USDA Chief Veterinary Officer On BSE Case

If you cannot trust the USDA... oh wait.. nevermind.

ammoniated beef i.e. LFTB's aka pink slime, does not kill the mad cow disease agent. you cannot cook the mad cow disease agent out of your meat. you cannot kill the mad cow agent on your surgical and dental instruments i.e. standard autoclave does not kill the TSE PrPSc prion agent. atypical L AND H BSE are transmissible to humans (Fong et al), with L-BSE having a 50 percent shorter incubation period. L-BSE and TME, there seems to be a link. if so, that would mean that L-BSE in N-USA for decades

Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease.

We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.

transmissiblespongiformencepha­lopathy.blogspot.com/2012/11/t­ransmission-of-new-bovine-prio­n-to.html

rare disease is “not generally associated with an animal consuming infected feed.”

The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown, one of the world’s experts on this type of disease who retired recently from the National Institutes of Health. "(The agency) has no foundation on which to base that statement.”

“We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an official with the USDA during the Clinton Administration now at Mississippi State.

Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.

*** It also suggests a similar cause or source for atypical BSE in these countries.

neuroprion . o r g

Spontaneous BSE has been shown and documented in several peer reviewed and published research papers. Spongiform encephalopathies arise from a misfolding of endogenous proteins in the nervous system. These proteins then act as a template causing others to misfold leading to destructive amyloid plaques. Spontaneous spongiform encephalopathies arise when this happens spontaneously. The weight of the scientific community accepts this. There are still experts who deny global warming too.

That is a response to the question. To draw out the implications that I perhaps answered to subtly, the relation of risk between the disease stated here (BSE), what I eat (in this case beef) and my health (the possibility of a single animal entering the food chain causing nvCJD in a single individual, much less me being that individual) is almost non existent. The question as you phrased it is too broad and naive to deserve a response outside of the context in which it was asked.

Thanks for skirting the question. Good luck.

i'm saying, and i am agreeing with Paul Brown, spontaneous BSE is a myth. never proven nor documented in any natural field case. i also don't believe that 85% of all CJD i.e. sporadic, is spontaneous. feed IS a factor for atypical BSE. atypical BSE is transmissible orally. nothing spontaneous about that...to believe that atypical BSE is a spontaneous happening, or to believe that 85%+ of all human TSE i.e. sporadic cjd is spontaneous, is a myth, one that continues to help spread this disease.

I really feel the risk factor for contracting nvCJD from eating beef, especially considering the low rate of occurrence of BSE, is negligible and therefor will continue to eat beef without prejudice. Seriously.