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Mad Cow Class Action Against Federal Government IS A GO

flounder

Well-known member
Mad Cow Class Action Against Federal Government Obtains Green Light from Quebec Court


MONTREAL, June 17 /CNW/ - In a landmark decision released late Friday,
June 15, 2007 Quebec Superior Court Justice Richard Wagner granted
authorization to a billion dollar class action suit, ruling that the mad cow
class action on behalf of some 20,000 Quebec cattle farmers against the
Federal Government will proceed to trial. This is an important step in
obtaining compensation for farmers following Canada's mad cow scandal
involving over 100,000 Canadian cattle farmers, including Quebec's
20,000 cattle farmers.
In April 2005, class action claims were filed cooperatively by a team of
lawyers in the courts of Quebec, Ontario, Saskatchewan and Alberta on behalf
of all commercial farmers of cattle resident in Canada as of May 20, 2003 (the
date at which Canada's International cattle and beef exports were frozen). The
claims allege that negligence on the part of the Federal Government caused the
BSE (Bovine Spongiform Encephalopathy) crisis in Canada and the corresponding
loss of income to Canadian cattle producers. The statements of claim may be
viewed at www.bseclassaction.ca
The class action lawsuits allege that the BSE crisis, the closing of the
U.S. and other international borders to Canadian cattle and beef, and the loss
of billions of dollars by the Canadian cattle industry were the result of
gross incompetence on the part of the Canadian government. Statistics Canada
confirmed in May of this year that Canadian cattle producers have lost more
than $9B in cash receipts since the BSE crisis began in May of 2003, an amount
which has been growing daily. To view this report, please visit
www.bseclassaction.ca
Quebec Attorney Gilles Gareau and Ontario's Cameron Pallett, co-counsel
in the Quebec action commented, "We applaud this decision as an important
milestone for all of Quebec's and Canada's cattle producers. We are confident
it will lead to eventual redress for hard-working farmers who have suffered
extensive damage and whose livelihoods have been compromised. It is a view
held by many experts that the BSE crisis would never have happened if the
Federal Government had not been asleep at the wheel. We would recommend that
all potential members of the class retain their financial records going as far
back as possible, as these records may be critical in determining the
financial damages they are entitled to recover.
According to documents filed in Quebec Court, government officials
jeopardized the safety of the Canadian food supply in failing to inform the
public that they had allowed 80 British cattle that were supposed to be in a
'monitoring program', to enter the human and animal food chain in Canada.
These same government officials' own risk analysis indicated that there was a
95% chance that 6 or more of these animals had BSE."
Although findings of liability against the Federal Government remain to
be made at trial, Mr. Gareau and his colleagues from across the country find
this a tremendous development for all Canadian cattle producers and urge them
to visit the BSE class action website to register and for more information
www.bseclassaction.ca

ABOUT CANADA'S BSE SCANDAL
--------------------------
BSE is an incurable neurological disease of cattle that is transmitted
when healthy cattle eat the remains of infected cattle or other ruminants. The
claim alleges that the federal government was negligent in enacting, or
failing to enact in a timely fashion, regulations with respect to permissible
ingredients in cattle feed. It is also alleged that the federal government
negligently allowed more than 80 British cattle to enter the human and animal
food chain, and failed to warn cattle producers of the dangers posed by this
release of BSE into the cattle food chain when the government realized what
they had done.



For further information: please contact the following attorneys who will
be available to comment Sunday and Monday: Québec, Me Gilles Gareau, Adams
Gareau, Telephone: (514) 848-9363, Cell: (514) 966-7555,
[email protected]; Ontario, Cameron Pallett, Barrister & Solicitor,
Telephone: (416) 923-1776, Cell: (416) 473-0460, [email protected];
Saskatchewan, Reynold Robertson, Robertson Stromberg Pedersen LLP, Telephone:
(306) 933-1348, Cell: (306) 230-9980, [email protected]; Alberta,
Clint Docken, Q.C., Docken & Company, Telephone: (403) 269-7656, Cell: (403)
619-3612, [email protected]

http://www.newswire.ca/en/releases/archive/June2007/17/c5678.html

TSS
 

flounder

Well-known member
PORKER said:
www.bseclassaction.ca


Welcome to the BSE class action website.

