Ronnie Dunn Cross Examination, slaughtering cattle, or killing deer ? TRANSCRIPT EXCERPT OF JURY TRIAL
Ronnie Dunn Cross Examination, slaughtering cattle, or killing deer ?
IN THE UNITED STATES DISTRICT COURT FOR THE NORTHERN DISTRICT OF INDIANA
SOUTH BEND DIVISION UNITED STATES OF AMERICA, vs. RUSSELL G. BELLAR, Defendant.
___________________________
)))))))))
Cause No.: 3:04cr00068-AS South Bend, Indiana January 4, 2005 9:30 a.m.
TRANSCRIPT EXCERPT OF JURY TRIAL (TESTIMONY OF: RONNIE DUNN AND RUSTY CAMP)
BEFORE THE HONORABLE ALLEN SHARP
snip...
Ronnie Dunn Cross Examination
Q. Mr. Dunn, at one point I believe you told the federal agents that Mr. Bellar told you that this was a private deer farm and shooting deer on that farm was like slaughtering cattle; is that correct?
A. I don't know if I used the word "slaughter," but it was, yeah, like that.
Q. You don't know if that was your word, "slaughtering cattle"?
A. I don't know that.
Q. Well, did he give you the idea of killing cattle?
A. Yes, it was the same principle.
Q. Mr. Dunn, at one point I believe you told the federal agents that Mr. Bellar told you that this was a private deer farm and shooting deer on that farm was like slaughtering cattle; is that correct?
A. I don't know if I used the word "slaughter," but it was, yeah, like that.
Q. You don't know if that was your word, "slaughtering cattle"?
A. I don't know that.
Q. Well, did he give you the idea of killing cattle?
A. Yes, it was the same principle.
snip...
see full text ;
BUCK FEVER
Thursday, September 18, 2014
*** Risk behaviors in a rural community with a known point-source exposure
to chronic wasting disease
Saturday, September 20, 2014
*** North Carolina Captive cervid licenses and permits Senate Bill 744
Singeltary Submission
Description The proposed changes to 15A NACA 10H .0301 would allow the
Commission to issue new captivity licenses and permits for the purpose of
holding cervids in captivity and allow certified herd owners to sell or transfer
cervids to any licensed facility. Also, mandatory testing for CWD will be raised
from all cervids that die at age 6 months or older to all cervids that die at
age 12 months or older.
Rule Text Click here
North Carolina Captive cervid licenses and permits Senate Bill 744
Singeltary Submission
*** p.s. please add this to my submission, very important
information...
Saturday, February 04, 2012
*** Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing
Protocol Needs To Be Revised
Approximately 4,200 fawns, defined as deer under 1 year of age, were
sampled from the eradication zone over the last year. The majority of fawns
sampled were between the ages of 5 to 9 months, though some were as young as 1
month.
*** Two of the six fawns with CWD detected were 5 to 6 months old.
All six of the positive fawns were taken from the core area of the CWD
eradication zone where the highest numbers of positive deer have been
identified.
Saturday, February 04, 2012
*** Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing
Protocol Needs To Be Revised
*** Conclusion. CWD prions (as inferred by prion seeding activity by
RT-QuIC) are shed in urine of infected deer as early as 6 months post
inoculation and throughout the subsequent disease course. Further studies are in
progress refining the real-time urinary prion assay sensitivity and we are
examining more closely the excretion time frame, magnitude, and sample variables
in relationship to inoculation route and prionemia in naturally and
experimentally CWD-infected cervids.
SNIP...SEE FULL TEXT ;
Saturday, September 20, 2014
*** North Carolina Captive cervid licenses and permits Senate Bill 744
Singeltary Submission
Wednesday, September 17, 2014
*** Cervid Health Business Plan Fiscal Years 2014 to 2018 Animal and Plant
Health Inspection Service Veterinary Services ***
Friday, September 05, 2014
*** CFIA CWD and Grain Screenings due to potential risk factor of spreading
via contamination of grain, oil seeds, etc. ***
Wednesday, September 17, 2014
*** Cervid Health Business Plan Fiscal Years 2014 to 2018 Animal and Plant
Health Inspection Service Veterinary Services ***
Sunday, September 21, 2014
INFORM: Cervid Health and States Indemnity FY 2015
Wednesday, September 17, 2014
Cost benefit analysis of the development and use of ante-mortem tests for
transmissible spongiform encephalopathies
Sunday, August 24, 2014
*** USAHA 117TH ANNUAL MEETING USDA-APHIS–VS CWD Herd Certification Program
Goals TSE PRION October 17 – 23, 2013
*** We conclude that TSE infectivity is likely to survive burial for long
time periods with minimal loss of infectivity and limited movement from the
original burial site. However PMCA results have shown that there is the
potential for rainwater to elute TSE related material from soil which could lead
to the contamination of a wider area. These experiments reinforce the importance
of risk assessment when disposing of TSE risk materials.
