America's Mad Cow Crisis by John Stauber
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America's Mad Cow Crisis
John Stauber
Americans might remember that when the first mad cow was confirmed in the
United States in December, 2003, it was major news. The United States Department
of Agriculture (USDA) and the Food and Drug Administration (FDA) had been
petitioned for years by lawyers from farm and consumer groups I worked with to
stop the cannibal feeding practices that transmit this horrible, always fatal,
human and animal dementia. When the first cow was found in Washington state, the
government said it would stop such feeding, and the media went away. But once
the cameras were off and the reporters were gone nothing substantial changed.
In the United States, dairy calves are still taken from their mothers and
fed the blood and fat of dead cattle. This is no doubt a way to infect them with
the mad cow disease that has now been incubating here for decades, spread
through such animal feeding practices. No one knows how the latest dairy cow was
infected, the fourth confirmed in the United States. Maybe it was nursed on
cow's blood. Perhaps it was fed feed containing cattle fat with traces of cattle
protein. Or perhaps there is a mad cow disease in pigs in the United States,
which simply has not been found yet, because pigs are not tested for it at all,
even though pigs are fed both pig and cattle byproducts, and then the blood, fat
and other waste parts of these pigs are fed to cattle.
All these U.S. cattle feeding methods are long banned and illegal in other
countries that suffered through but eventually dealt properly with mad cow
disease. Here, rather than stopping the transmission of the disease by stopping
the cannibal feeding, mad cow is simply covered up with inadequate testing and
very adequate public relations. US cattle are still fed mammalian blood, fat and
protein, risking human deaths and threatening the long term safety of human
blood products, simply to provide the U.S. livestock industry with a cheap
protein source and a cheap way to get rid of dead animal waste.
I began researching this issue around 1989, long before the disease was
confirmed to have jumped from cattle to the people eating them, as announced by
the British government in 1996. In 1997 I co-authored <http://www.prwatch.org/books/madcow.html>
Mad Cow USA, warning that the disease was likely already here and spreading,
since the animal cannibalism that caused its outbreak in Britain and spread it
to other countries was actually more widespread in the United States than
anywhere.
Some years ago responsible U.S. beef companies wanted to test their animals
for mad cow disease and label their beef as being disease free, but they were
forbidden under penalty of law from doing so. Only the USDA can test for mad
cows in America. In 2004 and 2005, after two additional mad cows were discovered
in Texas and Alabama, the United Sates government declared that obviously mad
cow wasn't much of a problem and gutted it's anemic testing program. Today only
about 40,000 cattle a year are tested, out of tens of millions slaughtered. It's
amazing that the California cow was even detected given this pathetic testing
program that seems well designed to hide rather than find mad cows.
The prevention of mad cow disease is relatively simple. If your country has
it, test each animal before it goes to slaughter to keep the diseased animals
out of the food chain. Cheap, accurate and easy tests are now available in other
countries but illegal here. Testing cattle both identifies the true extent of
the disease, and keeps infected animals from being eaten in your sausage or
hamburger. In this manner countries like Britain, Germany, France and Japan have
controlled their problem through testing and a strict ban on cannibal
feed.
Once mad cow disease moves into the human population of a country, all bets
are off as to what could happen next. It's a very slow disease, it develops
invisibly over decades in someone who has been infected, and it is always fatal.
We'll know a lot more in fifty years, but the future looks worrisome. In Britain
people are dying from mad cow disease, people who never consumed infected meat.
They used medical products containing human blood, and that blood was infected
because it was from infected people. There is no test to identify infectious
prions, the causal agent, in blood.
Almost none of this information appeared in news stories about the
California mad cow. Instead the headlines and the talking heads fed us the line
that the United States fixed this problem long ago, and the fact that only 4 mad
cows have been detected so far is proof of our success. Oprah Winfrey once tried
via her talk show to warn about this, way back in 1996, but Texas cattlemen
dragged her and her guest Howard Lyman into court and she had to spend many
millions of dollars defending herself from the supposed crime of slandering
meat.
Oprah won her case, which was probably unfortunate for the rest of us
because had she been convicted the ensuing appeals court trial might have gotten
enough attention to wake up Americans to the truth. Instead Oprah learned her
lesson - shut up and you won't get sued. Other media learned too that if the
government and industry can silence Oprah, they can muzzle anyone. (One of the 4
confirmed U.S. mad cows was later found in Texas, appropriately enough.)