On May 20, 2003 cattle producers were struck with the worst disaster to hit
the Canadian agriculture industry since the Great Depression. Bovine
spongiform encephalopathy (also known as BSE or mad cow disease) was
diagnosed in one cow in Alberta, triggering the immediate closing of
international borders to Canadian cattle and beef. Canadian cattle
producers have lost billions of dollars in revenue as a result. Farms that
have been in the same family for generations have been sold. Many producers
have been forced to turn their back on farming altogether. Families have
suffered and continue to suffer. This national class action is intended to
recover every penny lost by Canadian cattle producers from those who caused
their losses.


http://www.bseclassaction.ca/



SADLY, the families that have lost loved ones directly from animal TSEs or
indirectly via friendly fire from animal TSE, well, there just **** out of
luck, INDUSTRY RULES! it's all spontaneous/sporadic/ukbsenvcjd only. only
cows can get TSE orally, and only cattle ranchers can be compensated, even
though these animal TSE transmit orally to primate. and we know they
transmit via the medical and surgical arena. don't you just love political
junk science. ...



> USA MAD COW STRAIN MORE VIRULENT TO HUMANS THAN UK STRAIN
>
> 18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
> December 2006 are now available.
>
>
> snip...
>
>
>
> 64. A member noted that at the recent Neuroprion meeting, a study was
> presented showing that in transgenic mice BSE passaged in sheep may be
more
> virulent and infectious to a wider range of species than bovine derived
BSE.
>
> Other work presented suggested that BSE and bovine amyloidotic spongiform
> encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in
the
> prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO
A
> MUTATION FOUND IN CASES OF SPORADIC CJD.
>
>
> snip...
>
>
>
> http://www.seac.gov.uk/minutes/95.pdf
>
>
>
>
> 3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse
>
> Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western
> Reserve
> University
>
> Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain
> discovered recently in Italy, and similar or different atypical BSE cases
> were also reported in other countries. The infectivity and phenotypes of
> these atypical BSE strains in humans are unknown. In collaboration with
> Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have
> inoculated transgenic mice expressing human prion protein with brain
> homogenates from BASE or BSE infected cattle. Our data shows that about
half
> of the BASE-inoculated mice became infected with an average incubation
time
> of about 19 months; in contrast, none of the BSE-inoculated mice appear to
> be infected after more than 2 years.
>
> ***These results indicate that BASE is transmissible to humans and suggest
> that BASE is more virulent than
> classical BSE in humans.***
>
>
> 6:30 Close of Day One
>
>
> http://www.healthtech.com/2007/tse/day1.asp
>
>
>
>
> 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
>
>
>
> There is a growing number of human CJD cases, and they were presented last
> week in San Francisco by Luigi Gambatti(?) from his CJD surveillance
> collection.
>
> He estimates that it may be up to 14 or 15 persons which display
selectively
> SPRPSC and practically no detected RPRPSC proteins.
>
>
> http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
>
>
> http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
>
>
> USDA VOLUNTARY MAD COW TAINTED FOOD RECALL ''DON'T ASK, DON'T TELL''
POLICY
>
>
> AS ONE LEGISLATOR THAT MOU SHOULD BE TERMINATED IMMEDIATELY
>
> IT IS A FRONT TO THE PUBLIC
>
> THAT YOU WOULD ON YOUR OWN ACCORD, IN THAT KIND OF SECRECY, AND CALL THAT
> GOVERNMENT
>
> THAT'S NOT WHAT WERE HERE FOR, WERE HERE FOR TRANSPARENCY, WERE NOT HERE
TO
> DO SECRET DEALS,
>
> ''WERE NOT THE CIA'' !!!
>
> THERE ARE OTHER WAYS TO GET TO THE GOAL OF REACHING THE CONSUMER WITHOUT
> DEALING WITH USDA THAT FINDS IT UNACCEPTABLE TO SHARE INFORMATION WITH THE
> PUBLIC
>
>
>
> http://maddeer.org/video/embedded/02snip.rpm
>
>
>
> STANLEY PRUSINER NOBEL PEACE PRIZE WINNER ON THE PRION SLAMS USDA ON BSE
>
> US AG SEC AND LAYCRAFT
>
> "nothing ELSE matters, except beef from canada under 30 months bones beef
> product, that's ALL THAT MATTERS!"
>
>
> STAN THE MAN
>
> question for stan ;
>
> is this a demonstrated threat to public health safety ?
>
> stan states ;
>
> yes i think they (prions) are bad to eat, and you can die from them.
>
>
> http://maddeer.org/video/embedded/08snip.ram
>
>
>
> THE LINKs YOU JUST WATCHED WAS OF THE FOLLOWING HEARING ON THE WASHINGTON
> MAD COW and what little ramifications there after, and to this day,
nothing
> has changed much, except more secrecy. ...TSS
>
>
>
> 022404 Senate Info-Hearing Agriculture / Water Resources / Health and
Human
> Services / Government Oversight: Mad Cow Disease
>
>
> Entire 5 hour hearing - The California Channel
>
> (scroll down to "022404 Senate Info-Hearing")
>
> http://www.calchannel.com/february2004.htm
>
>
>
> Sporadic creutzfeldt-jakob disease in two adolescents
>
> http://jnnp.bmj.com/cgi/content/abstract/jnnp.2006.104570v1
>
>
> FULL TEXT SPORADIC CJD, THE BIG LIE
>
>
> http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0705&L=sanet-mg&T=0&P=25276
>
>
> 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
>
>
> vCJD in the USA * BSE in U.S.
> 15 November 1999
>
>
> http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406
>
>
> BMJ
>
>
> U.S. Scientist should be concerned with a CJD epidemic in the U.S., as
> well...
> 2 January 2000
>
>
> 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:
>
> [email protected]
>
> 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/fulltext
>
>
http://download.thelancet.com/pdfs/journals/1473-3099/PIIS1473309903007151.pdf
>
>
> see history of cjd questionnaire
>
> http://brain.hastypastry.net/forums/showthread.php?t=2408
>
>
> TSS
>
>
>
>
 