*** The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
PRION 2014 CONFERENCE
CHRONIC WASTING DISEASE CWD
A FEW FINDINGS ;
Conclusions. To our knowledge, this is the first established experimental
model of CWD in TgSB3985. We found evidence for co-existence or divergence of
two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice.
Finally, we observed phenotypic differences between cervid-derived CWD and
CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway
to characterize these strains.
We conclude that TSE infectivity is likely to survive burial for long time
periods with minimal loss of infectivity and limited movement from the original
burial site. However PMCA results have shown that there is the potential for
rainwater to elute TSE related material from soil which could lead to the
contamination of a wider area. These experiments reinforce the importance of
risk assessment when disposing of TSE risk materials.
The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
Our data establish that meadow voles are permissive to CWD via peripheral
exposure route, suggesting they could serve as an environmental reservoir for
CWD. Additionally, our data are consistent with the hypothesis that at least two
strains of CWD circulate in naturally-infected cervid populations and provide
evidence that meadow voles are a useful tool for CWD strain typing.
Conclusion. CWD prions are shed in saliva and urine of infected deer as
early as 3 months post infection and throughout the subsequent >1.5 year
course of infection. In current work we are examining the relationship of
prionemia to excretion and the impact of excreted prion binding to surfaces and
particulates in the environment.
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC)
are shed in urine of infected deer as early as 6 months post inoculation and
throughout the subsequent disease course. Further studies are in progress
refining the real-time urinary prion assay sensitivity and we are examining more
closely the excretion time frame, magnitude, and sample variables in
relationship to inoculation route and prionemia in naturally and experimentally
CWD-infected cervids.
Conclusions. Our results suggested that the odds of infection for CWD is
likely controlled by areas that congregate deer thus increasing direct
transmission (deer-to-deer interactions) or indirect transmission
(deer-to-environment) by sharing or depositing infectious prion proteins in
these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely
controlled by separate factors than found in the Midwestern and endemic areas
for CWD and can assist in performing more efficient surveillance efforts for the
region.
Conclusions. During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature.
see full text and more ;
Monday, June 23, 2014
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by
heat treatment in yellow grease produced in the industrial manufacturing process
of meat and bone meals
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute
and R(D)SVS; University of Edinburgh; Roslin, Scotland UK
Scrapie and chronic wasting disease probably spread via environmental
routes, and there are also concerns about BSE infection remaining in the
environment after carcass burial or waste 3disposal. In two demonstration
experiments we are determining survival and migration of TSE infectivity when
buried for up to five years, as an uncontained point source or within bovine
heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters
containing either sandy or clay soil. Migration from the boluses is being
assessed from soil cores taken over time. With the exception of a very small
amount of infectivity found 25 cm from the bolus in sandy soil after 12 months,
no other infectivity has been detected up to three years. Secondly, ten bovine
heads were spiked with TSE infected mouse brain and buried in the two soil
types. Pairs of heads have been exhumed annually and assessed for infectivity
within and around them. After one year and after two years, infectivity was
detected in most intracranial samples and in some of the soil samples taken from
immediately surrounding the heads. The infectivity assays for the samples in and
around the heads exhumed at years three and four are underway. These data show
that TSE infectivity can survive burial for long periods but migrates slowly.
Risk assessments should take into account the likely long survival rate when
infected material has been buried.
The authors gratefully acknowledge funding from DEFRA.
