2 replies [Last post]
Offline
Joined: 01/01/2006
Posts: 230
CWD experts address first meeting of advisory committee

Outdoors: CWD experts address first meeting of advisory committee
Tim Eisele — 8/22/2007 10:46 am

Why should we care?

That was a rhetorical question asked by Scott Craven, professor of Wildlife
Ecology at UW-Madison, in leading off the second CWD Stakeholder Advisory
Committee meetings in Madison last Saturday.

The meeting, held at Lowell Inn and Conference Center on the UW-Madison
campus, drew a surprisingly small public attendance, less than 10 people.
However, the reason for the meeting was for the 16-member committee to hear
from experts about what is known about chronic wasting disease.

The committee will meet monthly between August and January and then come up
with recommendations for the DNR on how it should change its CWD management
program.

The meetings are open to the public and, theoretically, this would have been
an important meeting for members of the public who cared to attend and learn
from experts directly, with the opportunity to question them following their
presentations.

Craven said that he was influenced by CWD both personally and
professionally. He participated in a deer hunting camp located just six
miles from where the first three CWD-positive deer were shot in the 2001
deer hunting season. During the next three years that deer hunting camp
disappeared as hunters moved on. He and his son have since killed two deer
that turned out to be CWD positive.

"I obviously care for both personal and professional reasons, but this issue
is just not on people's radar screen like it was three years ago," he said.
"One of the most important challenges that you face, as liaisons to groups
of citizens and hunters, is to bring that back."

Craven said the discovery of CWD followed a long period of general
satisfaction of deer management and deer hunting opportunities. Until CWD
was discovered, deer hunting couldn't get any better. Hunter numbers were
high, the harvest was 500,000 every year and people knew about the trophy
potential of several Wisconsin counties.

"Then all of a sudden on that fateful February day in 2002, CWD was
discovered and the world of deer and deer hunting in the state changed very
dramatically," Craven said. "Even though deer are only one of about 500
vertebrate species in the state, they remain incredibly important."

Deer have great economic potential, plus social and recreational values.
Though they can cause environmental complications, such as deer/vehicle
collisions and crop damage, Craven said these problems were on their way to
being managed.

But, when the discovery of CWD was announced, there was confusion, concern
and anxiety.

"The response from the DNR was immediate and firm, and although that has
caused anxiety over time I don't think it could have been done any other
way," Craven said. "Surveys were conducted to find the scope of the problem,
teams set up to handle the science, public health aspects (if any)
communications and field management all over a weekend."

Some of the plans were not palatable to some landowners and hunters within
the area affected by CWD. Talk of deer eradication, anxiety over venison
safety, constantly changing hunting regulations, and the uncertainty over
many aspects of CWD caused much concern and resistance to DNR actions.

Five years after the discovery of CWD, Craven said that millions of dollars
and many human resources were expended, a Herculean effort to reduce deer
numbers, and scientists have learned much about CWD.

"But CWD is still present and it has been found over a much larger area in
southern Wisconsin and northern Illinois," he said. "Many deer remain on the
landscape. Progress is slow, but there has been progress."

Craven believes people underestimated the passionate response to the
devastating impact of CWD on Wisconsin's rich deer hunting traditions. In
some cases it has been divisive, pitting neighbor against neighbor.

Craven said that he believes that people do care, but that CWD must be
brought back on the radar screen for the average hunter and landowner.

"Deer are too important to stand idly by and watch CWD run its course
whatever course that may be," he said. "Most experts feel CWD can only get
worse. If they are correct, the finger pointing and accusations that will
occur in 10, 20 or 30 years will be far worse than the current unfortunate
situation."

"There really is no choice, we have to care, and we have to act on the best
information and advice we can muster from any conceivable source," he said.
"For people to care, there must be hope and for that, people must believe
that a solution is possible and I believe that to be the case."

Craven asked the committee to base their opinion on facts and not on rumors.
This meeting was a presentation of facts by the experts and the committee
needed to blend its opinion and perspectives with the facts to come up with
a set actions that people can get behind.

Still lots of unknowns: Jim Kazmierczak, epidemiologist with the Wisconsin
Division of Public Health, gave the CWD Advisory Committee a primer on prion
diseases, or Transmissible Spongiform Encephalopathies. They are caused by
abnormal prions and include: scrapie in sheep and goats; mink transmissible
encephalopathy; Bovine Spongiform Encephalopathy otherwise known as "mad cow
disease" in cattle, CWD in deer and elk and Creutzfeldt-Jakob Disease (CJD)
in humans.

He noted that CJD is not found more frequently in states where chronic
wasting disease occurs in wildlife.

"And, according to the World Health Organization there is no scientific
evidence that CWD causes human illness," Kazmierczak said. He went on to
talk about the species barrier, saying that the CWD prion is very
inefficient at converting the normal human prion into an abnormal form.

All of the research is reassuring that CWD can not jump the species barrier,
he said, but there still are some concerns, such as:

** Saliva and blood from CWD positive deer have been shown to be infectious
for other deer.

** Muscle tissue from CWD-infected deer has been found to contain infectious
prions.

** Passage of prions through intermediary hosts has been shown to infect
other species.

Chad Johnson, assistant scientist in the UW-Madison School of Veterinary
Medicine, talked about CWD risks to other species, reporting that a moose
was diagnosed with CWD in 2005 and picked up the disease in the natural
environment.

Whether CWD can be transmitted to domestic animals is under research.
Johnson said that, so far, there have been no clinical signs of CWD in
cattle that were inoculated with CWD. However, it can not be concluded that
it can't happen.

Researchers know that raccoon, opossum, dog, skunk, coyote, cat, fox and
mice all eat deer carcasses. Tests are being done to see if they are
susceptible to CWD.

Joel Pedersen, associate professor of Soil Science at UW-Madison, emphasized
that if abnormal prions get into the environment they will not go away
rapidly. He noted a study of scrapie in Iceland where a new flock of sheep
came down with scrapie 16 years after the diseased original flock was
eliminated.

Tim Eisele — 8/22/2007 10:46 am

http://www.madison.com/tct/sports/206627

----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Cc:
Sent: Wednesday, August 22, 2007 11:31 AM
Subject: re-Outdoors: CWD experts address first meeting of advisory
committee

re---Outdoors: CWD experts address first meeting of advisory committee
Tim Eisele - 8/22/2007 10:46 am

Why should we care?
http://www.madison.com/tct/sports/206627

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

----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Cc: ; ;
; ; ;
; ;
; ;
; ; ;
;
Sent: Thursday, August 16, 2007 8:30 PM
Subject: Pathobiology and diagnosis of animal transmissible spongiform
encephalopathies: current knowledge, research gaps, and opportunities

Hello CWD Stakeholder Advisory Group,

A kind greetings from Bacliff, Texas!

i have wasted some decade it seems on human and animal transmissible
spongiform encephalopathies of humans and animals.

before your upcoming meeting, i urge you to read some data on CWD, you may
not have been aware of.

I wish to send you the following data on CWD. Please use as you wish. i say
now, and i say again almost a decade later,
cwd is but a small part, of a much larger problem, one that is not going
away anytime soon. ...