rkaiser

Well-known member
Terry writes -
SADLY, the families that have lost loved ones directly from animal TSEs or
indirectly via friendly fire from animal TSE, well, there just s*** out of
luck, INDUSTRY RULES! it's all spontaneous/sporadic/ukbsenvcjd only. only
cows can get TSE orally, and only cattle ranchers can be compensated, even
though these animal TSE transmit orally to primate. and we know they
transmit via the medical and surgical arena. don't you just love political
junk science. ...

Hard to know if this is commentary from yourself or what this is Terry - I am assuming it is your thoughts.

Why on earth are you taking this important step as "**** out of luck" for folks like yourself. Start your own damn lawsuit.

Cameron and I talked for an hour yesterday about this major step on the road to some kind of financial recovery for the producers of our country - and by the way old boy - he has no problem with our theory of metal contamination. In fact our friendship has developed over my commitment to this theory and a reminder to him, every time we talk to not let his guard down to wako's like yourself who have a whole different agenda when it comes to BSE.
 

DiamondSCattleCo

Well-known member
This is at least a step in the right direction. Hopefully the feds will get off the dime for BSE testing now.

Although, I think the CCA should have been lumped in with the feds on this suit. They're as much to blame for the whole fiasco as the feds.

Rod
 

rkaiser

Well-known member
As Cam Pallette kept reminding me yesterday "Don't wish for the dogs to be let in to the fight". I talked about how I wished it was Cargill rather than Ridley included in the suit, however the fight would have lasted for years, and the Cargill hounds may have gotten out the Mafia tactics to stop this thing.

As far as the CCA - whipping pups for the big Dogs. Leaving them (Cargill - Tyson and CCA) totally on the outside of this will be better in the long run.

Personally, I was shocked with this announcement. Always hope in Quebec they say.
 

flounder

Well-known member
rkaiser said:
Terry writes -
SADLY, the families that have lost loved ones directly from animal TSEs or
indirectly via friendly fire from animal TSE, well, there just s*** out of
luck, INDUSTRY RULES! it's all spontaneous/sporadic/ukbsenvcjd only. only
cows can get TSE orally, and only cattle ranchers can be compensated, even
though these animal TSE transmit orally to primate. and we know they
transmit via the medical and surgical arena. don't you just love political
junk science. ...