*** Susceptibility of UK red deer (Cervus alaphus elaphus) to oral BSE
transmission Project Code: M03024 ***
02/08/2011
The project confirmed that U.K red deer are susceptible to both oral and
intra-cerebral inoculation with the cattle BSE agent. Six clinically positive
(from 26-42 months post inoculation) i.c inoculated and one (56 months post
inoculation) orally dosed deer that tested positive for TSE by
immunohistochemistry and Western blotting using several primary antibodies
demonstrated widespread accumulation of disease specific prion protein in the
central nervous system, peripheral nervous system and enteric nervous system but
none in lymphoreticular system. All showed several brain sites positive for
disease specific prion protein and presented immunohistochemistry and Western
blotting phenotypes with similarities to BSE in sheep, goats and cattle but
unlike those seen in chronic wasting disease (CWD) in elk or scrapie in sheep.
The vacuolar pathology and distribution of disease specific prion protein in red
deer resembled that of CWD in most major respects however we have shown that BSE
can be clearly differentiated from CWD by existing immunohistochemical and
biochemical methods that are in routine use.
The knowledge gained as a result of this work will permit rapid and
accurate diagnosis should a TSE ever be detected in European red deer and will
also enable effective disease control methods to be quickly put in place.
Results
We confirmed that U.K red deer are susceptible to both oral and
intra-cerebral inoculation with the cattle BSE agent. Six clinically positive
(from 26-42mpi) i.c inoculated and one (56mpi) orally dosed deer that tested
positive for TSE by IHC and WB using several primary antibodies demonstrated
widespread accumulation of disease specific PrP in CNS, PNS and ENS but none in
LRS. All showed several brain sites positive for disease specific PrP and
presented IHC and WB phenotypes with similarities to BSE in sheep, goats and
cattle but unlike those seen in CWD in elk or scrapie in sheep. The vacuolar
pathology and distribution of PrPd BSE in red deer resembled that of CWD in most
major respects however we have shown that BSE can be clearly differentiated from
CWD by existing immunohistochemical and biochemical methods that are in routine
use.
Final technical report MO3024 01/04/2003 – 31/03/2010 Susceptibility of UK
red deer (Cervus elaphus elaphus) to oral BSE transmission. Stuart Martin - VLA
Lasswade Pentlands Science Park Bush Loan Penicuik EH26 0PZ Page 2 of 21 Further
work undertaken August 2009 – March 2010. Genetic analysis - Wilfred Goldmann;
Roslin NPD.
Negative controls and the remaining 5 orally dosed deer culled at 72mpi
tested negative by IHC and Western blot however analysis of the PrP ORF of these
deer (kindly carried out by Wilfred Goldmann of the Roslin NPD) identified a Q
to E polymorphism at codon 226 that may influence the efficiency of oral
transmission (not published).
In the experimental BSE challenge of red deer six out of six deer succumbed
to BSE when challenged by intracerebral routes but only one of six deer
challenged by the oral route succumbed to infection. Deer killed at 190 days or
365 days post oral challenge showed no evidence of abnormal PrP accumulation
when tested by immunocytochemistry. The PrP gene of red deer includes a Q to E
polymorphism at codon 226. The table shows the distribution of these codon 226
polymorphisms within experimental challenge groups.
snip...
Research article Open Access
Immunohistochemical and biochemical characteristics of BSE and CWD in
experimentally infected European red deer (Cervus elaphus elaphus)
Stuart Martin*1, Martin Jeffrey1, Lorenzo González1, Sílvia Sisó1, Hugh W
Reid2, Philip Steele2, Mark P Dagleish2, Michael J Stack3, Melanie J Chaplin3
and Aru Balachandran4 Address: 1Veterinary Laboratories Agency (VLA-Lasswade),
Pentlands Science Park, Bush Loan, Penicuik, Midlothian, EH26 0PZ, UK, 2Moredun
Research Institute, Pentlands Science Park, Bush Loan, Penicuik, Midlothian,
EH26 0PZ, UK, 3VLA-Weybridge, Addlestone, Surrey, KT15 3NB, UK and 4Animal
Diseases Research Institute, Canadian Food Inspection Agency, Ottawa, Ontario,
K2H 8P9, Canada
Abstract
Background: The cause of the bovine spongiform encephalopathy (BSE)
epidemic in the United Kingdom (UK) was the inclusion of contaminated meat and
bone meal in the protein rations fed to cattle. Those rations were not
restricted to cattle but were also fed to other livestock including farmed and
free living deer. Although there are no reported cases to date of natural BSE in
European deer, BSE has been shown to be naturally or experimentally
transmissible to a wide range of different ungulate species. Moreover, several
species of North America's cervids are highly susceptible to chronic wasting
disease (CWD), a transmissible spongiform encephalopathy (TSE) that has become
endemic. Should BSE infection have been introduced into the UK deer population,
the CWD precedent could suggest that there is a danger for spread and
maintenance of the disease in both free living and captive UK deer populations.
