5 replies [Last post]
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Joined: 01/01/2006
Posts: 230
CWD UPDATE SEPTEMBER 2007

P04.01
Chronic Wasting Disease in a Captive White-Tailed Deer Farm

Keane, D1; Barr, D1; Bochsler, P1; Hall, M2; Gidlewski, T3; O’Rourke, K4; Spraker, T5
1University of Wisconsin, USA; 2US Department of Agriculture, USA; 3US Department
of Agriculture, USA; 4USDA ARS-ADRU, Washington |State University, USA; 5Veterinary
Diagnostic Laboratory, Colorado State University, USA

A white-tailed deer farm in Portage, Wisconsin, was depopulated in January 2006,
after chronic wasting disease (CWD) had been initially discovered on the property in
September 2002. Prior to the depopulation, a total of 22 positive animals had been
removed from the property: one in 2002, six in 2003, ten in 2004, four in 2005 and one
in 2006. At the time of depopulation a total of 76 animals remained: 47 females and 29
males. Age was assessed by visual examination of teeth at the time of death and
revealed 26 adult, 8 fawn and 42 yearling animals. The following tissues were
examined by immunohistochemistry for PrPCWD using Ab99/97.6.1: obex, tonsil,
retropharyngeal, submandibular, parotid, prescapular, axillary, inguinal, prefemoral and
popliteal lymph nodes, recto-anal mucosal tissue and eye. Seventy-nine percent of
animals (sixty) were found to be positive in at least one tissue; 49 were obex positive,
58 retropharyngeal positive, 56 tonsil positive, 48 recto-anal mucosal associated
lymphoid tissue positive and 4 animals were positive for PrPCWD in the retina. Prion
genotype was determined for all animals.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf

P04.61

Survival of PrPSc during Simulated Wastewater Treatment Processes

Pedersen, J1; Hinckley, G1; McMahon, K2; McKenzie, D3; Aiken, JM3
1University of Wisconsin, Soil Science/Civil and Environmental Engineering,
USA; 2University of Wisconsin, Civil and Environmental Engineering, USA;
3University of Wisconsin, Comparative Biosciences, USA

Concern has been expressed that prions could enter wastewater treatment systems through sewer and/or septic systems (e.g., necropsy laboratories, rural meat processors, private game dressing) or through leachate from landfills that have received TSE-contaminated material. Prions are highly resistant to degradation and many disinfection procedures raising concern that they could survive conventional wastewater treatment. Here, we report the results of experiments examining the partitioning and survival of PrPSc during simulated wastewater treatment processes including activated and mesophilic anaerobic sludge digestion. We establish that PrPSc
can be efficiently extracted from activated and anaerobic digester sludges
with 1% sodium dodecyl sulfate, 10% sodium undecyl sulfate, and 1% sodium N-lauryl sarcosinate. Activated sludge digestion does not result in significant
degradation of PrPSc. The protein partitions strongly to the activated sludge solids and is expected to enter biosolids treatment processes. A large fraction of PrPSc survived simulated mesophilic anaerobic sludge digestion. Our results suggest that if prions were to enter municipal waste water treatment systems, most of the agent would partition to activated sludge solids, survive mesophilic anaerobic digestion, and be present in treated biosolids. Land application of biosolids containing prions could represent a route for their unintentional introduction into the environment. Our results argue for
excluding inputs of prions to municipal wastewater treatment facilities that
would result in unacceptable risk of prion disease transmission via contaminated
biosolids.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf

http://www.microbes.info/forum

Chronic Wasting Disease (CWD) continues to spread
Sports
RONALD E. MCCALL | Thursday, September 27, 2007 at 12:30 am

http://savannahnow.com/node/366050

re-CHRONIC WASTING DISEASE SPREADING and USA MAD COW H-BASE and SPORADIC CJD

http://savannahnow.com/node/366082

Terry S. Singeltary Sr.
P.O. Box 42

Offline
Location: Summit, IL
Joined: 10/22/2006
Posts: 706
CWD UPDATE SEPTEMBER 2007