........good luck!

kindest regards,
terry

----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Sent: Saturday, August 11, 2007 3:36 PM
Subject: [BSE-L] Pathobiology and diagnosis of animal transmissible
spongiform encephalopathies: current knowledge, research gaps, and
opportunities

Research Project: Transmission, Differentiation, and Pathobiology of
Transmissible Spongiform Encephalopathies
Location: Virus and Prion Diseases of Livestock

Title: Pathobiology and diagnosis of animal transmissible spongiform
encephalopathies: current knowledge, research gaps, and opportunities

Authors

Kehrli, Marcus
O`rourke, Katherine
Hamir, Amirali
Richt, Juergen
Nicholson, Eric
Silva, Christopher
Edelman, Daniel - FOOD AND DRUG ADMINISTRAT
Gay, Cyril

Submitted to: Government Publication/Report
Publication Type: Government Publication
Publication Acceptance Date: May 1, 2007
Publication Date: July 1, 2007

Citation: Kehrli, Jr., M.E., O'Rourke, K.I., Hamir, A.N., Richt, J.A.,
Nicholson, E.M., Silva, C.J., Edelman, D., Gay, C.G. 2007.

Pathobiology and diagnosis of animal transmissible spongiform
encephalopathies: current knowledge, research gaps, and opportunities
[government white paper]. Beltsville, MD: Interagency Working Group on Prion
Science, Subcommittee on Pathobiology and Diagnostics. USDA, Agriculture
Research Service. 33 p.

Technical Abstract:

Transmissible spongiform encephalopathies (TSEs) are fatal neurologic
diseases that can affect several animal species and human beings. There are
four animal TSE agents found in the United States: scrapie of sheep and
goats; chronic wasting disease (CWD) of deer, elk, and moose; transmissible
mink encephalopathy (TME) and bovine spongiform encephalopathy (BSE).
Although the animal TSEs do not cause major death losses among US livestock
populations, they are important because of international trade issues. The
experience of the United Kingdom and Europe in dealing with the vast
majority of the world's BSE cases, serves as a reminder of the need for
continuing vigilance in monitoring risks for public health and research to
answer remaining questions around the pathogenesis and transmission of these
diseases. There remain questions on 1) cross-species transmissibility of
TSEs in livestock and wildlife; 2) the pathobiology of TSEs in natural and
secondary hosts; pathogenesis and transmission of CWD; and 4) pathogenesis
and ante mortem detection of typical and atypical BSE. Our understanding of
the pathogenesis and transmission of these diseases continues to evolve as
ongoing, global TSE research efforts focus on defining tissue sites of
abnormal prion accumulation, routes of infection, methods of strain
differentiation, genetics of susceptibility and ante-mortem diagnostics. In
this paper, a Subcommittee on Pathobiology and Diagnostics of TSEs for an
Interagency Working Group on Prion Science summarizes the science of animal
TSEs in order to identify knowledge gaps for the purpose of prioritizing
animal prion research needs. Because of substantial losses involving
international trade and potential risk for interspecies transmission to
susceptible livestock and possibly humans, the presence of BSE, CWD, scrapie
and TME in the United States presents a liability to U.S. domestic and
alternative livestock industries. In addition, the proven risk of BSE to
agriculture and public health from subclinical or clinically sick animals
requires science-based surveillance for any silent, unrecognized epizootic
expansions of these diseases in populations of animals that could either
directly or indirectly affect food animals. CWD is an example of an
uncontrolled expanding epidemic that threatens not only cervids but possibly
other livestock. CWD also has elicited public health surveillance programs
to monitor for scientific evidence of a prion disease in humans that consume
venison. Therefore, some of the research needs are precautionary, but the
risks to animal and human health from being caught unaware are high. Efforts
are being made by both federal and state regulatory agencies to eradicate
scrapie and CWD, and to determine the prevalence of BSE. The effectiveness
of these programs will depend heavily on having accurate information about
the nature of these diseases, not only in the original hosts, but also in
other species that may be in contact with infected animals.

http://arsserv0.tamu.edu/research/publications/Publications.htm?seq_no_1...

Summary of Selected Disease Events January-March 2007

Scrapie: Nor98-like-Wyoming On March 16, 2007, the USDA Animal and Plant
Health Inspection Service (APHIS) notified stakeholders that an aged female
sheep had tested positive for scrapie, consistent with the Nor98 type. The
ewe was slaughtered in Michigan, where it was tested as part of USDA's
ongoing regulatory scrapie slaughter surveillance program. The ewe was
traced back to a flock in Wyoming. This is the first time this particular
type of scrapie has been found in the United States. The Nor98 type of
scrapie is uncommon even in Europe, with fewer than 300 similar cases
diagnosed since it was identified in 1998.

http://www.aphis.usda.gov/vs/ceah/cei/taf/iw_2007_files/Summary/quarterl...

ORAL-04
EPIDEMIOLOGY OF CHRONIC WASTING DISEASE IN NORTH AMERICAN CERVIDS
M. W. Miller
Colorado Division of Wildlife, Wildlife Research Center, Fort Collins,
Colorado, USA.
Chronic wasting disease (CWD) occurs naturally in North American deer
(Odocoileus spp.), wapiti,
and moose (collectively called "cervids"). CWD presently occurs in scattered
foci throughout North
America, both in the wild and in commercial facilities. CWD is contagious
among its natural hosts,
and epidemics can persist under both captive and free-ranging conditions,
resulting in remarkably
high infection rates. The precise mechanism of contagion remains unclear,
although accumulations of
disease-associated prion protein (PrPCWD) in lymphatic tissues associated
with the gastrointestinal
tract suggest shedding via feces and perhaps saliva. Analyses of epidemic
data suggest that indirect
(animal-environment-animal) transmission may be the dominant force in
epidemic dynamics, and the
CWD agent has been shown to persist in environments contaminated by excreta
or carcass remains
for years. Variation in cellular prion protein appears to influence CWD
pathogenesis, and may provide
a biological mechanism for emergence of variant strains within and among the
four naturally
susceptible species. The long-term implications of CWD for public,
livestock, and wildlife health
remain uncertain. Unfortunately, limitations of existing technology
available to combat prion diseases
make control of CWD ineffective or infeasible under most conditions.
23

