From Reuters, 6/20/06: USDA to reduce mad cow testing program by 90 pct
WASHINGTON (Reuters) - The U.S. government will scale down its mad cow surveillance program by 90 percent to reflect a smaller presence of the disease in the United States, but reduced testing should not slow efforts to reopen a foreign markets to U.S. beef, Agriculture Secretary Mike Johanns said on Thursday.
The U.S. Department of Agriculture will reduce its cattle-testing level to 40,000 head per year. That will be down from an average of about 30,000 head each month since June 2004, after discovery of animals with the disease prompted fears that resulted in Japan, Korea and other countries banning U.S. beef.
The reduced testing level, to take effect after 30 days, will cost $8 million a year, down from $1 million per week at the height of testing. USDA said it will focus on the "most at-risk animals" that show telltale signs of the disease.
As sad as I am to say it, we're swearing off beef. We were wary before and have done limited bursts of not eating beef, but the USDA's irresponsibility on this is too much to ignore. (Having said that, I'm open to eating organic beef, though Shane remains suspicious.)
"Those who are attempting to cause consumers to believe that somehow they're protected by testing really aren't being fair with consumers," said Johanns. "It's pretty blunt, but it's true," he said.
Interesting: Johanns is essentially saying that the USDA's lack of oversight regarding cattle feeding policies has resulted in a culinary crap shoot anytime anyone wants to tuck into a steak. How comforting.
What happens if you are infected with "mad cow"? Here's an excerpt from Wikipedia:
Unlike the other kinds of infectious disease which are spread by microbes, the infectious agent in BSE [Bovine spongiform encephalopathy, aka mad cow] is a specific type of protein. Misshapen ("misfolded") prion proteins carry the disease between individuals and cause deterioration of the brain. BSE is a type of transmissible spongiform encephalopathy (TSE). [...] Transmission can occur when healthy animals consume tainted tissues from others with the disease. In the brain these proteins cause native cellular prion protein to deform into the infectious state
which then goes on to deform further prion protein in an exponential cascade. These aggregate to form dense plaque fibers, which lead to the microscopic appearance of "holes" in the brain, degeneration of physical and mental abilities and ultimately death. Some TSE's are resistant to extreme temperatures and are not affected by household disinfectants.
The human version of BSE is Variant Creutzfeldt-Jakob Disease (vCJD). "Regular" Creutzfeldt-Jakob Disease is a bit different from vCJD, but the symptoms are similar. From Wikipedia:
The first symptom of CJD is rapidly progressive dementia, leading to memory loss, personality changes and hallucinations. This is accompanied by physical problems such as speech impairment, jerky movements (myoclonus), balance and coordination dysfunction (ataxia), changes in gait, rigid posture, and seizures. The duration of the disease varies greatly, but sporadic (non-inherited) CJD can be fatal within months or even weeks (Johnson, 1998). In most patients, these symptoms are followed by involuntary movements and the appearance of a typical diagnostic electroencephalogram tracing.
The symptoms of CJD are caused by the progressive death of the brain's nerve cells, which is associated with the build-up of abnormal prion proteins. When brain tissue from a CJD patient is examined under a microscope, many tiny holes can be seen where whole areas of nerve cells have died. The word 'spongiform' in 'transmissible spongiform encephalopathies' refers to the 'spongy' appearance of the brain tissue.
Of vCJD, Wikipedia reports it is:
distinguished from the classical type by its early onset (usually in the 20s) and a predominance of psychiatric and sensory symptoms. The prions in this form are thought to be transmitted by consuming the nervous tissue of bovines with so-called mad cow disease (Bovine Spongiform Encephalopathy), although there is no definite proof of this association as yet. It has been shown, however, that PRPSc particles accumulate in gastrointestinal lymphoid tissue (specifically, Peyer's patches) in animals after oral infection (Maignien et al 1999; Beekes and McBride, 2000;
Shmakov and Ghosh, 2001; Ghosh 2002). Furthermore, in vitro studies have shown the uptake of these particles by human gastrointestinal tract cells (Morel et al, 2005). Further suggestive of an oral route of transmission in humans is the fact that over 95% of identified cases of vCJD are in Britain, which suffered a mad cow disease epidemic in the mid-80s. There are very few cases of vCJD. In Britain in 2005, 5 people died from vCJD. There are currently 5 people alive with vCJD in Britain.
You might notice that the connection between BSE and vCJD isn't proven and that "there are very few cases of vCJD." Dementia, personality changes, hallucinations, speech imparement, seizures? ONE case of vCJD is one too many. I shudder at the thought of contracting this disease, let alone someone I love. The kids are disappointed -- adiós burgers -- but no more beef.
I'll miss you, but I'd miss my mind more.