See here is a problem. While they are reporting, and that is fantastic that they actually are, the findings need to be broken down to where the common individual can understand it. I went to college and had some advanced biology and I even had to think to decipher that report. To make it easier to understand I believe what they are saying is that the CWD is being introduced to the waste water facilities by way of processors draining the blood from infected game animals and depositing the skins into land fills thereby getting into the water table. The report is also suggesting that the virus/bacteria is also very resistant to treatments that are commonly used by waste treatment plants. Im not saying in any way that the common individual is in any way stupid. Im saying that not everyone understands the meaning that these reports are trying to get accross.

Easy explination for us less educated people that have a hard time figuring out those scientific terms.

Dont put your skins in the trash to be picked up. Burn them in a pile. Dont wash the blood into a drain thats connected to a public sewer system.

While these reports are great and very much needed, for them to be any good for the public they need to be broken down to plain old common English.

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Joined: 01/01/2006
Posts: 230
CWD UPDATE SEPTEMBER 2007
cam69conv wrote:
Ya gots ta KILL it before ya can GRILL it!!!!.

New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication Paul Brown*,dagger , Edward H. RauDagger , Bruce K. Johnson*, Alfred E. Bacote*, Clarence J. Gibbs Jr.*, and D. Carleton Gajdusek§

* Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, and Dagger Environmental Protection Branch, Division of Safety, Office of Research Services, National Institutes of Health, Bethesda, MD 20892; and § Institut Alfred Fessard, Centre National de la Recherche Scientifique, 91198 Gif sur Yvette, France

Contributed by D. Carleton Gajdusek, December 22, 1999

Abstract

One-gram samples from a pool of crude brain tissue from hamsters infected with the 263K strain of hamster-adapted scrapie agent were placed in covered quartz-glass crucibles and exposed for either 5 or 15 min to dry heat at temperatures ranging from 150°C to 1,000°C. Residual infectivity in the treated samples was assayed by the intracerebral inoculation of dilution series into healthy weanling hamsters, which were observed for 10 months; disease transmissions were verified by Western blot testing for proteinase-resistant protein in brains from clinically positive hamsters. Unheated control tissue contained 9.9 log10LD50/g tissue; after exposure to 150°C, titers equaled or exceeded 6 log10LD50/g, and after exposure to 300°C, titers equaled or exceeded 4 log10LD50/g. Exposure to 600°C completely ashed the brain samples, which, when reconstituted with saline to their original weights, transmitted disease to 5 of 35 inoculated hamsters. No transmissions occurred after exposure to 1,000°C. These results suggest that an inorganic molecular template with a decomposition point near 600°C is capable of nucleating the biological replication of the scrapie agent.

transmissible spongiform encephalopathy | scrapie | prion | medical waste | incineration

Introduction

The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin. It also has been assumed that the replication of these agents is a strictly biological process (1), although the notion of a "virus" nucleant of an inorganic molecular cast of the infectious beta -pleated peptide also has been advanced (2). In this paper, we address these issues by means of dry heat inactivation studies.

see full text:

http://www.pnas.org/cgi/content/full/97/7/3418

Interactions of prion proteins with soil

Liviana Leitaa,, Flavio Fornasiera, Maria De Nobilib, Alessandro Bertolic,

Sacha Genovesic, Paolo Sequid

aC.R.A. Consiglio per la Ricerca e Sperimentazione in Agricoltura—Istituto Sperimentale per la Nutrizione delle Piante, Sezione di Gorizia,

via Trieste 23, I-34170 Gorizia, Italy

bDipartimento di Scienze Agrarie ed Ambientali, Universita` di Udine, via delle Scienze 208, I-33100 Udine, Italy

cDipartimento di Chimica Biologica, Universita` di Padova, viale G. Colombo 3, I-35121 Padova, Italy

dC.R.A. Consiglio per la Ricerca e Sperimentazione in Agricoltura—Istituto Sperimentale per la Nutrizione delle Piante, via della Navicella 2,

