staff will be there, taking samples to send to the laboratories.”

Pennsylvania can expect a quick turnaround on sampling, since it can avail itself of labs in Harrisburg, University Park, and the new Bolton Center at the University of Pennsylvania.

Rogers described the hunting in Hampshire as “pretty slow,” below turnouts from past seasons when the region has either led or ranked near the top in total kills at the end of the two-week hunt.

“There’s plenty of deer but the hunting pressure is off,” Rogers said. “But it’s been down a few years now.”

Rogers acknowledged the well-publicized discovery of CWD-infected deer might be having a negative impact on hunting there, but only when the final tally is in will the DNR know for sure.

Even with a noticeable dip in Hampshire hunters, Rogers said the apparent decline is far less than dramatic than the negative response when CWD turned up a few years ago in Wisconsin. Even with the major drop in hunters, within a few seasons, their ranks swelled to normal proportions.

“They realized that the disease is not going to wipe out the deer population,” he said.

Rogers said he, personally, isn’t worried about the appearance of the disorder.

“I’m going to keep eating deer from Hampshire County,” the biologist added.

— E-mail:

mannix@register-herald.com

http://www.register-herald.com/cnhi/registerherald/ourcommunity/local_story_325230133.html?keyword=topstory

Published: November 21, 2005 09:19 am

Officials confirm another sick deer

By Michael Sawyers
CUMBERLAND TIMES-NEWS (CUMBERLAND, Md.)
ROMNEY, W.Va. —

A 7 1/2-year-old Hampshire County whitetail doe that was found alive but weak and disoriented three weeks ago was confirmed Friday to have chronic wasting disease, bringing to five the number of infected deer within the county.

“This deer showed clinical signs of having the disease,” said Rich Rogers, wildlife biologist with the West Virginia Division of Natural Resources. “Besides being weak, it was drooling, though it did not appear thin.”

The deer was first spotted on private land along Cold Stream Road, north of Capon Bridge and U.S. Route 50. Rogers said the site is seven miles from the location of the first positive deer, a road kill near Slanesville, and three miles from the scene of the other diseased deer that were later discovered after agency shooting teams killed and checked more than 200 animals.

It is also just four miles from the Virginia state line. Virginia had already banned importation of deer carcasses from Hampshire County.

The West Virginia buck season begins Monday. Rogers said he and other agency officials will be at wildlife checking stations in Hampshire County asking to take brain stem samples from harvested deer.

“This will give us a more complete picture of where the disease exists in the county,” he said.

New York and West Virginia are the only two states in the extreme eastern United States where the disease has been confirmed. The illness, which attacks the animals’ brains, is always fatal. CWD had previously been confirmed in deer from Colorado, South Dakota, Wisconsin and other Rocky Mountain and northern plains states as well as some Canadian provinces.

CWD has not been known to jump species barriers and infect humans.

Michael A. Sawyers writes for the Cumberland (Md.) Times-News.

http://www.news-tribune.net/cnhi/newstribune/features/cnhinsoutdoors_story_325091944.html?keyword=topstory


Article Last Updated: 11/23/2005 12:32:35 AM

Officials are probing if man's death linked to wasting disease
By Ronnie Lynn
The Salt Lake Tribune


Health officials are investigating whether a northern Utah man died earlier this month of a rare disease some fear may be linked to the chronic wasting disease found in some deer populations.
Bear River Health Department Director Lloyd Berentzen expects test results back from a Cleveland lab within four weeks.
The lab is analyzing whether the man died of Creutzfeldt-Jakob Disease (CJD), a degenerative brain disorder that, according to the National Institute of Neurological Disorders and Stroke, causes death in 90 percent of patients within one year of the first symptom.
Residents of northern Utah worry the man, whose name and age are being withheld for privacy, may have contracted CJD from contact with a deer infected with chronic wasting disease, a similarly lethal brain disorder sometimes referred to as mad cow disease.
That's unlikely, Berentzen said.
"There is no evidence to suggest any public health threat," he said. "We don't think there's a reason to panic."
Berentzen acknowledged, however, that the man's death raised enough suspicion to warrant a health department investigation.
"The person's deterioration was very rapid, so that raises questions," he said. "It could be an advanced case of Alzheimer's. The chances of it being CJD are extremely remote."
There are about 200 cases of CJD in the United States each year, and the chances of getting it are one in a million worldwide, according to the National Institute of Neurological Disorders and Stroke.
Even rarer are cases in which CJD is contracted through contact with infected brain or nervous system tissue. Most cases, about 85 percent, are classified as "sporadic," which means the disease appears for no