Hard to know if this is commentary from yourself or what this is Terry - I am assuming it is your thoughts.

Why on earth are you taking this important step as "s*** out of luck" for folks like yourself. Start your own damn lawsuit.

Cameron and I talked for an hour yesterday about this major step on the road to some kind of financial recovery for the producers of our country - and by the way old boy - he has no problem with our theory of metal contamination. In fact our friendship has developed over my commitment to this theory and a reminder to him, every time we talk to not let his guard down to wako's like yourself who have a whole different agenda when it comes to BSE.





TORT REFORM BY THE INDUSTRY AND THERE LAWYERS, the system only protects it's own my friend, the consumer has no chance in hell anymore.

and metals are not transmissible.



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&list_uids=6997404&dopt=Abstract



1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8



Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.

Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.

PMID: 8006664 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract


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




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: [email protected] )

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


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 [log in to unmask]


Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References

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




QUESTION, IS U.S.A. FOOD PRODUCTION SYSTEM POISONING US ?



What Do We Feed to Food-Production Animals? A Review of Animal Feed
Ingredients and Their Potential Impacts on Human Health


Amy R. Sapkota,1,2 Lisa Y. Lefferts,1,3 Shawn McKenzie,1 and Polly Walker1
1Johns Hopkins Center for a Livable Future, Bloomberg School of Public
Health, Baltimore, Maryland, USA; 2Maryland Institute for
Applied Environmental Health, College of Health and Human Performance,
University of Maryland, College Park, Maryland, USA;
3Lisa Y. Lefferts Consulting, Nellysford, Virginia, USA


snip...



Table 1. Animal feed ingredients that are legally used in U.S. animal feeds



Animal


Rendered animal protein from Meat meal, meat meal tankage, meat and bone
meal, poultry meal, animal the slaughter of food by-product meal, dried
animal blood, blood meal, feather meal, egg-shell production animals and
other meal, hydrolyzed whole poultry, hydrolyzed hair, bone marrow, and
animal animals digest from dead, dying, diseased, or disabled animals
including deer and elk Animal waste Dried ruminant waste, dried swine waste,
dried poultry litter, and undried processed animal waste products


snip...


Conclusions


Food-animal production in the United States has changed markedly in the past
century, and these changes have paralleled major changes in animal feed
formulations. While this industrialized system of food-animal production may
result in increased production efficiencies, some of the changes in animal
feeding practices may result in unintended adverse health consequences for
consumers of animal-based food products. Currently, the use of animal feed
ingredients,
including rendered animal products, animal waste, antibiotics, metals, and
fats, could result in higher levels of bacteria, antibioticresistant
bacteria, prions, arsenic, and dioxinlike compounds in animals and resulting
animal-based food products intended for human consumption. Subsequent human
health effects among consumers could include increases in bacterial
infections (antibioticresistant and nonresistant) and increases in the risk
of developing chronic (often fatal) diseases
such as vCJD. Nevertheless, in spite of the wide range of potential human
health impacts that could result from animal feeding practices, there are
little data collected at the federal or state level concerning the amounts
of specific ingredients that are intentionally included in U.S. animal feed.
In addition, almost no biological or chemical testing is conducted on
complete U.S. animal feeds; insufficient testing is performed on retail meat
products; and human health effects data are not appropriately linked to this
information. These surveillance inadequacies make it difficult to conduct
rigorous epidemiologic studies and risk assessments
that could identify the extent to which specific human health risks are
ultimately associated with animal feeding practices. For example, as noted
above, there are insufficient data to determine whether other human
foodborne bacterial illnesses besides those caused by S. enterica serotype
Agona are associated with animal feeding practices. Likewise, there are
insufficient data to determine the percentage of antibiotic-resistant human
bacterial infections that are attributed to the nontherapeutic use of
antibiotics in animal feed. Moreover, little research has been conducted to
determine whether the use of organoarsenicals in animal feed, which can lead
to elevated levels of arsenic in meat products (Lasky et al. 2004),
contributes to increases in cancer risk. In order to address these research
gaps, the following principal actions are necessary within the United
States: a) implementation of a nationwide reporting system of the specific
amounts and types of feed ingredients of concern to public health that are
incorporated into animal feed, including antibiotics, arsenicals, rendered
animal products, fats, and animal waste; b) funding and development of
robust surveillance systems that monitor biological, chemical, and other
etiologic agents throughout the animal-based food-production chain “from
farm to fork” to human health outcomes; and c) increased communication and
collaboration among feed professionals, food-animal producers, and
veterinary and public health officials.