I-00184 Roma, Italy

Received 10 September 2004; received in revised form 3 November 2005; accepted 7 November 2005

Abstract

Prions, are proteinaceous particles recognized as the agents of a class of neurodegenerative disorders, called transmissible spongiform

encephalopathies (TSE), or prion diseases. Epidemiological data suggest that TSE-contaminated environments may serve as source of

infectivity, but there is no information about adsorption of prions onto soil. We carried out experiments by mixing, healthy, or scrapieinfected

hamster brains homogenates with three types of soil suspended in different buffers: (i) two saline buffers, i.e., phosphate buffer

solution (PBS) and CaCl2 solution; (ii) a mix of nondenaturing detergents, i.e., Triton X-100 and sodium deoxycholate (DOC) solution;

(iii) a non-ionic detergent, i.e., lauryl maltoside; (iv) two anionic detergents, i.e., Sarkosyl or sodium dodecyl sulphate (SDS); and (v) a

chaotropic agent, i.e., urea. The unbound prion proteins were detected in the supernatants (after centrifugation of soil suspension) by

Western blotting. Results clearly demonstrate that both the no infectious (PrPC) and infectious (PrPSc) forms are adsorbed by all soils.

Only 1% sodium dodecylsulphate (SDS) partially impeded the association of PrPC, but not that of PrPSc with the sandy loam soil.

Agents with different interacting properties towards hydrophilic and/or hydrophobic domains failed to extract PrPSc from sediments of

soil–brain homogenate mixtures. The strong interaction of PrPSc with soil favors the accumulation of prions in soils, especially if

amended with prion-containing organic fertilizers and/or whenever TSE-affected animal carcasses, placenta, and excreta in general are

buried or laid at the soil surface.

snip...

In conclusion, although these results cannot precisely

define the nature of the bonds between prions and soil

components, especially if they are reversible under conditions

other than those tested in the present study, the

apparent strength of such interactions suggests that prions

can be retained, and accumulate in soil, especially if

amended with prion-containing organic fertilizers and/or

whenever TSE-affected animal carcasses, placenta, and

excreta in general are buried or laid at the soil surface

(Miller et al., 2004). If the adsorbed prions also retain their

pathological activity (Brown and Gajdusek, 1991; Leita et

al., unpublished results), they could represent a hazardous

environmental source of infectivity, and provide a further

explanation for the horizontal transmissibility of TSE

forms, such as scrapie and CWD.

r 2006 Elsevier Ltd. All rights reserved.

0038-0717/$ - see front matter r 2006 Elsevier Ltd. All rights reserved.

doi:10.1016/j.soilbio.2005.11.018

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

PAUL BROWN SCRAPIE SOIL TEST

http://www.bseinquiry.gov.uk/files/sc/seac07/tab03.pdf

Some unofficial information from a source on the inside looking out - personal/private communication

Confidential!!!!

As early as 1992-3 there had been long studies conducted on small
pastures containing scrapie infected sheep at the sheep research station
associated with the Neuropathogenesis Unit in Edinburgh, Scotland.
Whether these are documented...I don't know. But personal recounts both
heard and recorded in a daily journal indicate that leaving the pastures
free and replacing the topsoil completely at least 2 feet of thickness
each year for SEVEN years....and then when very clean (proven scrapie
free) sheep were placed on these small pastures.... the new sheep also
broke out with scrapie and passed it to offspring. I am not sure that TSE
contaminated ground could ever be free of the agent!!
A very frightening revelation!!!

