Thursday, September 25, 2014

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

 

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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.

 

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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.

 

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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 ***

 


 

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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

 

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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.

 

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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

 


 

 

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