apparent reason.
State wildlife officials say they found cases of chronic wasting disease near Vernal in 2002 and Fountain Green in 2004, but never in northern Utah.
"We've tested heavily in that area since 2001, and so far, we're confident it's not there," said Leslie McFarlane, a wildlife disease specialist with the Utah Division of Wildlife Resources.
The division has tested more than 900 deer in the region since 2001, McFarlane said.
Even had they found chronic wasting disease in the area, there is no documented connection between that disease and Creutzfeldt-Jakob Disease, said Ermias Belay, an epidemiologist who studies both diseases for the national Centers for Disease Control and Prevention.
"There is no evidence that chronic wasting disease has been transmitted to humans, but additional studies are needed to clarify whether [it] might pose a threat," he said. "CJD as a disease occurs without any link to hunting or venison consumption."
Those studies are ongoing but take years to complete because the incubation period - the period from exposure to the first symptom - is several years, he said.

http://www.sltrib.com/utah/ci_3244217


First study of CWD on humans is announced
BINGHAMTON, N.Y., Nov. 22 (UPI) -- Binghamton University scientists are conducting the first study to determine if chronic wasting disease in deer can infect humans who eat deer meat.

Ralph Garruto, professor of biomedical anthropology, is leading the study that monitors the health of a group of people known to have consumed venison infected with CWD.

Recently discovered in both wild and captive deer, CWD is similar to mad cow disease in that it concentrates in the spinal cord and brain.

Garruto hopes the study will determine if the disease can affect humans in the same way mad cow disease has been shown to cause neurological disease in those who consume infected beef.

The study focuses on a group of people who attended a Sportman's feast in Verona, N.Y., earlier this year. At least some of the attendees consumed venison from a deer infected with CWD.

The study will monitor the health of the participants during a six-year period.

CWD, first discovered in Colorado in 1967, has been documented in several Rocky Mountain and Midwestern states. This year, New York became the first state west of the Mississippi to report CWD in both privately owned and wild deer herds.

Copyright 2005 by United Press International. All Rights Reserved

http://www.sciencedaily.com/upi/index.php?feed=Science&article=UPI-1-20051122-19220300-bc-us-chronicwasting.xml