There are a handful of dedicated activists such as Howard Lyman who have
been sounding the alarm on this. They include the ecologist Dr. Michael Hansen
of Consumers Union and Dr. Michael Greger, a physician. Terry Singeltary Sr.,
whose mom died of a version of the human form of mad cow disease, has been a
relentless, unpaid activist on this issue.
Despite their dedicated work, there is no indication that anything is going
to change here in America. The U.S. government refuses to implement the feed ban
and the animal testing necessary. It doesn't matter if the President is named
Clinton, Bush or Obama because their bureaucrats in the USDA and FDA stay the
course and keep the cover up going. Docile, eating what they are fed, trusting
the rancher all the way to the slaughterhouse. Is that just the cows, or is it
us too?
-- John Stauber: <http://sourcewatch.org/index.php?title=John_Stauber>
is an independent author and activist. He founded the Center for Media and
Democracy in 1993, retiring in 2009. Way back in 1997 he co-authored Mad Cow
USA. <http://www.prwatch.org/books/madcow.html>
http://www.commondreams.org/view/2012/04/26-1
http://www.electricpolitics.com/2012/04/americas_mad_cow_crisis.html
Tell the USDA to Stop the Spread of Mad Cow Disease!
Terry Singeltary P.O. Box 42 Bacliff, TX 77518-0042
April 25, 2012
Administrator Gregory Parham
12th & Jefferson Drive, SW Whitten Bldg., Room 313-E Washington, DC
20250 Re: Docket No. APHIS-2008-0010
Dear Administrator Parham:
In order to stop the spread of bovine spongiform encephalopathy (BSE or mad
cow disease), the US Department of Agriculture should adopt and enforce the same
strict standards required by the European Union and Japan:
* Mandatory testing for all cattle brought to slaughter, before they enter
the food chain.
* Ban the feeding of blood, manure, and slaughterhouse waste to
animals.
In the meantime, the USDA must stop harassing farmers and food processors
who are interested in independently testing their own beef for mad cow
disease.
Ironically, the news that mad cow is still in our food supply comes at a
time that the U.S. Department of Agriculture Animal and Plant Health Inspection
Service (APHIS) is proposing to drop significant protections the U.S. has
against the importation of cattle infected with mad cow disease.
APHIS proposes to open United States' borders to cattle from countries that
have had thousands of cases of BSE, and where new BSE cases continue to be
found. The importation of a single infected cow from Canada in 2001 set in
motion restrictions on U.S. beef exports that cost the beef industry billions of
dollars and that still exist today in several major export markets.
APHIS also proposes to drop important measures that have been used to
protect U.S. consumers from these imported cattle and meat products (which have
a much higher chance of being infected with BSE than U.S.-raised cattle), and
intends to rely almost exclusively on slaughtering techniques, particularly the
removal of specified risk materials (SRMs), which we know on occasion is not
employed fully or effectively, and which has not been practiced long enough to
determine whether it is indeed the panacea APHIS assumes, given the long
gestation time of variant Creutzfeldt-Jakob Disease (vCJD) in humans.
I support the view of R-CALF USA CEO Bill Bullard:
"Seventy-six farm and consumer organizations, representing tens of millions
of U.S. citizens, recently urged Secretary Vilsack to strengthen, not weaken,
our already lax BSE policies by reversing the so-called 'over-thirty-month
rule,' which allows Canadian cattle born during the time the BSE agent was known
to be circulating in Canada's feed system to be imported into the United States.
"Secretary Vilsack has again ignored our concerns and is putting the
self-interests of corporate meatpackers that want access to more meat supplies
regardless of risk to humans and livestock, ahead of the health and safety
concerns of U.S. citizens.
"The USDA is touting its proposed rule as a trade rule, claiming it will
strengthen the United States' negotiating position in trade agreements. This is
the same failed argument the Bush Administration used when it first relaxed our
U.S. BSE policies in 2004, and the result of that failed argument is that many
important export markets imposed long-lasting export restrictions on U.S. beef.
"USDA's proposal amounts to a unilateral disarmament of essential disease
protections for U.S. citizens and livestock. It will disadvantage U.S. producers
in the global market because other major beef exporters, including Brazil,
Australia, and India continue to maintain adequate import standards while the
U.S. relaxes its own. This will create unnecessary and avoidable anxieties among
other beef consuming nations for U.S. beef.
"Exposing U.S. consumers and U.S. livestock to a heightened risk of BSE
introduction is irresponsible and contrary to pledges made by the Obama
Administration during his campaign."