REFERENCES...snip...end


Sapkota et al.
668 VOLUME 115 | NUMBER 5 | May 2007 • Environmental Health Perspectives


http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1867957&blobtype=pdf


look at the decline in BSE cases in reference to feed ban of tainted materials ;

http://www.defra.gov.uk/animalh/bse/statistics/bse/overview.html

http://www.defra.gov.uk/animalh/bse/controls-eradication/feedban-bornafterban.html


The measures taken by the UK Government, in particular the feed ban, have already resulted in a sharp decline in the incidence of BSE. ...

http://www.defra.gov.uk/animalh/bse/controls-eradication/index.html


TSS
 

DiamondSCattleCo

Well-known member
rkaiser said:
As far as the CCA - whipping pups for the big Dogs. Leaving them (Cargill - Tyson and CCA) totally on the outside of this will be better in the long run.

You're probably right, but it would be nice for those fools to get a slap in the face from a group that says 'Hey, a-holes, you're not actually representing producers anymore'. Producers tell them that all the time, but it just doesn't seem to sink in.

Rod
 

rkaiser

Well-known member
metals are not transmissible?

Is that all you can come up with Terry? And then post a whole bunch more crap that no one and I mean no one will read AGAIN.

Misfolded prions are not transmissible Mr. Science. Metals can definitely be passed from one animal to another - ie transmissible.

BUT we both agree that this case is good ---- NOT?

We are going to work on the Alberta Governement once more for support Rod, but as far as CCA and ABP well - you know what I think of that puppet trunk.
 
A

Anonymous

Guest
I can't believe it-- Canadian cattlemen and producers suing their government over their perceived inept actions and misdeeds of said government-- and when US cattlemen and producers sued the US government over their perceived inept actions and misdeeds, the Canadians called the US cattlemen every nasty name in the book :wink: :lol: :lol: :lol:
 

Kathy

Well-known member
flounder...
and metals are not transmissible

Dr. Vitaly Vodyanoy:

within patent application 20070122799 USA

"[0298] Seeds, Proteon Nucleating Centers (PNCs)

[0299] Hypothesis Metal clusters (Gonzalez-Morega, 1993; Aiken & Finke, 1999) play a role in the seeds in proteons, Metals involved in the natural folding and misfolding of proteins are not in the ion state, but rather in the clusters of metal atoms. These atoms are directly bonded to each other creating a polyatomic metallic nucleus that can exist alone or are associated with a given number of ligands.

[0300] Rationale: The most remarkable property of metal clusters is that they provide a binding template for folding and aggregation of proteins (Liu and Xu, 2002). High symmetry is one of the main characteristics of metal clusters (Gonzalez-Moraga, 1993). Packing of secondary structures prefers geometrical patterns (Gracy et al., 1993; Onuchic et al., 1997). Many disorders arise from misfolding and aggregation of an underlying protein (Carrel and Lormas, 1997; Sato, 2001). The same disorders were shown to depend on metal misbalance (Bush, 2000). Copper, iron or manganese are involved in the aging and neurological disorders. Metals are involved in prion diseases (Lehman, 2002, Thackray, et al., 2002). Among 327 possible protein folds (Chothia, et al., 1997) only 230 folds are unique. The number of unique space groups applied to inorganic clusters is also equal to 230! (Hahn, 1987). The mathematical accuracy and stability of geometrical patterns and a large number of structural arrangements of metal clusters make them uniquely qualified as perfect templates for protein folding.