JOURNAL OURNAL OF VIROLOGY IROLOGY, Nov. 2005, p. 13794–13796 Vol. 79, No.
21
0022-538X/05/$08.00 !0 doi:10.1128/JVI.79.21.13794–13796.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
NOTES
Interspecies Transmission of Chronic Wasting Disease Prions to
Squirrel Monkeys (Saimiri sciureus sciureus)
Richard F. Marsh, 1† Anthony nthony E. Kincaid, 2 Richard A. Bessen, 3 and
Jason C. Bartz Bartz4*
Department of Animal Health and Biomedical Sciences, University of
Wisconsin, Madison 53706 537061; Department of
Physical Therapy Therapy2 and Department of Medical Microbiology and
Immunology, 4 Creighton University, Omaha,
Nebraska 68178; and Department of Veterinary Molecular Biology, Montana
State University, Bozeman, Montana 59718 597183
Received 3 May 2005/Accepted 10 August 2005
Chronic wasting disease (CWD) is an emerging prion disease of deer and elk.
The risk of CWD transmission
to humans following exposure to CWD-infected tissues is unknown. To assess
the susceptibility of nonhuman
primates to CWD, two squirrel monkeys were inoculated with brain tissue from
a CWD-infected mule deer. The
CWD-inoculated squirrel monkeys developed a progressive neurodegenerative
disease and were euthanized at
31 and 34 months postinfection. Brain tissue from the CWD-infected squirrel
monkeys contained the abnormal
isoform of the prion protein, PrP-res, and displayed spongiform
degeneration. This is the first reported
transmission of CWD to primates.
Chronic wasting disease (CWD) is a prion disease of elk and
deer in North America that was first identified at cervid re- research
search facilities in Colorado and Wyoming in the late 1960s
(17, 18). CWD has been identified on cervid game farms from
Montana to New York and has been diagnosed in wild deer
and elk in Colorado, Wyoming, Nebraska, South Dakota, Wis- Wisconsin,
consin, New Mexico, Illinois, and Utah and in Saskatchewan,
Canada (1, 14, 15). The geographic distribution of CWD in
deer and elk has been expanding and will likely result in an
increase in human exposure to the CWD agent. Although
there have been no cases of human prion disease linked to
CWD infection, the risk of interspecies transmission of CWD
to humans following consumption of CWD-infected tissues is
uncertain (5, 13).
One approach to assess the susceptibility of humans to an- animal
imal prion diseases is by experimental transmission to nonhu- nonhuman
man primates (9–11). To investigate the susceptibility of non- nonhuman
human primates to CWD, two adult female squirrel monkeys
(Saimiri sciureus sciureus) were intracerebrally (i.c.) inoculated with 200
"l of a 20% (wt/vol) brain homogenate from a female mule
deer in the clinical phase of CWD (inoculum was a gift from
Elizabeth Williams, Department of Veterinary Sciences, Uni- University
versity of Wyoming, Laramie, WY). Both CWD-inoculated
squirrel monkeys developed a progressive neurological disease
and were euthanized at the terminal stages of disease at 31 and
34 months postinfection, respectively (data on clinical symp- symptoms
toms and the time to onset of disease were not available).
To determine whether the abnormal form of the prion pro- protein,
tein, PrP-res, was present in the CWD-infected squirrel mon- monkeys,
keys, brain homogenates were analyzed by Western blotting as
previously described using the anti-PrP monoclonal antibody
6H4 (Prionics AG, Switzerland) (2). For this analysis, a 5%
(wt/vol) brain homogenate in Dulbecco’s phosphate-buf buffered fered
saline (Mediatech, Inc.) from CWD-infected squirrel monkeys,
a CWD-infected elk, or an uninfected mouse was either di- digested
gested with proteinase K (PK) (4 U/ml; United States Bio- Biochemical)
chemical) fo for 1 h a r at 37°C with agitation or was not digested
with PK. In the samples that were not digested with PK, PrP
migrated between 21 and 35 kDa in the CWD-infected squirrel
monkeys (Fig. 1, lanes 1 and 2) and between 30 and 35 kDa in
the CWD-infected elk (Fig. 1, lane 3) and in the uninfected
mouse sample (Fig. 1, lane 4). In the samples that were di- digested
gested with PK, PrP-res were detected in the two CWD-in- infected
fected squirrel monkeys (Fig. 1, lanes 5 and 6) and in the
CWD-infected elk sample (Fig. 1, lane 7). In the PK-digested
uninfected mouse brain, PrP was not detected (Fig. 1, lane 8),
indicating that PK digestion completely removed the PK-sen- sensitive
sitive isoform of PrP. In both CWD-infected squirrel monkeys,
the migration of the three PrP-res polypeptides on sodium
dodecyl sulfate-polyacrylamide gels was similar. The diglyco- diglycosylated
sylated PrP-res polypeptide migrated at 30 kDa similar to what