ORAL-19
IINTERSPECIES PRION TRANSMISSION IS CONTROLLED BY CONFORMATIONAL
COMPATIBILITY BETWEEN PRPSC AND HETEROTYPIC PRPC
K.M. Green*1, S.R. Browning*1,6, T.S. Seward2, M. Green4, E.A. Hoover5, G.C.
Telling1,2,3,7
1Department of Microbiology, Immunology and Molecular Genetics, 2Sanders
Brown Center on
Aging,3Department of Neurology, 4UK Transgenic Facility University of
Kentucky, Lexington, Ky USA.
5Department of Microbiology, Immunology and Pathology, Colorado State
University, Fort Collins, Co, USA
6Present address: Department of Infectology, Scripps Research Institute,
Jupiter, Florida, USA
7To whom correspondence should be addressed:gtell2@uky.edu
* These authors contributed equally
The threats to humans and livestock from interspecies prion transmission are
difficult to assess
because the factors controlling this process remain uncertain. To address
this we have used
transgenic mouse models to understand the roles played by PrP primary
structure, prion strains and
the species specificity of protein X in controlling interspecies prion
infection in the context of cervid
transmission barriers. Cervid prions are of particular concern because
chronic wasting disease
(CWD) of North American and South Korean cervids is the only recognized
prion disease of wild
animals and its increasing geographic range, contagious nature, and
environmental persistence have
raised concerns about prion dissemination and the potential for further
interspecies transmission. We
show that conformational compatibility of PrPSc in a prion strain and PrP
primary structure in a new
host is the most important determinant of interspecies prion transmission
barriers. Although prion
strains can acquire totally new host range properties following heterologous
conversion of PrPP
C in a
new host, the strain-related biochemical properties of PrPSc may remain
relatively stable. We also
show that the cervid PrP polymorphism at residue 132, which is equivalent to
the human PrP 129
polymorphism, is a crucial determinant of cervid prion transmission and has
a profound controlling
effect on PrPSc-related prion strain properties. Our transgenic approaches
modeling trans-species
prion susceptibility in cervids also speak to the possible origins of CWD
since cervid transgenic mice
are also vulnerable, to varying degrees, to sheep scrapie prions, the degree
of susceptibility being
strain related. One particularly well-characterized sheep scrapie isolate,
SSBP/1, caused disease as
efficiently as CWD prions from diseased deer or elk. Finally, while
transmissions in transgenic mice
based on the protein X model of prion propagation produced chimeric prions,
passage of which
resulted in novel cervid prions with an extended host range compared to
CWD-cervid prions, the
unexpected susceptibilities of such mice to CWD and mouse prions are
inconsistent with the
previously hypothesized role of protein X in prion propagation.

GEN-13
PRION PROTEIN GENES AFFECT SUSCEPTIBILITY OF CERVIDS TO CHRONIC WASTING
DISEASE
C. Johnson1, J. Johnson1, J.P. Vanderloo1, D. Keane2, P. Bochsler2, J.M.
Aiken1, D. McKenzie1
1Department of Animal Health and Biomedical Sciences and 2Wisconsin
Veterinary Diagnostic Laboratory,
University of Wisconsin, Madison, WI, USA mckenzie@svm.vetmed.wisc.edu
The primary sequence of the prion protein affects susceptibility to
transmissible spongiform
encephalopathies (TSE; prion disease) in mice, sheep and humans. The Prnp
sequence of freeranging,
Wisconsin white-tailed deer was determined and the Prnp genotypes of
CWD-positive and -
negative deer compared. Six amino acid (AA) changes were identified; two of
which were located in
pseudogenes. Two alleles, a glutamine to lysine polymorphism at codon 226
and a single
octapeptide repeat insertion into the pseudogene, have not been previously
reported. The
predominant alleles, wild-type (glutamine at AA95, glycine at AA96 and
glutamine at AA226) and a
glycine to serine polymorphism at AA96 (G96S), comprise almost 98% of the
Prnp alleles in the
Wisconsin white-tailed deer population. Comparison of the allelic
frequencies in the CWD-positive
and -negative deer suggests that G96S and a glutamine to histidine
polymorphism at AA 95 (Q95H)
are linked to a reduced susceptibility to CWD. The G96S allele does not,
however, provide complete
resistance, as a CWD-positive G96S/G96S deer was identified. The G96S allele
is also linked to
slower progression of disease in CWD-positive deer based on the deposition
of PrPCWD in the obex
region of the medulla oblongata. To further determine the effect of
variations of the cervid Prnp alleles
on susceptibility, deer with known Prnp genotypes were orally dosed with CWD
inocula prepared from
wild-type/wild-type homozygous animals. The experimentally infected
wild-type/wild-type animals
have succumbed to disease, animals heterozygous for Prnp alleles have not.

PA-03
PRIONS IN SKELETEL MUSCLE OF CWD INFECTED DEER
R.C. Angers*1, S.R. Browning*1,6, T.S. Seward2, C.J. Sigurdson4, 7, M.W.
Miller5, E.A. Hoover4, G.C. Telling1,
2, 3, 8
1Department of Microbiology, Immunology and Molecular Genetics, University
of Kentucky, Lexington, KY 40536, 2Sanders
Brown Center on Aging, University of Kentucky, 3Department of Neurology,
University of Kentucky, 4Department of
Microbiology, Immunology and Pathology, Colorado State University, 5Colorado
Division of Wildlife, Wildlife Research Center,
Fort Collins, CO 80526; 6 Present address: Department of Infectology,
Scripps Research Institute, 5353 Parkside Drive, RF-2,
Jupiter, Florida, 33458; 7 Present address: Institute of Neuropathology,
University of Zurich, Schmelzbergstr 12, 8091 Zurich,
Switzerland; 8 To whom correspondence should be addressed: e-mail: gtell2@
uky.edu; * These authors contributed equally to
this work
The zoonotic potential of chronic wasting disease (CWD) has become a public
health concern since the
transmission of bovine spongiform encephalopathy (BSE) prions to humans
resulting in variant Creutzfeldt-
Jakob disease (vCJD). Studies in mice, sheep and humans indicated that PrPSc
could be detected in the skeletal
muscles. Since the most probable route of human exposure to CWD is through
consumption or handling of
meat from infected animals, it is important to assess whether skeletal
muscle from affected cervids harbors
prions. CWD-susceptible Tg(CerPrP) mice were intracranially inoculated with
brain and matched skeletal
muscle homogenates from moribund as well as non-infected control deer. Tg
mice inoculated with either brain
or muscle homogenates from CWD-infected deer developed clinical illness with
characteristic prion disease
symptoms and the brains of recipients accumulated cervid PrPSc. The mean
incubation times for animals
inoculated with brain material ranged between 231 and 283 days, whereas mice
receiving muscle tissue had
average incubation periods between 360 and 492 days. Tg mice inoculated with
material from CWD-negative
deer did not develop prion disease or accumulate PrPSc. Brain and muscle
samples used to inoculate Tg(CerPrP)
mice were analyzed for the presence of PrPSc. Brain samples producing the
shortest incubation times had levels
of PrPP
Sc detectable by Western blotting in 25 µg total protein, whereas PrPSc
P was detectable only after sodium
phosphotungstate (NaPTA) precipitation of 0.5 mg for isolates with the
longest incubation periods. No
protease-resistant material was detected in muscle when 50 mg total protein
was precipitated with NaPTA and
analyzed by Western blot. Although a possible role of prion strain
variability cannot currently be dismissed,
these results suggest variable prion titers in the CNS and skeletal muscle
from different CWD-infected deer in
the same phase of disease.