----------

> ===========================================
>
> Furthermore, an unpublished study had indicated low
>
> level absorption of PrP from soil by tomato plants although it
>
> should be noted that this study had not been repeated. Details of
>
> this work would be sent to the SEAC Secretary.
>
> ========================
>
>

http://www.seac.gov.uk/minutes/draft91.pdf

TSS

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Joined: 01/01/2006
Posts: 230
CWD UPDATE SEPTEMBER 2007

P01.47

Quantifying the Species Barrier in Chronic Wasting Disease by a Novel in vitro Conversion Assay

Li, L1; Coulthart, MB2; Balachandran, A3; Chakrabartty, A4; Cashman, NR1
1University of British Columbia, Brain Research Centre, Canada; 2Public Health Agency
of Canada, National Microbiology Laboratory, Canada; 3Animal Diseases Research
Institute, Canada Food Inspection Agency, National Reference Laboratory for Scrapie
and CWD, Canada; 4Ontario Cancer Institute and Department of Medical Biophysics,
University of Toronto, Canada

Background: Chronic wasting disease (CWD) is a transmissible spongiform
encephalopathy that can affect North American cervids (deer, elk, and moose).
Although the risk of CWD crossing the species barrier and causing human disease is
still unknown, however, definite bovine spongiform encephalopathy (BSE) transmission
to humans as variant CJD (vCJD), it would seem prudent to limit the exposure of
humans to CWD.

Aim: In view of the fact that BSE can be readily transmitted to non-bovid species, it is
important to establish the species susceptibility range of CWD.

Methods: In vitro conversion system was performed by incubation of prions with
normal brain homogenates as described before, and protease K (PK) resistant PrP was
determined by immunoblotting with 6H4 monoclonal prion antibody.

Results: Our results demonstrate that PrPC from cervids (including moose) can be
efficiently converted to a protease-resistant form by incubation with elk CWD prions,
presumably due to sequence and structural similarities between these species.
Interestingly, hamster shows a high conversion ratio by PrPCWD. Moreover, partial
denaturation of substrate PrPC can apparently overcome the structural barriers
between more distant species.

Conclusions: Our work correctly predicted the transmission of CWD to a wild moose.
We find a species barrier for prion protein conversion between cervids and other
species, however, this barrier might be overcome if the PrPC substrate has been
partially denatured in a cellular environment. Such an environment might also promote
CWD transmission to non-cervid species, *** including humans.
Acid/GdnHCl-treated brain PrPC was a superior substrate for the in vitro conversion
than PrPC treated at physiological pH. This has implications for the process by which
the prion protein is converted in disease.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf

From: "Terry S. Singeltary Sr."
Subject: CWD UPDATE 88 AUGUST 31, 2007

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

Date: Wed, 29 Aug 2007 21:13:08 -0500
From: "Terry S. Singeltary Sr."
Subject: CWD NEW MEXICO RECORDS IT'S 19 CASE (near Texas border again)

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=26079

Monitoring the Potential Transmission of Chronic Wasting Disease to Humans
Using a Hunter Registry Database in Wyoming (405 lines)
From: Terry S. Singeltary Sr.
Date: Thu, 30 Aug 2007 21:23:42 -0500

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

J Biol Chem. 2007 Aug 20; : 17709374

Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a
new prion strain.

####################################

our results raise the possibility that CJD cases
classified as VV1 may include cases caused by
iatrogenic transmission of sCJD-MM1 prions or
food-borne infection by type 1 prions from animals,
e.g., chronic wasting disease prions in cervid. In fact,
two CJD-VV1 patients who hunted deer or
consumed venison have been reported (40, 41). The
results of the present study emphasize the need for
traceback studies and careful re-examination of the
biochemical properties of sCJD-VV1 prions.

###################################

FULL TEXT ;

http://www.jbc.org/cgi/content/abstract/M704597200v1?maxtoshow=&HITS=10&...

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=21267

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

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

TSS

Offline
Joined: 08/27/2004
Posts: 1964
CWD UPDATE SEPTEMBER 2007

Unreal I dont even wanna know whats going to pop up in the next 5 years.

Good read Flounder.