has been reported for squirrel monkeys infected with sporadic
Creutzfeldt-Jakob disease (CJD), kuru, and scrapie (4). The
relative abundance of PrP-res in the brain from the squirrel
monkey that was sacrificed at 34 months postinfection (Fig. 1,
lane 5) was greater than that in the squirrel monkey sacrificed
at 31 months postinfection (Fig. 1, lane 6) and may represent
dif differences ferences in the state of disease progression when the
animals
were sacrificed.
Histological examination of the brain, brain stem, and spinal
cord from the squirrel monkey that was euthanized at 31
months postinfection revealed widespread spongiform changes
that are consistent with CWD-induced neurodegeneration.
* Corresponding author. Mailing address: Department of Medical
Microbiology and Immunology, Creighton University, 2500 California
Plaza, Omaha, NE 68178. Phone: (402) 280-1811. Fax: (402) 280-1875.
E-mail: jbartz@creighton.edu.
† Deceased.
13794
Spongiform lesions in the neuropil were predominantly located
in subcortical gray matter structures of the forebrain. There
was widespread spongiform change in the putamen, caudate
nucleus, nucleus accumbens, lateral and medial hypothalamus,
hippocampal formation (CA 1), amygdala, and dorsomedial
thalamus (Fig. 2). Dif Diffuse fuse spongiosis was found in the interpe-
interpeduncular
duncular nucleus and substantia nigra in the midbrain and in
the reticular formation of the pons and medulla. Due to the
limited number of histological sections, a detailed comparison
of the neuropathology in CWD-infected squirrel monkeys and
other prion transmission studies in squirrel monkeys was not
possible.
The time to terminal disease following inoculation of squir- squirrel
rel monkeys with the CWD agent, 31 and 34 months, was
longer than for squirrel monkeys that were i.c. inoculated with
transmissible mink encephalopathy agent (9 to 12 months) and
scrapie agent (16 months) but is within the reported range of
the time to terminal disease following i.c. inoculation with
sporadic CJD (11 to 37 months) and kuru (10 to 48 months) (6,
8). This variation in disease progression following experimen- experimental
tal transmission of sporadic CJD, kuru, and CWD to squirrel
monkeys could be due to dif differences ferences in the inoculation dose,
strain of the prion agent, or the ability to establish infection
upon interspecies transmission. Regardless, this study illus- illustrates
trates that a nonhuman primate can develop a prion disease
following i.c. inoculation with a brain homogenate from a
CWD-infected mule deer.
Direct comparison of the ability of the CWD agent to cause
disease in squirrel monkeys following experimental i.c. inocu- inoculation
lation and the susceptibility of humans to CWD infection must
be interpreted with caution. Although squirrel monkeys are
susceptible to experimental infection with kuru and CJD, they
are also susceptible to experimental infection with scrapie (8),
and there is no epidemiological evidence to suggest that
scrapie can be transmitted to humans (16). These data suggest,
following direct cerebral inoculation, squirrel monkeys may
not be a good experimental model for assessing human sus- susceptibility
ceptibility to animal prion diseases. Oral exposure is the likely
natural route of human exposure to CWD, and in experimental
animals, this route is much less ef efficient ficient at causing disease
than
i.c. inoculation (3, 7, 12). Therefore, the ability of scrapie and
CWD to cause disease in primates by oral infection needs to be
established to further resolve the issue of susceptibility of hu- humans
mans to CWD infection.
Richard Marsh, who performed the experimental transmission of
CWD to squirrel monkeys, died in 1997 before these experiments were
completed. Due to the emergence of CWD in deer and elk and the
potential risk for CWD transmission to humans, we present his find- findings
ings with additional tissue analysis.
We thank Al Jenny, USDA-APHIS-VS-NVSL for the gift of the
CWD-infected elk tissue.
We dedicate the manuscript to Elizabeth Williams for her pioneer- pioneering
ing work on CWD.
REFERENCES
1. Animal and Plant Health Inspection Services, Marketing and Regulatory
Programs, U.S. Department of Agriculture. 2005. [Online.] http://www.aphis
.usda.gov/vs/nahps/cwd/cwd-distribution.html.
FIG. 1. Deposition of the abnormal isoform of the prion protein,
PrP-res, in the brain of squirrel monkeys inoculated with chronic
wasting disease. Western blot analysis of 250- "g tissue equivalents of
brain homogenates digested with proteinase K or not digested with
proteinase K was performed. The brain homogenates were from a
CWD-infected squirrel monkey that was sacrificed at 34 months (lanes