This is no time to relax our essential protections against the introduction
of mad cow disease.
so, USDA et al accidently find two atypical mad cows in Texas and Alabama
during the infamous enhanced BSE cover up back in 2004 and 2005, and then shut
the testing down to numbers so low, it's almost impossible to find another mad
cow case, unless your country is to a point that mad cow disease can be found in
1 in 40,000, and STILL FIND MAD COW DISEASE, HOUSTON, WE HAVE A PROBLEM. ...
PLEASE UNDERSTAND, the USDA et al are lying about atypical BSE being a
spontaneous mutation, NOT caused by feed. spontaneous BSE has NEVER been proven
in any natural field case of BSE. feed is the most likely route. ...tss
As previously stated most of the characteristics of atypical BSE have not
been defined. In addition to the origin, the risk to other cattle by means of
natural transmission, the risk to humans and other animal species suck as
chickens and pigs is still unknown as is the distribution of infectivity
throughout the body of a bovine. There is little information on clinical
manifestation if it occurs at all in certain of the cases. Documented L cases
have been diagnosed from samples taken from older ''healthy'' cattle presented
for routine slaughter.
While additional surveillance and research is being conducted, it is
important for policy make to consider the implications of atypical BSE. They may
need to rethink what populations are appropriate targets. It would probably be
unwise to prematurely lessen or discontinue the current BSE protection measures.
SNIP...
Atypical BSE: What is it and what is the significance
Linda A. Detwiler, Paul Brown, Lisa M. McShane, and Gianluigi Zanusso
When atypical cases were first reported there was some speculation that
these may merely be protein accumulation disorders associated with old age. It
has now been shown that both the Land H types of atypical BSE are at least
experimentally transmissible. Homogenates from L cases have been transmitted to
bovinized transgenic mice, humanized transgenic mice, Cynomolgus monkeys and 1
breed of cattle (Buschmann et al. 2006; Book of abstracts (2006), International
Conference on Prion Diseases, Turin, Italy). H cases have been transmitted to
bovinized transgenic (Tgbov) and ovinized transgenic mice (Béringue et al.
2006). The incubation times for atypical L cases of BSE were shorter in the
Tgbov mice than classical BSE inoculated into Tgbov mice and the H cases had
longer incubations.
A variation or mutation of the classical BSE strain
A different route of exposure or exposure at an older
age A strain of Scrapie transmitted to cattle
Sporadic or a spontaneous occurrence of BSE At his
point in time, there is no evidence to conclude that any of the theories are or
are not a possibility. There is considerable interest in the sporadic theory. If
a form of BSE were to ocnaturally, this may suggest that certain control and
prevention measure would have to remain in place indefinitely. Proving or
disproving the occurrence of a relatively rare sporadic disease poses a
significant challenge. It would require between 3 and 4.5 million tests
performed on brain samples randomly taken from cattle over 7 years of age in a
country with no evidencrisk from orally acquired BSE. It is unlikely that any
country would have the will or resources to perform such a study. Lacking this
type of evidence, systematic surveillance over a long time period may provide
evidence about the nature of atypical BSE.
snip...see full text ;
When L-type BSE was inoculated into ovine transgenic mice and Syrian
hamster the resulting molecular fingerprint had changed, either in the first or
a subsequent passage, from L-type into C-type BSE. In addition, non-human
primates are specifically susceptible for atypical BSE as demonstrated by an
approximately 50% shortened incubation time for L-type BSE as compared to
C-type. Considering the current scientific information available, it cannot be
assumed that these different BSE types pose the same human health risks as
C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk
material (SRM) in atypical BSE. The incumbent of this position will develop new
and transfer existing, ultra-sensitive methods for the detection of atypical BSE
in tissue of experimentally infected cattle.
BY the way, ammonia treated beef DOES NOT KILL MAD COW DISEASE !!!
Tuesday, April 24, 2012
MAD COW DISEASE USA 4TH CASE DOCUMENTED ATYPICAL BSE CALIFORNIA
Wednesday, April 25, 2012
4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012
Wednesday, April 25, 2012
ACTUALITY - USDA Chief Veterinary Officer On Surveillance And Milk Safety
and BSE aka MAD COW DISEASE
Wednesday, April 25, 2012
USA MAD COW DISEASE AND CJD THERE FROM SINGELTARY ET AL 1999 - 2012
layperson
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
flounder9@verizon.net
Sincerely, Terry Singeltary
powered by CQ Roll Call ©2012
Confirmation Your e-mail message was sent to: Administrator Gregory Parham,
Administrator, Animal and Plant Health Inspection Service
TSS
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