***PLEASE SEE FULL TEXT 234 PAGES *** ;

http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf

sporadic cjd

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0705&L=sanet-mg&P=25276

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0705&L=sanet-mg&T=0&P=25276

Colorado Surveillance Program for Chronic Wasting Disease
Transmission to Humans (TWO SUSPECT CASES, see GSS)

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0704&L=sanet-mg&T=0&P=1165

1
© SEAC 2007
NINETY SEVENTH MEETING OF THE SPONGIFORM
ENCEPHALOPATHY ADVISORY COMMITTEE

The Spongiform Encephalopathy Advisory Committee held its 97th
meeting in London on 10th May 2007, and discussed the following:
CURRENT ISSUES

SEAC was informed about the following issues, both of which were
discussed later in the agenda:

. United Kingdom Chief Dental Officers recently issued
guidance to dentists to limit certain dental instruments to
single use as a precautionary measure to reduce the potential
risk of variant Creutzfeldt-Jakob Disease (CJD) transmission1.
. The first unusual case of Bovine Spongiform Encephalopathy
(BSE) in the UK.
ATYPICAL SCRAPIE CASE AUDIT
SEAC was updated on investigations of an atypical scrapie case in
a sheep flock previously considered free of transmissible
spongiform encephalopathies (TSEs). An independent audit of the
processes used to manage the flock found no evidence of errors in
the collection of the samples for testing, or any major breaches in
biosecurity in the importation and subsequent management of the
flock. SEAC concluded that there was insufficient evidence to
determine the origin of the case and that it was unlikely the origin
would ever be unambiguously determined. There was no
evidence for importation of the disease from New Zealand,
although this could not be definitively excluded. It was noted that
an investigation, by the Veterinary Laboratories Agency, of the
1

http://www.gnn.gov.uk/environment/fullDetail.asp?ReleaseID=279256&NewsAr...

2
© SEAC 2007
flock had not identified other confirmed atypical scrapie cases,
although further analyses are continuing.

ATYPICAL SCRAPIE RESEARCH CONTINGENCY PLANNING

To inform contingency planning, the Food Standards Agency
(FSA) asked SEAC to consider possible scenarios, which might
arise from research underway on atypical scrapie, and how these
might change the understanding of the risk to human health.
SEAC stated it was difficult to assess changes to understanding of
the risk in the absence of hard scientific data, and that no one data
set on its own was likely to be definitive. Studies comparing the
properties of atypical scrapie and other TSE agents using the
same animal model, especially humanised mice or non-human
primates, would be most informative in the short term.
Surveillance data to assess any association between CJDs and
atypical scrapie prevalence would be most persuasive but are
unlikely to become available in the short term. In assessing the
risk it would be important to consider all the information available,
rather than data from single studies considered in isolation.

FATEPRIDE

SEAC was updated about FATEPriDE, a recently completed multicentre
European Union funded project, examining the possible
influence of environmental trace elements on the occurrence of
TSEs. The committee noted that interactions between trace
elements and other environmental factors and the occurrence of
TSEs are likely to be complex. No link between the vast majority
of environmental factors studied, including organophosphates, and
TSEs was found. The only environmental factor found to influence
TSEs was manganese, at a molecular and cellular level. It is
possible, but hard to prove in the field, that environmental
manganese may influence susceptibility to, or spread of, some
TSEs, possibly by increasing retention in the soil.
UPDATE ON PREVALENCE STUDIES
SEAC was updated about progress on approaches to obtain better
estimates of the prevalence of subclinical vCJD:
3
© SEAC 2007
. The National Anonymous Tonsil Archive was on track to
report to the SEAC Epidemiology Subgroup in June 2007 the
analysis of tonsils collected to date from the age group likely
to be at most risk of BSE infection.
. A report from an expert group considering the feasibility of
collecting tissues from autopsies for testing would be
published in the near future. The recommendations of the
report would then be considered by the Department of Health
(DH).
. Tenders received from manufacturers of prototype blood tests
for the analysis of a large number of anonymous blood
samples would be considered in late May 2007 by an expert
group convened by the HPA.

FUTURE ASSESSMENT OF LIKELY vCJD INFECTIVITY
ASSOCIATED WITH PLASMA PRODUCTS

SEAC agreed to a DH request to reassess, at SEAC 98, the likely
removal of infectivity from blood contaminated with the vCJD agent
during plasma product production. In addition, to estimate the
timing of the time window for possible infections arising from use of
plasma products prior to the sourcing plasma from countries
considered free from BSE.

UNUSUAL CASES OF SPONGIFORM ENCEPHALOPATHY IN
CATTLE

SEAC received presentations from international experts on
unusual cases of BSE. This item was discussed in the reserved
business session as unpublished research was considered, which
is consistent with the SEAC Code of Practice.
SEAC noted such cases are very rare. They had been identified
predominantly by active surveillance and predominantly in older
animals in a number of European countries and elsewhere. It now
appears that the cases can be categorised into two types, H-type
or L-type, on the basis of their biochemical characteristics which
differ from those of classical BSE. The neuropathological and
transmission properties of unusual BSE types also differed from
classical BSE. It is not yet clear whether or not conversion to
classical BSE may occur on secondary transmissions. The origin
4
© SEAC 2007
of unusual BSE is not clear and it might possibly be spontaneous.
SEAC agreed that, given current knowledge, procedures appeared
to be in place to prevent an epidemic of unusual BSE. Further
data, particularly on tissue distribution and transmissibility via the
oral route, is needed. SEAC agreed to publish a position
statement.

UPDATE ON DENTAL RESEARCH

SEAC was updated on preliminary findings from research to
estimate the potential risk of vCJD transmission via dental
procedures. This item was discussed in the reserved business
session as unpublished research was considered, which is
consistent with the SEAC Code of Practice.
SEAC agreed that the data and conclusions appeared robust,
while recognising they are preliminary data from an animal model
and that the studies are not yet complete. The research
suggested that there may be a significant risk that vCJD can be
transmitted via some dental procedures in man, although the level
of risk remains difficult to quantify. The committee welcomed the
Chief Dental Officers' recent guidance to dentists who were
advised to ensure that all dental files and reamers were treated as
single use, but sought reassurance that compliance in both private
and NHS practice would be closely monitored. SEAC considered
it important that a comprehensive assessment of the potential risks
of vCJD transmission from all dental procedures be conducted as
a priority. This could allow possible additional precautionary
measures to be identified. SEAC agreed to publish a position
statement in the near future.

http://www.seac.gov.uk/summaries/seac97_summary.pdf

SUMMARY

http://www.seac.gov.uk/minutes/97.pdf

MAY SCRAPIE REPORT 2007 (atypical NOR-98 like disease documented Wyoming,
USA)

http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/download...

Atypical scrapie in a swiss goat and implications for transmissible
spongiform encephalopathy surveillance
Torsten Seuberlich1, Catherine Botteron, Sylvie L. Benestad, Hervé
Brünisholz, Reto Wyss, Ulrich Kihm, Heinzpeter Schwermer, Martina Friess,
Alexandra Nicolier, Dagmar Heim and Andreas Zurbriggen
Correspondence: 1 Corresponding Author: Torsten Seuberlich, NeuroCenter,
Department of Clinical Veterinary Medicine, Vetsuisse Faculty,
Bremgartenstrasse 109a, CH-3001 Berne, Switzerland, e-mail:
torsten.seuberlich@itn.unibe.ch