[0301] Experimental evidence: When PNCs were removed from blood plasma by filtration through a 5-kDa filter, the amount of protein in the retentate was equivalent to that of the non-filtered sample, and no protein was found in the filtrate (data not shown). Proteons could not be produced from the retentate until an aliquot of the filtrate was added back, and proteon production was dependent on the amount of filtrate added (data not shown). Interestingly, proteons cound be produced in this matter even after the filtrate was carbonized at 660.degree. C., but production was quenched by 10 mM EDTA, and a metal-chelating agent (data not shown)(Irving and Al-Jarrah, 1975). Adsorption spectra (GTW Analytical Services) of the filtrate revealed the presence of metals, namely Cu, ZN and Fe (data not shown). [note - healthy blood examined]

[0302] TEM showed that the bulk of the drived PNC-containing filtrate was amorphous, and that it contained crystalline metallic nanoparticles 1-2 nm in diameter. Selected area diffraction (SAD) patterns from different regions of the samples were consistent with both face-centered cubic (FCC) and body centered cubic (BCC) metals. Furthermore, both copper and iron were identified from EDS spectra acquired from regions containing the nanoparticles (data not shown) that the diffraction patterns were not consistent with an organometallic structure number of metal atoms. For example, the volume of a 1 nm diameter Cu particle is approximately equivalent to 10 Cu (or 20 .alpha.-Fe) unit cells (Borchardt-Ott, 1993). Given that FCC and BCC metals contain four and two atoms per unit cell, respectively (Borchardt-Ott, 1993), there data suggest that a particle containing .about.40 atoms is formed regardless of the lattice type. Furthermore, the very fact that the metallic nanoparticles exist implies that the environment in which they formed prevented both oxidation and coarsening of the particles.

[0303] Proposed Role of PNCs

[0304] PNCs consist of 1-2-nm metal nanoparticles that contain 40-300 atoms. Given that proteons contain both PNCs and fragments of the Hb .alpha.-chain (see FIG. 1C), we conclude that PNCs play an important role in capturing Hb released to blood plasma. Released Hb is normally captured by haptoglobin, which is then recognized by Hb scavenger receptors and endocytosed by macrophages (Kristiansen et al., 2001). We speculate that when haptoglobin is depleted during critically elevated hemolysis (Delss, 1999), released Hb is collected by PNCs. We estimate that about 7.times.10.sup.13 PNCs/ml are present in human blood, and that only about 0.004% of the entire PNC pool is normally linked to proteins to form proteons. On average, a 160-nm diameter proteon can bind about 100,000 protein molecules that are the size of Hb. TEM data indicated that blood contains abundant copper nanoparticles, suggesting that proteons result from the nucleation and growth (Eaton and Hofrichter, 1990) of misfolded Hb on copper PNCs. This process may offer insights into the mechanisms of some blood disorders associated with intravascular hemolysis, which results in Hb aggregation (Kannan et al., 1988; Schluter and Drenckhahn, 1986; Papalexis et al, 2001). Indeed, copper plays a critical role in other protein conformation-based disorders such as prion disease, Parkinson's disease, Alzheimers disease and familial amyotrophic lateral sclerosis (Brown et al., 1997). Metal clusters in blood may have many other functions. We were surprised to discover that small concentrations of PNCs were lethal to cultured cancer cells, whereas non-cancerous cells were much less affected (Samaylov et al., 2005).

[0305] Small metal nanoclusters meet requirements to serve as nuclei for aggregation of proteins and their fragments: i.e. Small, a few nm or smaller; Large quantity, about 10.sup.13 PNCs/cm.sup.3 of blood or tissue; Abundant source for replenishing; Binding sites and strong affinity to proteins; Variability to bind different proteins; Stability to resist extreme physical and biochemical conditions (high temperature, pressure, acid and alkaline environments, oxygen, organic solvents, detergents, antibiotics, proteases, lipases).

Inhale, consume or absorb {or even produce within the body?} the wrong metal nanoparticles (PNCs) which irreversibly alter, misfold, polymerize and aggregate protein fragments (many of which are similar in their fragment structure) and you have a problem.

The metal PNCs are the "TEMPLATE" AND THUS THE CAUSATIVE AGENT!
 