1 and 5) or at 31 months postinfection (lanes 2 and 6), a CWD-infected
elk (lanes 3 and 7), and an uninfected mouse (lanes 4 and 8). The
arrow indicates the location of the 29-kDa molecular mass marker.
FIG. 2. Spongiform degeneration in brain tissue from a squirrel
monkey inoculated with chronic wasting disease and euthanized at 31
months postinfection. (A) Low-power view of the lentiform nucleus,
showing the distribution of spongiform changes in the putamen (Pu)
and lack of spongiosis in the globus pallidus (Gp). Ac, anterior com-
commissure.
missure. (B) High-power view of the area outlined in panel A that
exhibits widespread spongiosis. Bars # 100 microns.
VOL OL. 79, 2005 NOTES 13795
2. Bartz, J. C., J. M. Aiken, and R. A. Bessen. 2004. Delay in onset of
prion
disease for the HY strain of transmissible mink encephalopathy as a result
of
prior peripheral inoculation with the replication-deficient DY strain. J.
Gen.
Virol. 85: 265–273.
3. Bartz, J. C., A. E. Kincaid, and R. A. Bessen. 2003. Rapid prion
neuroinva- neuroinvasion
sion following tongue infection. J. Virol. 77: 583–591.
4. Beekes, M., E. Baldauf, S. Cassens, H. Diringer, P. Keyes, A. C. Scott,
G. A.
Wells, P. Brown, C. J. Gibbs, Jr., and D. C. Gajdusek. 1995. Western blot
mapping of disease-specific amyloid in various animal species and humans
with transmissible spongiform encephalopathies using a high-yield purifica-
purification
tion method. J. Gen. Virol. 76: 2567–2576.
5. Belay, E. D., P. Gambetti, L. B. Schonberger, P. Parchi, D. R. Lyon, S.
Capellari, J. H. McQuiston, K. Bradley, G. Dowdle, J. M. Crutcher, and
C. R. Nichols. 2001. Creutzfeldt-Jakob disease in unusually young patients
who consumed venison. Arch. Neurol. 58: 1673–1678.
6. Brown, P., C. J. Gibbs, Jr., P. Rodgers-Johnson, D. M. Asher, M. P.
Sulima,
A. Bacote, L. G. Goldfarb, and D. C. Gajdusek. 1994. Human spongiform
encephalopathy: the National Institutes of Health series of 300 cases of
experimentally transmitted disease. Ann. Neurol. 35: 513–529.
7. Diringer, H., J. Roehmel, and M. Beekes. 1998. Ef Effect fect of repeated
oral
infection of hamsters with scrapie. J. Gen. Virol. 79: 609–612.
8. Gibbs, C. J., Jr., and D. C. Gajdusek. 1973. Experimental subacute
spongi- spongiform
form virus encephalopathies in primates and other laboratory animals. Sci-
Science
ence 182: 67–68.
9. Gibbs, C. J., Jr., and D. C. Gajdusek. 1972. Transmission of scrapie to
the
cynomolgus monkey (Macaca fascicularis). Nature 236: 73–74.
10. Lasmezas, C. I., J. P. Deslys, R. Demaimay, K. T. Adjou, F. Lamoury, D.
Dormont, O. Robain, J. Ironside, and J. J. Hauw. 1996. BSE transmission to
macaques. Nature 381: 743–744.
11. Lasmezas, C. I., J. G. Fournier, V. Nouvel, H. Boe, D. Marce, F.
Lamoury, N.
Kopp, J. J. Hauw, J. Ironside, M. Bruce, D. Dormont, and J. P. Deslys. 2001.
Adaptation of the bovine spongiform encephalopathy agent to primates and
comparison with Creutzfeldt-Jakob disease: implications for human health.
Proc. Natl. Acad. Sci. USA 98: 4142–4147.
12. Prusiner, S. B., S. P. Cochran, and M. P. Alpers. 1985. Transmission of
scrapie in hamsters. J. Infect. Dis. 152: 971–978.
13. Raymond, G. J., A. Bossers, L. D. Raymond, K. I. O’Rourke, L. E. McHol-
McHolland,
land, P. K. Bryant, M. W. Miller, E. S. Williams, M. Smits, and B. Caughey.
2000. Evidence of a molecular barrier limiting susceptibility of humans,
cattle and sheep to chronic wasting disease. EMBO J. 19: 4425–4430.
14. Sigurdson, C. J., and M. W. Miller. 2003. Other animal prion diseases.
Br.
Med. Bull. 66: 199–212.
15. Spraker, T. R., M. W. Miller, E. S. Williams, D. M. Getzy, W. J. Adrian,
G. G. Schoonveld, R. A. Spowart, K. I. O’Rourke, J. M. Miller, and P. A.
Merz. 1997. Spongiform encephalopathy in free-ranging mule deer
(Odocoileus hemionus), white-tailed deer (Odocoileus virginianus) and
Rocky Mountain elk (Cervus elaphus nelsoni) in northcentral Colorado.
J. Wildl. Dis. 33: 1–6.
16. van Duijn, C. M., N. Delasnerie-Laupretre, C. Masullo, I. Zerr, R. de
Silva,
D. P. Wientjens, J. P. Brandel, T. Weber, V. Bonavita, M. Zeidler, A. Alp-
Alperovitch,
erovitch, S. Poser, E. Granieri, A. Hofman, R. G. Will, and European Union
(EU) Collaborative Study Group of Creutzfeldt-Jakob disease (CJD). 1998.
Case-control study of risk factors of Creutzfeldt-Jakob disease in Europe
during 1993–95. Lancet 351: 1081–1085.
17. Williams, E. S., and S. Young. 1980. Chronic wasting disease of captive
mule
deer: a spongiform encephalopathy. J Wildl. Dis. 16: 89–98.
18. Williams, E. S., and S. Young. 1982. Spongiform encephalopathy of Rocky
Mountain elk. J. Wildl. Dis. 18: 465–471.
13796 NOTES J. VIROL IROL.TSS