Different types of transmissible spongiform encephalopathies (TSEs) affect
sheep and goats. In addition to the classical form of scrapie, both species
are susceptible to experimental infections with the bovine spongiform
encephalopathy (BSE) agent, and in recent years atypical scrapie cases have
been reported in sheep from different European countries. Atypical scrapie
in sheep is characterized by distinct histopathologic lesions and molecular
characteristics of the abnormal scrapie prion protein (PrPsc).
Characteristics of atypical scrapie have not yet been described in detail in
goats. A goat presenting features of atypical scrapie was identified in
Switzerland. Although there was no difference between the molecular
characteristics of PrPsc in this animal and those of atypical scrapie in
sheep, differences in the distribution of histopathologic lesions and PrPsc
deposition were observed. In particular the cerebellar cortex, a major site
of PrPsc deposition in atypical scrapie in sheep, was found to be virtually
unaffected in this goat. In contrast, severe lesions and PrPsc deposition
were detected in more rostral brain structures, such as thalamus and
midbrain. Two TSE screening tests and PrPsc immunohistochemistry were either
negative or barely positive when applied to cerebellum and obex tissues, the
target samples for TSE surveillance in sheep and goats. These findings
suggest that such cases may have been missed in the past and could be
overlooked in the future if sampling and testing procedures are not adapted.
The epidemiological and veterinary public health implications of these
atypical cases, however, are not yet known.

http://www.jvdi.org/cgi/content/abstract/19/1/2

1: Vet J. 2007 Jun 14; [Epub ahead of print]Lack of PrP(sc) immunostaining
in intracranial ectopic lymphoid follicles in a sheep with concomitant
non-suppurative encephalitis and Nor98-like atypical scrapie: A case
report.Vidal E, Tortosa R, Costa C, Benavides J, Francino O, Sánchez-Robert
E, Pérez V, Pumarola M.
Priocat Laboratory, CReSA, Autonomous University of Barcelona, 08193
Bellaterra (Cerdanyola del Vallès), Spain.

During active surveillance for transmissible spongiform encephalopathies
(TSEs) in sheep, an initial reactor was detected using a rapid test on a
brain sample. Immunohistochemistry confirmed an atypical TSE presentation
that closely resembled the previously described Nor98 cases. Sequencing of
the prnp gene confirmed the ARQ/AHQ genotype with the L141F mutation at
codon 141 associated with this phenotype. The head, including the brain and
cranial lymphoid tissues, was sampled and examined thoroughly. Non-purulent
encephalitis, with ectopic lymphoid follicle formation within the brain, was
diagnosed concomitant to the TSE. When scrapie-associated prion protein
(PrP(sc)) deposition was studied by immunohistochemistry there was a
noticeable lack of lymphotropism. The distribution of PrP(sc) in the brain
differed considerably from that of classical scrapie cases. Astrogliosis and
microgliosis were demonstrated by histochemical procedures.

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&Te...

Published online before print October 20, 2005

Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0502296102
Medical Sciences

A newly identified type of scrapie agent can naturally infect sheep with
resistant PrP genotypes

( sheep prion | transgenic mice )

Annick Le Dur *, Vincent Béringue *, Olivier Andréoletti , Fabienne Reine *,
Thanh Lan Laï *, Thierry Baron , Bjørn Bratberg ¶, Jean-Luc Vilotte ||,
Pierre Sarradin **, Sylvie L. Benestad ¶, and Hubert Laude *
*Virologie Immunologie Moléculaires and ||Génétique Biochimique et
Cytogénétique, Institut National de la Recherche Agronomique, 78350
Jouy-en-Josas, France; Unité Mixte de Recherche, Institut National de la
Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions
Hôte Agent Pathogène, 31066 Toulouse, France; Agence Française de Sécurité
Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels,
69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut
National de la Recherche Agronomique, 37380 Nouzilly, France; and
¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway

Edited by Stanley B. Prusiner, University of California, San Francisco, CA,
and approved September 12, 2005 (received for review March 21, 2005)

Scrapie in small ruminants belongs to transmissible spongiform
encephalopathies (TSEs), or prion diseases, a family of fatal
neurodegenerative disorders that affect humans and animals and can transmit
within and between species by ingestion or inoculation. Conversion of the
host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a
misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission
and pathogenesis. The intensified surveillance of scrapie in the European
Union, together with the improvement of PrPSc detection techniques, has led
to the discovery of a growing number of so-called atypical scrapie cases.
These include clinical Nor98 cases first identified in Norwegian sheep on
the basis of unusual pathological and PrPSc molecular features and "cases"
that produced discordant responses in the rapid tests currently applied to
the large-scale random screening of slaughtered or fallen animals.
Worryingly, a substantial proportion of such cases involved sheep with PrP
genotypes known until now to confer natural resistance to conventional
scrapie. Here we report that both Nor98 and discordant cases, including
three sheep homozygous for the resistant PrPARR allele (A136R154R171),
efficiently transmitted the disease to transgenic mice expressing ovine PrP,
and that they shared unique biological and biochemical features upon
propagation in mice. These observations support the view that a truly
infectious TSE agent, unrecognized until recently, infects sheep and goat
flocks and may have important implications in terms of scrapie control and
public health.

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

Author contributions: H.L. designed research; A.L.D., V.B., O.A., F.R.,
T.L.L., J.-L.V., and H.L. performed research; T.B., B.B., P.S., and S.L.B.
contributed new reagents/analytic tools; V.B., O.A., and H.L. analyzed data;
and H.L. wrote the paper.

A.L.D. and V.B. contributed equally to this work.

To whom correspondence should be addressed.

Hubert Laude, E-mail: laude@jouy.inra.fr

http://www.pnas.org/cgi/doi/10.1073/pnas.0502296102

http://www.pnas.org/cgi/content/abstract/0502296102v1

An evaluation of scrapie surveillance in the United States
From: Terry S. Singeltary Sr.
Date: Sun, 5 Aug 2007 13:05

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=3427

SEAC New forms of Bovine Spongiform Encephalopathy 1 August 2007
From: Terry S. Singeltary Sr.
Date: Sun, 5 Aug 2007 13:09:38 -0500

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=3573

FSE: FIRST CONFIRMED CASE REPORTED IN PORTUGAL AND POTENTIAL MAD CAT ESCAPES
LAB IN USA (204 lines)
From: Terry S. Singeltary Sr.
Date: Thu, 9 Aug 2007 16:58:42 -0500

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=7062

Owens, Julie
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)
Page 1 of 98
8/3/2006

Greetings FSIS,

I would kindly like to comment on the following ;

[Federal Register: July 12, 2006 (Volume 71, Number 133)]
[Notices]
[Page 39282-39283]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr12jy06-35]
-----------------------------------------------------------------------
DEPARTMENT OF AGRICULTURE
Food Safety and Inspection Service
[Docket No. FSIS-2006-0011]
Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
Update; Notice of Availability and Technical Meeting

snip...

http://a257.g.akamaitech.net/7/257/2422/01jan20061800/edocket.access.gpo...

MY comments/questions are as follows ;

1. SINCE the first Harvard BSE Risk Assessment was so flawed and fraught
with error after the PEER REVIEW
assessment assessed this fact, how do you plan on stopping this from
happening again, will there be another peer
review with top TSE Scientist, an impartial jury so-to-speak, to assess this
new and updated Harvard BSE/TSE risk
assessment and will this assessment include the Atypical TSE and SRM issues
?

*** Suppressed peer review of Harvard study October 31, 2002 ***

http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf

2. WITH A RECENT NATION WIDE MAD COW FEED BAN RECALL in the past few months
that consisted of
some 10,878.06 TONS, then another Mad Cow feed ban warning letter in May, IT
should seem prudent to ask why our
feed bans continue to fail in 2006, and continue to fail today ?

snip...

full text 98 pages ;

http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf

[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

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....

full text 17 pages ;

https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000...