Offline
Joined: 01/01/2006
Posts: 230
BSE TRANSMITS TO RED DEER

for you info. ...tss

Subject: Clinical Observations of BSE Infection in Red Deer
Date: October 4, 2007 at 9:05 am PST

P04.80

Clinical Observations of BSE Infection in Red Deer

Steele, P1; Martin, S2; Jeffrey, M2; González, L2; Sisó, S2; Finlayson, J1;
Hamilton, S1;
Eaton, Samatha L1; Reid, Hugh W1; Todd, R1; Pang, Y1; Chianini, F1;
Dagleish, MP1
1Moredun Research Institute, UK; 2Veterinary Laboratory Agency, Lasswade, UK

Observation of clinical signs is often the first step in the diagnosis of
TSE diseases in
experimental, farmed and wild animals. Clinical presentation of chronic
wasting
disease (CWD) infected deer varies widely as disease progresses and many
clinical
signs observed can be non-specific to TSE infection, however by terminal
stage the
majority of cases involve behavioural changes and loss of body condition.
We present here the first description of clinical disease in deer
experimentally infected
with BSE. These data are part of the results of an ongoing project to
investigate the
susceptibility of UK red deer (Cervus elaphus elaphus) to BSE infection
either by
alimentary or intra-cerebral infection.
Eighteen European red deer calves (mean 64 days old) were challenged
intragastrically
with 25g of BSE-infected bovine brain. Six challenged and 2 control deer
were culled at 6 and 12 month post infection. These animals showed no
clinical signs
and no disease-specific PrP (PrPd) on immunohistochemistry (IHC) examination
of a
wide range of tissues collected at post-mortem. Six BSE-dosed and 4 negative
control
deer are still alive at time of writing (1384 dpi).
Subsequently, 6 red deer of the same cohort (mean 341 days old) were
challenged with
0.05g of BSE positive bovine brain material and 2 with sterile saline by the
intracerebral
route. Currently (1106 dpi), five of the six challenged animals have
developed
clinical signs and terminal disease confirmed by IHC and western blot
detection of
PrPd.
Clinical signs similar to CWD cases have been observed including behavioral
change,
wide stance, lowered head, and excessive salivation. All animals had
significant weight
loss attributed to inability or unwillingness to feed, with inhalation
pneumonia occurring
in the case of one animal which is commonly observed in CWD cases. The first
animal
to show clinical signs was markedly different to the four subsequent cases.
This animal had to be culled following several behavioral episodes causing
physical
injury. Our results prove for the first time that UK red deer are
susceptible to intra-cerebral
BSE infection and shows that the clinical presentation of disease shares
many
similarities to that recorded for CWD.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf

M03024: Susceptibility of red deer (Cervus elaphus elaphus) to BSE
Thursday 09 October 2003

This research project aims to determine whether BSE can be transmitted to UK
red deer by including infected material in their feed.

Study Duration: April 2003 to April 2010

Contractor: Veterinary Laboratories Agency

Background
The major cause of the spread of the BSE epidemic was attributed to the
feeding of contaminated meat and bonemeal (MBM) in the protein rations fed
to cattle. The use of MBM in animal feed was not restricted to cattle
rations and it is known that MBM was included in the concentrates fed to
farmed deer. BSE has been shown to be naturally or experimentally
transmissible to a wide range of different ungulate species and deer are
known to be susceptible to an endemic TSE (chronic wasting disease, CWD)
which is prevalent in North America. However, to date, no TSE infections of
UK deer have been reported.
Should BSE infection have been transmitted into the UK red deer population,
the CWD precedent would suggest that there is potential for both spread and
maintenance of the disease in both free living and captive UK deer
populations. The purpose of this study is to investigate the susceptibility
of UK red deer to BSE infection and to determine the clinical and
pathological phenotype.

Research Approach
The initial objective of the study is to determine whether orally infected
UK red deer are susceptible to bovine BSE agent. Groups of orally dosed deer
will be sacrificed at 6, 12 and 60 months post inoculation and necropsies
carried out. A range of tissue samples will be retained for further analysis
such as immunohistochemistry. All animals will also be monitored clinically
throughout the experiment to define any clinical phenotype.

http://www.food.gov.uk/science/research/researchinfo/bseresearch/tserese...