This study compares the immunohistochemical and biochemical characteristics of
BSE and CWD in experimentally-infected European red deer (Cervus elpahus
elaphus).
Results: After intracerebral or alimentary challenge, BSE in red deer more
closely resembled natural infection in cattle rather than experimental BSE in
small ruminants, due to the lack of accumulation of abnormal PrP in lymphoid
tissues. In this respect it was different from CWD, and although the
neuropathological features of both diseases were similar, BSE could be clearly
differentiated from CWD by immunohistochemical and Western blotting methods
currently in routine use.
Conclusion: Red deer are susceptible to both BSE and CWD infection, but the
resulting disease phenotypes are distinct and clearly distinguishable.
SNIP...
Results
Clinical disease
All six deer challenged i.c. with BSE developed clinical disease between
794 and 1260 days post-inoculation with a mean incubation period of 1027 days. A
detailed description of the clinical signs was provided in an earlier report
[8]. Briefly, affected deer showed variable degrees of ataxia, anorexia,
circling and apparent blindness, together with failure of seasonal change of
coat, weight loss and 'panic attacks'. In addition, one of six red deer orally
dosed with BSE developed clinical disease 1740 days after challenge, and this
animal presented with a short clinical duration of two days; the other five deer
from this group remain healthy at the time of writing (65 months after
challenge). Sequential rectal biopsies taken at five different time points from
orally and i.c. inoculated deer were negative for PrPd.
All four deer orally challenged with CWD started to show behavioural
changes between 577 and 586 days post challenge;
these progressed to definite neurological disease between 742 and 760 days
post-challenge (Table 1).
Clinical signs were similar to the BSE challenged deer and included
nervousness, weight loss, excessive salivation, roughness of coat, and
progressive ataxia. All these CWD inoculated deer showed PrPd accumulation in
the secondary follicles of rectal biopsies taken at 7 months post
infection.
Conclusion
European red deer are susceptible to infection with the cattle BSE agent,
not only by the intra-cerebral but also by the oral route, and although the
clinical signs and spong- iform change are similar to those of CWD in the same
species, these two infections can be easily differentiated. The lack of lymphoid
involvement, the PrPd truncation pattern both "in vivo" and "in vitro", and the
predominantly intracellular accumulation of PrPd are features of deer BSE that
are in contrast with those of deer CWD. However, only one of six deer developed
disease after alimentary exposure to 25 g of a BSE brain pool homogenate after
an incubation period of nearly 5 years; this suggests a strong species barrier
but if a TSE in European red deer should ever be identified then BSE/CWD
discrimination would be an urgent priority. To determine whether there are
potential naturally occurring BSE-like strains and to determine the degree to
which there is strain variation, it would be necessary to examine many more
naturally occurring CWD cases. These results will support the ongoing European
surveillance for natural TSEs in red deer and the further assessment of
potential risk to human health.
Published: 27 July 2009 BMC Veterinary Research 2009, 5:26
doi:10.1186/1746-6148-5-26 Received: 12 February 2009 Accepted: 27 July 2009
This article is available from: http://www.biomedcentral.com/1746-6148/5/26
© 2009 Martin et al; licensee BioMed Central Ltd. This is an Open Access article
distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium,
provided the original work is properly cited.
Monday, May 05, 2014
*** Member Country details for listing OIE CWD 2013 against the criteria of
Article 1.2.2., the Code Commission recommends consideration for listing ***
snip...
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
*** Overall, therefore, it is considered there is a __greater than
negligible risk___ that (nonruminant) animal feed and pet food containing deer
and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In
Animal Feed
EMC 1 Terry S. Singeltary Sr. Vol #: 1
see my full text submission here ;
Sunday, December 15, 2013
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s the
risk to humans and pets?
Tuesday, July 01, 2014
*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND
POTENTIAL RISK FACTORS THERE FROM
TSS
posted by Terry S. Singeltary Sr. at
2:25 PM
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