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

Docket

No. 04-047-l

No. 04-021ANPR

No. 2004N-0264

NEW BSE SAFEGUARDS

Federal Measures to Mitigate BSE Risks: Considerations for Further Action

http://www.fda.gov/cvm/index/updates/bseanprm.htm

Greetings FDA, USDA and APHIS et al,

I would kindly like to comment on the continued delay of the regulations
that have been proposed for years to reduce the risk of BSE/TSE in the
USA. Each day that is wasted debating this issue allows this agent to
spread,
and many many more humans and animals become needlessly exposed to
this agent via a multitude of potential routes and sources right here in the
USA. TO continue to ignore the new findings from several scientists
about the fact that BSE is not the only strain of TSE in cattle, the fact
that
new atypical strains of TSE are showing up in not only cattle, but
sheep and the fact that the new strain of TSE in cattle seems to be
more similar to sporadic CJD as opposed to the nv/v CJD, to continue
to ignore these findings will only further spread this agent. ..............

full text ;

https://web01.aphis.usda.gov/regpublic.nsf/168556f5aa7a82ba85256ed00044e...

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

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

Docket Management Docket: 02N-0276 - Bioterrorism Preparedness ...
General Comments, Subject: Docket No: 02-088-1 RE-Agricultural ...
From: Terry S. Singeltary Sr.

To: regulations@aphis.usda.gov

Docket No: 02-088-1 Title: ...

Greetings FDA and public,

if you go to the below site, and search all BSE known countries and check
out their air traffic illegal meat they have confiscated, and check out the
low number checked, compared to actual passenger traffic, would not take too
much for some nut to bring in FMD/TSEs into the USA as a 'suitcase bomb'.

[[Under APHIS-PPQ's agricultural quarantine inspection monitoring, 284 air
passengers from Israel were sampled for items of agricultural interest in
fiscal year 2001. Seven of these passengers, or 2 percent, carried a total
of 11 kg of meat items that could potentially harbor the pathogen that
causes BSE. None of these passengers from whom meat items were confiscated
reported plans to visit or work on a ranch or farm during their visit to the
U.S.]]

if they were to have questioned the terrorist that bombed the Twin Towers
with jets, if they were to have questioned them at flight school in the USA,
i am sure that they would have said they did not intend to visit the Twin
Towers as a flying bomb either. what am i thinking, they probably did ask
this? stupid me. ...

full text ;

http://www.fda.gov/ohrms/DOCKETS/dockets/02n0276/02N-0276-EC-254.htm

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 ...

Greetings again Dr. Freas and Committee Members,

I wish to submit the following information to the
Scientific Advisors and Consultants Staff
2001 Advisory Committee (short version).

I understand the reason of having to shorten my submission,
but only hope that you add it to a copy of the long version,
for members to take and read at their pleasure,
(if cost is problem, bill me, address below).
So when they realize some time in the near future
of the 'real' risks i speak of from human/animal TSEs and
blood/surgical products. I cannot explain the 'real' risk
of this in 5 or 10 minutes at some meeting,
or on 2 or 3 pages, but will attempt here:

remember AIDS/HIV, 'no problem to heterosexuals in the U.S.?
no need to go into that, you know of this blunder.

DO NOT make these same stupid mistakes again with
human/animal TSE's aka MADCOW DISEASE. I lost my Mom to hvCJD,
and my neighbor lost his Mother to sCJD as well (both cases
confirmed). I have seen many deaths, from many diseases.
I have never seen anything as CJD, I still see my Mom laying helpless,
jerking tremendously, and screaming "God, what's wrong
with me, why can't I stop this". I still see this, and will
never forget. Approximately 10 weeks from 1st of symptoms to death.
This is what drives me. I have learned more in 3 years about not only
human/animal TSE's but the cattle/rendering/feeding industry/government
than i ever wished to.

I think you are all aware of CJD vs vCJD, but i don't think
you all know the facts of human/animal TSE's as a whole,
they are all very very similar, and are all tied to the
same thing, GREED and MAN.

I am beginning to think that the endless attempt to track
down and ban, potential victims from known BSE Countries
from giving blood will be futile. You would have to ban
everyone on the Globe eventually? AS well, I think we
MUST ACT SWIFTLY to find blood test for TSE's,
whether it be blood test, urine test, eyelid test,
anything at whatever cost, we need a test FAST.

DO NOT let the incubation time period of these TSEs fool you.............

full text 6 pages ;

http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf

SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...

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

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.

http://jama.ama-assn.org/http://www.neurology.org/cgi/eletters/60/2/176#535

BRITISH MEDICAL JOURNAL

BMJ

http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406

BMJ

http://www.bmj.com/cgi/eletters/320/7226/8/b#6117

JOURNAL OF NEUROLOGY

MARCH 26, 2003

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

THE PATHOLOGICAL PROTEIN
Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9

June 2003

BY Philip Yam

CHAPTER 14 LAYING ODDS

Answering critics like Terry Singeltary, who feels that the U.S. under-
counts CJD, Schonberger conceded that the current surveillance system
has errors but stated that most of the errors will be confined to the older
population.

http://www.thepathologicalprotein.com/

doi:10.1016/S1473-3099(03)00715-1
Copyright © 2003 Published by Elsevier Ltd.
Newsdesk

Tracking spongiform encephalopathies in North America

Xavier Bosch

Available online 29 July 2003.

Volume 3, Issue 8, August 2003, Page 463

"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."

............................

http://www.thelancet.com/journals/laninf/article/PIIS1473309903007151/fu...

http://download.thelancet.com/pdfs/journals/1473-3099/PIIS14733099030071...

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&lis...

look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused
7% (1 of 14) of the cows to come down with BSE;

Risk of oral infection with bovine spongiform encephalopathy agent in
primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,
Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie
Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe
Deslys
Summary The uncertain extent of human exposure to bovine spongiform
encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease
(vCJD)--is compounded by incomplete knowledge about the efficiency of oral
infection and the magnitude of any bovine-to-human biological barrier to
transmission. We therefore investigated oral transmission of BSE to
non-human primates. We gave two macaques a 5 g oral dose of brain homogenate
from a BSE-infected cow. One macaque developed vCJD-like neurological
disease 60 months after exposure, whereas the other remained free of disease
at 76 months. On the basis of these findings and data from other studies, we
made a preliminary estimate of the food exposure risk for man, which
provides additional assurance that existing public health measures can
prevent transmission of BSE to man.

snip...

BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%)
1/15 (7%)

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum
used in our study with primates against a bovine brain inoculum with a
similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals
positive/number of animals surviving at the time of clinical onset of
disease in the first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. ic
ip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected
orally with similar BSE brain inocula

Published online January 27, 2005

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

It is clear that the designing scientists must also have shared Mr Bradley's
surprise at the results because all the dose levels right down to 1 gram
triggered infection.

http://www.bseinquiry.gov.uk/files/ws/s145d.pdf

2

6. It also appears to me that Mr Bradley's answer (that it would take less
than say 100

grams) was probably given with the benefit of hindsight; particularly if one

considers that later in the same answer Mr Bradley expresses his surprise
that it

could take as little of 1 gram of brain to cause BSE by the oral route
within the

same species. This information did not become available until the "attack
rate"

experiment had been completed in 1995/96. This was a titration experiment

designed to ascertain the infective dose. A range of dosages was used to
ensure

that the actual result was within both a lower and an upper limit within the
study

and the designing scientists would not have expected all the dose levels to
trigger

infection. The dose ranges chosen by the most informed scientists at that
time

ranged from 1 gram to three times one hundred grams. It is clear that the
designing

scientists must have also shared Mr Bradley's surprise at the results
because all the

dose levels right down to 1 gram triggered infection.

http://www.bseinquiry.gov.uk/files/ws/s147f.pdf

2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)

http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml

SHORT COMMUNICATION

Oral Transmission of Chronic Wasting Disease in Captive Shira's Moose

Terry J. Kreeger1,3, D. L. Montgomery2, Jean E. Jewell2, Will Schultz1 and
Elizabeth S. Williams2

1 Wyoming Game and Fish Department, 2362 Highway 34, Wheatland, Wyoming
82201, USA;
2 Department of Veterinary Sciences, University of Wyoming, Laramie, Wyoming
82071, USA
3 Corresponding author (email: tkreeger@wildblue.net )

ABSTRACT: Three captive Shira's moose (Alces alces shirasi) were orally
inoculated with a single dose (5 g) of whole-brain homogenate prepared from
chronic wasting disease (CWD)-affected mule deer (Odocoileus hemionus). All
moose died of causes thought to be other than CWD. Histologic examination of
one female moose dying 465 days postinoculation revealed spongiform change
in the neuropil, typical of transmissible spongiform encephalopathy.
Immunohistochemistry staining for the proteinase-resistant isoform of the
prion protein was observed in multiple lymphoid and nervous tissues. Western
blot and enzyme-linked immunosorbent assays provided additional confirmation
of CWD. These results represent the first report of experimental CWD in
moose.
Key words: Alces alces shirasi, chronic wasting disease, enzyme-linked
immunosorbent assay, immunohistochemistry, moose, oral inoculation, prion,
PrPCWD.

http://www.jwildlifedis.org/cgi/content/abstract/42/3/640

http://www.usaha.org/committees/reports/2005/report-wd-2005.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

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 th

Offline
Joined: 01/01/2006
Posts: 230
CWD experts address first meeting of advisory committee

PART 2

REFERENCES

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

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....
===================================================

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...tss

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

SNIP...FULL TEXT ;

http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm

TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST
PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated,
net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated,
Recall # V-103-6;

*********************************

e) "Big Jim's" BBB Deer Ration, Big Buck Blend,
Recall # V-104-6;

*********************************

f) CO-OP 40% Hog Supplement Medicated Pelleted,
Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020,
Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete
Feed for Chickens from Hatch to 20 Weeks, Medicated,
Bacitracin Methylene Disalicylate, 25 and 50 Lbs,
Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying
Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED,
net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs,
Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs,
Recall # V-112-6
CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER
Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and
visit on June 9, 2006. FDA initiated recall is complete.
REASON
Animal and fish feeds which were possibly contaminated with ruminant based
protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
125 tons
DISTRIBUTION
AL and FL

END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html

snip...end...tss

NOW, please note what the FDA claims was a safe level ;

FDA has determined that each animal could have consumed, at most and in
total, five-and-one-half grams - approximately a quarter ounce -- of
prohibited material. These animals weigh approximately 600 pounds.

http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html

thats enough to expose and kill 100 cows.....tss

see history of cjd questionnaire

http://brain.hastypastry.net/forums/showthread.php?t=2408

Posted July 20, 2007

Hassett resigns DNR post; Doyle picks Frank for job
By Todd Richmond
Associated Press writer
MADISON - After years of battling chronic wasting disease, navigating
partisan politics and trying to win back outdoorsmen's trust, Wisconsin
Department of
Natural Resources Secretary Scott Hassett has resigned.
http://www.rhinelanderdailynews.com/articles/2007/07/21/news/news02.txt

==========

cant blame the head of wisconsin DNR. look what happened to the funding for
CWD. perhaps this person saw the writing on the wall. ...tss

wdin@usgs.gov

Greetings,

IN reply to ;

Cuts would reduce CWD budget by 60 percent

Published Monday, July 23, 2007 11:59:09 AM Central Time
By Lee Fahrney Times Outdoors Writer

http://www.themonroetimes.com/m0723cwd.htm

THIS disturbs me greatly, and should disturb every hunter in Wisconsin, and
neighboring states. With CWD spreading like it is, we should not be
cutting any funding for CWD by 60 %. It makes no sense, with CWD amplifying
and spreading still.

193 CONFIRMED POSITIVE CWD samples from 19,953 samples collected last time
in Wisconsin, and they want to reduce funding by 60% for CWD management
activities ???

this is not logical ???

do they now think that CWD is under control in Wisconsin ???

do they think that CWD is now NOT a potential threat to animal and or human
health, and or the environment ???

what is the logistics behind this decision ???

2006-2007 Harvest and CWD Testing
CWD Public Dialogue to Begin

Preliminary numbers show that during the
2006-07 deer seasons, 56,593 deer were
harvested from the CWD zones. This is a
decline of more than 15 percent from the 2005-
06 season. Antlerless harvest accounts for
this drop, having decreased 31 percent from
last year. Buck harvest, however, increased
by five percent.
Of the 19,953 samples collected last
season, 193 tested CWD-positive. Thirty-five
of these deer were harvested in the herd
reduction zone. The rest were harvested in
the disease eradication zones.
This brings the total number of free ranging
CWD-positive deer to 844 for all years. Fiftyfour
of these deer were harvested in the herd
reduction zone.
As part of the effort to confirm that CWD
has not spread out of the CWD zones of southern
Wisconsin, 9,308 samples were also
collected in west-central Wisconsin and areas
of south-central and south-east Wisconsin not
in a CWD zone. None of these samples tested
positive for the disease.

http://dnr.wi.gov/org/land/wildlife/whealth/issues/cwd/doc/07_05_news.pdf

CWD Update 87

July 6, 2007

State and Provincial Updates

Illinois:

Paul Shelton, Illinois Department of Natural Resources provides the
following: Illinois

Department of Natural Resources staff collected 6,733 usable CWD
surveillance samples during the period beginning July 1, 2006.
A few additional samples from suspect deer remain untested at this time.
Testing yielded 41 CWD-positive deer and 6,692 'not detected'.
Forty-one positives were detected in four counties in northern Illinois:
Winnebago (18), Boone (13), DeKalb (6), and McHenry (4). No
new counties were identified as having CWD, and no disease was detected in
Ogle County, in which CWD was first identified during the
2005-2006 sampling season. However, CWD was identified in southeastern
DeKalb County, more than 20 miles southeast of
previously-identified locations. Samples were collected from a variety of
sources, including deer check stations in high-risk counties (3,097),
sample drop-off locations for archery hunters (175), cooperating meat
processors (1,778), suspect deer (25), roadkills in CWD counties
(16), and culling efforts (1,642). Cooperating meat lockers were added as a
sampling source this year to provide a statewide sampling base
outside the identified CWD area. Hunter-harvested deer accounted for 17
(41%) of the positives identified, with the remainder coming from
suspect deer (4; 10%); roadkills (1; 2%); and sharpshooting (19; 46%).
Illinois DNR CWD information is available at:

http://dnr.state.il.us/cwd.

http://wildlifedisease.nbii.gov/documents/CWD%20Updates/Update%2087.pdf

Title: Susceptibility of cattle to first-passage intracerebral inoculation
with chronic wasting disease agent from white-tailed deer

http://www.ars.usda.gov/research/publications/Publications.htm?seq_no_11...

