Wednesday, April 25, 2012

America's Mad Cow Crisis by John Stauber

America's Mad Cow Crisis by John Stauber


Permission granted to reprint this article:


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

No comments:

Post a Comment