-------- Original Message --------
Subject: Susceptibility of red deer (Cervus elaphus elaphus) to BSE
Date: Mon, 8 Mar 2004 20:29:54 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de

TSE Project Details
Project Ref M03024
Theme Risk assessment of SEs
Sub Theme An evaluation of SEs transmission modalities from cattle to
man and other food animals, environment vectors
MRC Priority
Title Susceptibility of red deer (Cervus elaphus elaphus) to BSE
Funder(s)
Principle Investigator Dr Hawkins PI Department Veterinary Laboratories
Agency
PI Location Weybridge PI Organisation Veterinary Laboratories Agency

Last Year Cost £ This Year Cost £
Start Date 01/04/2003 End Date 01/04/2010
Status Current Total Cost £ 1,485,458
Abstract The major cause of the spread of BSE was attributed to the
feeding of contaminated meat and bone meal (MBM) in the protein rations
fed to cattle. The use of MBM in animal feed was not restricted to
cattle rations and it is known that MBM was included in the concentrates
fed to farmed deer. BSE has been shown to be naturally or experimentally
transmissible to a wide range of different ungulate species and deer are
known to be susceptible to an endemic TSE (chronic wasting disease, CWD)
which is prevalent in North America. However, to date, no TSE infections
of UK deer have been reported. The initial objective of the study is to
determine whether orally infected UK red deer are susceptible to bovine
BSE agent. Groups of orally dosed deer will be sacrificed at 6, 12 and
60 months post inoculation and necropsies carried out. A range of tissue
samples will be retained for further analysis such as
immunohistochemistry. All animals will also be monitored clinically
throughout the experiment to define any clinical phenotype.

©2004 Medical Research Council

http://www.mrc.ac.uk/index/current-research/current-tse_portfolio_search...

Virology
Susceptibility of Red Deer to BSE
Dagleish, M
FSA funded project in collaboration with VLA
No known cases of BSE have ever been reported in any species of deer.
However, an EU directive has decreed that provision must be made for all
ruminant species entering the human food chain to be screened for BSE and
free living and captive deer may have been exposed to the BSE agent. BSE has
affected a range of different hoof stock (domestic and exotic cattle, eland,
nyala, greater kudu, gemsbok and Arabian and scimitar-horned oryx) and
several species of cats (cheetah, puma, tiger, lion and domestic cats) by
presumed ingestion of contaminated meat and bone meal in food. As both
captive and free ranging UK deer enter the human food chain it is important
to determine their susceptibility to transmission of the BSE agent, the
nature of any possible resultant clinical disease and to develop methods of
screening deer tissues for the BSE agent to maintain the high standards of
food safety within the UK .

This study will determine in the first instance whether the BSE agent can
actually be transmitted to red deer. If this is possible the study will also
provide a description of any resultant clinical disease, pathological
changes and positive control tissue material all of which would aid
surveillance for BSE in deer within the UK .

Moredun Research Institute
Pentlands Science Park, Bush Loan, Penicuik, Midlothian, EH26 0PZ, Scotland
Telephone - 0131 445 5111, International +44 131 445 5111,
info@moredun.ac.uk

Site last updated: 22 Jun 2006

http://www.mri.sari.ac.uk/vir-dagleish-proj2.asp

http://www.ngpc.state.ne.us/cgi-bin/ultimatebb.cgi?ubb=print_topic;f=12;...

http://www.ngpc.state.ne.us/cgi-bin/ultimatebb.cgi?ubb=get_topic;f=12;t=...

CREUTZFELDT JAKOB DISEASE MAD COW BASE, CWD, SCRAPIE UPDATE OCT 2007

http://cjdmadcowbaseoct2007.blogspot.com/

CJD NEWS

http://disc.server.com/Indices/236650.html

CJD VOICE (voice for _all_ victims of human TSE)

http://members.aol.com/larmstr853/cjdvoice/cjdvoice.htm

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

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