----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Sent: Wednesday, October 19, 2005 10:47 AM
Subject: Interspecies Transmission of Chronic Wasting Disease Prions to
Squirrel Monkeys (Saimiri sciureus)


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

From: TSS ()
Subject: Interspecies Transmission of Chronic Wasting Disease Prions to
Squirrel Monkeys (Saimiri sciureus)
Date: October 19, 2005 at 8:33 am PST

0022-538X/05/$08.00+0 doi:10.1128/JVI.79.21.13794-13796.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Interspecies Transmission of Chronic Wasting Disease Prions to Squirrel
Monkeys (Saimiri sciureus)
Richard F. Marsh,1, Anthony E. Kincaid,2 Richard A. Bessen,3 and Jason C.
Bartz4*
Department of Animal Health and Biomedical Sciences, University of
Wisconsin, Madison 53706,1 Department of Physical Therapy,2 Department of
Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska
68178,4 Department of Veterinary Molecular Biology, Montana State
University, Bozeman, Montana 597183

Received 3 May 2005/ Accepted 10 August 2005

Chronic wasting disease (CWD) is an emerging prion disease of deer and elk.
The risk of CWD transmission to humans following exposure to CWD-infected
tissues is unknown. To assess the susceptibility of nonhuman primates to
CWD, two squirrel monkeys were inoculated with brain tissue from a
CWD-infected mule deer. The CWD-inoculated squirrel monkeys developed a
progressive neurodegenerative disease and were euthanized at 31 and 34
months postinfection. Brain tissue from the CWD-infected squirrel monkeys
contained the abnormal isoform of the prion protein, PrP-res, and displayed
spongiform degeneration. This is the first reported transmission of CWD to
primates.


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

* Corresponding author. Mailing address: Department of Medical Microbiology
and Immunology, Creighton University, 2500 California Plaza, Omaha, NE
68178. Phone: (402) 280-1811. Fax: (402) 280-1875. E-mail:
jbartz@creighton.edu .

Deceased.


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

Journal of Virology, November 2005, p. 13794-13796, Vol. 79, No. 21
0022-538X/05/$08.00+0 doi:10.1128/JVI.79.21.13794-13796.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.


http://jvi.asm.org/cgi/content/abstract/79/21/13794?maxtoshow=&HITS=10&hits=
10&RESULTFORMAT=&fulltext=cwd&searchid=1129736446553_4280&stored_search=&FIR
STINDEX=0&volume=79&issue=21&journalcode=jvi


TSS

#################### https://lists.aegee.org/bse-l.html
####################

#################### https://lists.aegee.org/bse-l.html ####################


----- Original Message -----
From: Terry S. Singeltary Sr.
To: doug_zellmer@thenorthwestern.com
Sent: Friday, October 28, 2005 12:18 PM
Subject: cwd


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


TSS
Animal Prion Diseases Relevant to Humans (unknown types?)
Thu Oct 27, 2005 12:05
71.248.128.109

About Human Prion Diseases /
Animal Prion Diseases Relevant to Humans

Bovine Spongiform Encephalopathy (BSE) is a prion disease of cattle. Since 1986, when BSE was recognized, over 180,000 cattle in the UK have developed the disease, and approximately one to three million are likely to have been infected with the BSE agent, most of which were slaughtered for human consumption before developing signs of the disease. The origin of the first case of BSE is unknown, but the epidemic was caused by the recycling of processed waste parts of cattle, some of which were infected with the BSE agent and given to other cattle in feed. Control measures have resulted in the consistent decline of the epidemic in the UK since 1992. Infected cattle and feed exported from the UK have resulted in smaller epidemics in other European countries, where control measures were applied later.

Compelling evidence indicates that BSE can be transmitted to humans through the consumption of prion contaminated meat. BSE-infected individuals eventually develop vCJD with an incubation time believed to be on average 10 years. As of November 2004, three cases of BSE have been reported in North America. One had been imported to Canada from the UK, one was grown in Canada, and one discovered in the USA but of Canadian origin. There has been only one case of vCJD reported in the USA, but the patient most likely acquired the disease in the United Kingdom. If current control measures intended to protect public and animal health are well enforced, the cattle epidemic should be largely under control and any remaining risk to humans through beef consumption should be very small. (For more details see Smith et al. British Medical Bulletin, 66: 185. 2003.)