DiamondSCattleCo

Well-known member
Oldtimer said:
and when US cattlemen and producers sued the US government over their perceived inept actions and misdeeds, the Canadians called the US cattlemen every nasty name in the book :wink: :lol: :lol: :lol:

Apples and oranges OT. You were suing your government to keep our livestock out of your country using baseless accusations and questionable mathematics. Did you really think that Canadians would applaud your actions? :roll:

Sue your own government for not allowing private BSE testing or screwing up your feed ban, and we Canadians will be right there cheering you on.

Rod
 
A

Anonymous

Guest
DiamondSCattleCo said:
Oldtimer said:
and when US cattlemen and producers sued the US government over their perceived inept actions and misdeeds, the Canadians called the US cattlemen every nasty name in the book :wink: :lol: :lol: :lol:

Apples and oranges OT. You were suing your government to keep our livestock out of your country using baseless accusations and questionable mathematics. Did you really think that Canadians would applaud your actions? :roll:

Sue your own government for not allowing private BSE testing or screwing up your feed ban, and we Canadians will be right there cheering you on.

Rod
If you read the lawsuit-- it was for the same reasons-- your government (Canadian) allowed importing high risk materials/cattle from a foreign country (Britain)- and not putting in enough safeguards to protect the Canadian cattle herd and Canadian cattle industry--
which is exactly what R-CALF did- sue the US government for what we perceive is higher risk cattle/product from Canada- without the proper safeguards in effect..... US cattleman are just trying to prevent what they have already seen happen in Canada, that is the basis of your lawsuit...

Sounds like HYPOCRISY to me...

Remember R-CALF/US cattlemen didn't sue Canadians- they sued the US government and USDA for their illegal/misguided/unscientific changing of the import rules just for the benefit of the Multinational Packers....
 
A

Anonymous

Guest
Kato said:
So why didn't you sue the US government for not monitoring British cattle imported into your country?

That could happen-- but at the time it was best to stop the current high risk before it happened- so we didn't have to go thru what Canadians were.....
Why didn't Canadian producers block the British cattle- instead of having to go thru the suffering and now suing for damages :???: .....
We've been taking lessons from Canada (going all the way back to the first NAFTA trade barriers--Anaplas/Blue tongue)...

The purpose of the suit is to look at all their safeguards- and methods/legalities/authority of implementing/changing such safeguards...In order to do this all the evidence needs to be laid out...

The final results of this suit will also impact USDA's/Packers ability to pick and choose parts of Argentina to import FMD cattle from- along with poulty from Asian countries with AI like China .....

As the ruling now stands the Packers thru their control of USDA have unlimited access to bring anything from anywhere into the US- no matter what the impact may be on US producers, consumers, or herds.....
 

flounder

Well-known member
UK Exports of Live Cattle by Value 1986-96

USA 697 LIVE CATTLE

CANADA 299 LIVE CATTLE

http://www.bseinquiry.gov.uk/files/mb/m11f/tab11.pdf


UK TABLE of Exports of meal of meat and meat offal; greaves 1979 - 1995

USA 24 TONS

CANADA 83 TONS

http://www.bseinquiry.gov.uk/files/mb/m12/tab12.pdf


HOWEVER, my files show 44 tons of greaves for USA. ...TSS


Subject: Re: exports from the U.K. of it's MBM to U.S.???
From: [email protected]
Date: Tue, 8 Feb 2000 14:03:16 +0000
To: [email protected] (Receipt Notification Requested) (Non Receipt Notification Requested)

Terry Meat and bonemeal is not specifically classified for overseas trade purposes. The nearest equivalent is listed as flours and meals of meat or offals (including tankage), unfit for human consumption; greaves. UK exports of this to the US are listed below:
Country Tonnes

1980
1981 12
1982
1983
1984 10
1985 2
1986
1987
1988
1989 20
1990

Data for exports between 1975 and 1979 are not readily available. These can be obtained (at a charge) from data retailers appointed by HM Customs and Excise: BTSL (Tel: 01372 463121) or Abacus (01245 252222). Best wishes Simon Pearsall Overseas trade statistics Stats (C&F)C ======================================


TSS
 
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