Title: Transmission of chronic wasting disease of mule deer to Suffolk sheep
following intracerebral inoculation

Submitted to: Journal of Veterinary Diagnostic Investigation
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 20, 2006
Publication Date: November 1, 2006
Citation: Hamir, A.N., Kunkle, R.A., Cutlip, R.C., Miller, J.M., Williams,
E.S., Richt, J.A. 2006. Transmission of chronic wasting disease of mule deer
to Suffolk sheep following intracerebral inoculation. Journal of Veterinary
Diagnostic Investigation. 18(6):558-565.

Interpretive Summary: Chronic wasting disease (CWD) has been identified in
captive and free ranging deer and elk since 1967. To determine the
transmissibility of CWD to sheep and to provide information about the
disease and tests for detection of CWD in sheep, 8 lambs were inoculated
with brain suspension from mule deer naturally affected with CWD. Two other
lambs were kept as controls. Only 1 sheep developed clinical disease at 35
months after inoculation. The study was terminated at 72 months after the
inoculation. At that time one other sheep was found to be positive for the
disease. It is proposed that the host's genetic makeup may play a role in
transmission of the disease to domestic sheep. Impact. This is the first
study which shows that it is possible to transmit CWD to a small number of
sheep.
Technical Abstract

snip...end

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_11...

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&h...

Chronic Wasting Disease and Potential Transmission to Humans
Ermias D. Belay,* 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

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

Chronic wasting disease (CWD) of deer and elk is endemic in a tri-corner
area of Colorado, Wyoming, and Nebraska, and new foci of CWD have been
detected in other parts of the United States. Although detection in some
areas may be related to increased surveillance, introduction of CWD due to
translocation or natural migration of animals may account for some new foci
of infection. Increasing spread of CWD has raised concerns about the
potential for increasing human exposure to the CWD agent. The foodborne
transmission of bovine spongiform encephalopathy to humans indicates that
the species barrier may not completely protect humans from animal prion
diseases. Conversion of human prion protein by CWD-associated prions has
been demonstrated in an in vitro cell-free experiment, but limited
investigations have not identified strong evidence for CWD transmission to
humans. More epidemiologic and laboratory studies are needed to monitor the
possibility of such transmissions.

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

May 2007

NIAID Research on Prion Diseases
OVERVIEW

snip...

More research is necessary to determine whether CWD poses any risk to
humans, particularly because it is spreading over a wider geographical area
in the United States. There have been several reported cases of CJD in
individuals who have consumed venison, most much younger than the typical
age associated with CJD. In each of these instances, careful investigations
by CDC have shown no causal link between CJD and CWD in deer and elk
populations. Continued surveillance is important, however, to assess any
possible risk of CWD transmission to humans.

http://www.niaid.nih.gov/factsheets/priondis.htm

> In each of these instances, careful investigations by CDC have shown no
_causal_ link between CJD and CWD in deer and elk populations.

WRONG !

BELAY ET AL STATES ;

''Our conclusion stating that we found no _strong_ evidence of CWD
transmission to humans''

THERE'S a big difference between ''casual'' and ''strong''. ...TSS

Colorado Surveillance Program for Chronic Wasting Disease
Transmission to Humans (TWO SUSPECT CASES)

From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST

From: "Belay, Ermias"
To:
Cc: "Race, Richard (NIH)" ; ; "Belay,
Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was
attached to your email), we did not say CWD in humans will present like
variant CJD.

That assumption would be wrong. I encourage you to read the whole
article and call me if you have questions or need more clarification
(phone: 404-639-3091). Also, we do not claim that "no-one has ever been
infected with prion disease from eating venison." Our conclusion stating
that we found no strong evidence of CWD transmission to humans in the
article you quoted or in any other forum is limited to the patients we
investigated.

Ermias Belay, M.D.
Centers for Disease Control and Prevention

full text ;

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0704&L=sanet-mg&T=0&P=1165

SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...

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

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.

http://jama.ama-assn.org/http://www.neurology.org/cgi/eletters/60/2/176#535

BRITISH MEDICAL JOURNAL

BMJ

http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406

BMJ

http://www.bmj.com/cgi/eletters/320/7226/8/b#6117

JOURNAL OF NEUROLOGY

MARCH 26, 2003

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

doi:10.1016/S1473-3099(03)00715-1
Copyright © 2003 Published by Elsevier Ltd.
Newsdesk

Tracking spongiform encephalopathies in North America

Xavier Bosch

Available online 29 July 2003.

Volume 3, Issue 8, August 2003, Page 463

"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."
............................

http://www.thelancet.com/journals/laninf/article/PIIS1473309903007151/fu...

http://download.thelancet.com/pdfs/journals/1473-3099/PIIS14733099030071...

thank you,

kindest regards,

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

p.s. RECENT UPDATE NOR-98 ATYPICAL SCRAPIE DETECTED IN 2 MORE STATES

From: "Terry S. Singeltary Sr."
Sent: Tuesday, August 21, 2007 9:50 AM
Subject: TWO MORE Nor98 atypical Scrapie cases detected in USA bringing
total to 3 cases to date

Infected and Source Flocks

As of June 30, 2007, there were .....

snip...

One field case and one validation case were consistent with Nor-98 scrapie.

http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/download...

IN the February 2007 Scrapie report it only mentions ;

''One case was consistent with Nor98 scrapie.''

http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/

(please note flocks of origin were in WY, CO, AND CA. PERSONAL COMMUNCATIONS
USDA, APHIS, VS ET AL. ...TSS)

NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=14553

An evaluation of scrapie surveillance in the United States

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=3427

FOIA REQUEST FOR ATYPICAL TSE INFORMATION ON VERMONT SHEEP

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=10451

SEAC New forms of Bovine Spongiform Encephalopathy 1 August 2007
From: Terry S. Singeltary Sr.
Date: Sun, 5 Aug 2007 13:09:38 -0500

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=3573

POTENTIAL MAD CAT ESCAPES LAB IN USA

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=7062

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

Offline
Joined: 01/01/2006
Posts: 230
CWD UPDATE 88 AUGUST 31, 2007

CWD UPDATE 88 AUGUST 31, 2007

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0709&L=sanet-mg&T=0&P=450

TSS

Related Forum Threads You Might Like

ThreadThread StarterRepliesLast Updated
Board of Game Emergency TeleconferenceChuck-n-Alaska103/29/2008 02:29 am
If you live in california you should read thiscsumerall206/19/2008 19:44 pm
Best Coyote and Fox round? ACMETRAPPER302/27/2012 11:53 am
Michigan Moose Hunting Soon?jaybe205/15/2011 14:08 pm
Tom Redmond's Archery ExpertsCVC1109/03/2007 16:18 pm