Chronic Wasting Disease (CWD) is a prion disease of elk and deer, both free range and in captivity. CWD is endemic in areas of Colorado, Wyoming, and Nebraska, but new foci of this disease have been detected in Nebraska, South Dakota, New Mexico, Wisconsin, Mississippi Kansas, Oklahoma, Minnesota, Montana, and Canada. Since there are an estimated 22 million elk and deer in the USA and a large number of hunters who consume elk and deer meat, there is the possibility that CWD can be transmitted from elk and deer to humans. As of November 2004, the NPDPSC has examined 26 hunters with a suspected prion disease. However, all of them appeared to have either typical sporadic or familial forms of the disease. The NPDPSC coordinates with the Centers for Disease Control and state health departments to monitor cases from CWD-endemic areas. Furthermore, it is doing experimental research on CWD transmissibility using animal models. (For details see Sigurdson et al. British Medical Bulletin. 66: 199. 2003 and Belay et al. Emerging Infectious Diseases. 10(6): 977. 2004.)

http://www.cjdsurveillance.com/abouthpd-animal.html

SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2004. SPORADIC CJD CASES TRIPLED, and that is with a human TSE surveillance system that is terrible flawed. in 1997 cases of the _reported_ cases of cjd were at 54, to 163 _reported_ cases in 2004. see stats here;

p.s. please note the 47 PENDING CASES to Sept. 2005

p.s. please note the 2005 Prion D. total 120(8) 8=includes 51 type pending, 1 TYPE UNKNOWN ???

p.s. please note sporadic CJD 2002(1) 1=3 TYPE UNKNOWN???

p.s. please note 2004 prion disease (6) 6=7 TYPE UNKNOWN???

http://www.cjdsurveillance.com/resources-casereport.html

CWD TO HUMANS = sCJD ???

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...

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

ATYPICAL TSEs in USA CATTLE AND SHEEP ?

http://www.bseinquiry.gov.uk/files/sc/seac17/tab03.pdf

TSS

#################### https://lists.aegee.org/bse-l.html ####################



Subject: HUMAN AND ANIMAL TSE TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY I.E. MAD COW DISEASEs [TSS SUBMISSIONS FEDERAL DOCKETS AND PEER REVIEW JOURNALS]


FYI, this goes far far beyond the mad cow hamburger and the UK nvCJD/BSE only theory. i have wasted almost 8 years of my life daily for nothing.
i am no doctor, i have no PhDs, and i am president and ceo of nothing, i only seek the truth.

YOU might be interested in some new studies in my submission;

Importation of Whole Cuts of Boneless Beef from Japan [Docket No. 05-004-1] RIN 0579-AB93 TSS SUBMISSION


http://docket.epa.gov/edkfed/do/EDKStaffItemDetailView?objectId=090007d480993808

http://docket.epa.gov/edkfed/do/EDKStaffAttachDownloadPDF?objectId=090007d480993808

http://docket.epa.gov/edkfed/do/EDKStaffCollectionDetailView?objectId=0b0007d48096b40d

From: TSS ()
Subject: [Docket No. 03-025IFA] SRMs and Non-Ambulatory disabled cattle[TSS]
Date: October 6, 2005 at 2:28 pm PST

[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle

03-025IFA
03-025IFA-2
Terry S. Singeltary


Page 1 of 17

From: Terry S. Singeltary Sr. [flounder9@verizon.net]

Sent: Thursday, September 08, 2005 6:17 PM

To: fsis.regulationscomments@fsis.usda.gov

Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements

for the Disposition of Non-Ambulatory Disabled Cattle

Greetings FSIS,

I would kindly like to submit the following to [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and

Requirements for the Disposition of Non-Ambulatory Disabled Cattle

THE BSE/TSE SUB CLINICAL Non-Ambulatory Disabled Cattle

Broken bones and such may be the first signs of a sub clinical BSE/TSE Non-Ambulatory Disabled Cattle ;

SUB CLINICAL PRION INFECTION

MRC-43-00

Issued: Monday, 28 August 2000

NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH

FINDINGS RELEVANT TO CJD AND BSE


Terry S. Singeltary Sr.

P.O. Box 42

Bacliff, Texas USA 77518

9/13/2005

http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf





Follow Ups:



Post a Followup

Name:
E-mail: (optional)
Subject:

Comments:

Optional Link URL:
Link Title:
Optional Image URL: