European protectionism

[Doug Henwood]

James Heartfield wrote:

>In message <p05010408b6ebca11ee8e@[216.254.77.128]>, Doug Henwood
><dhenwood at panix.com> writes
>>
>>James, do you still think there's no risk to humans from mad cow disease?
>
>Well, yes, this was recently confirmed by some Cambridge scientists here
>in a TV report. Bovine Spongiform Encephalitis and Creutzfeld Jakob
>Disease are, as far as anyone can tell, not directly related.

Best tell the Centers for Disease Control, which says 
<http://www.cdc.gov/ncidod/diseases/cjd/bse_cjd.htm>:

>Since 1996, evidence has been increasing for a causal relationship 
>between ongoing outbreaks in Europe of a disease in cattle, called 
>bovine spongiform encephalopathy (BSE, or "mad cow disease"), and a 
>disease in humans, called new variant Creutzfeldt-Jakob disease 
>(nvCJD). Both disorders are invariably fatal brain diseases with 
>unusually long incubation periods measured in years, and are caused 
>by an unconventional transmissible agent.
>
>Although there is strong evidence that the agent responsible for 
>these human cases is the same agent responsible for the BSE 
>outbreaks in cattle, the specific foods that may be associated with 
>the transmission of this agent from cattle to humans are unknown. 
>However, bioassays have identified the presence of the BSE agent in 
>the brain, spinal cord, retina, dorsal root ganglia (nervous tissue 
>located near the backbone), and the bone marrow of cattle 
>experimentally infected with this agent by the oral route.

and at <http://www.cdc.gov/ncidod/diseases/cjd/bse_cjd_qa.htm>

>[Q] What is the new variant form of CJD that the experts in the 
>United Kingdom believe might be related to the BSE outbreak in 
>cattle?
>
>[A] In contrast to the classic form of CJD, the new variant form in 
>the United Kingdom predominantly affects younger persons (median age 
>at death: 27.5 years as of October 2000), has atypical clinical 
>features, with prominent psychiatric or sensory symptoms at the time 
>of clinical presentation and delayed onset of neurologic 
>abnormalities, including ataxia within weeks or months, dementia and 
>myoclonus late in the illness, a duration of illness of at least 6 
>months, and a diffusely abnormal non-diagnostic electroencephalogram.
>
>The characteristic neuropathologic profile of new variant CJD 
>includes, in both the cerebellum and cerebrum, numerous kuru-type 
>amyloid plaques surrounded by vacuoles and prion protein (PrP) 
>accumulation at high concentration indicated by immunohistochemical 
>analysis.
>
>Recently published data show an increasing trend for the epidemic of 
>new variant CJD in the United Kingdom. A listing of monthly updated 
>numbers of new variant CJD cases in the United Kingdom is available 
>at: http://www.doh.gov.uk/cjd/cjd_stat.htm.
>
>
>[Q] Is there evidence directly linking this newly recognized variant 
>of CJD to BSE exposure?
>
>[A] There is strong epidemiologic and laboratory evidence for a 
>causal association between new variant CJD and BSE. The absence of 
>confirmed cases of new variant CJD in other geographic areas free of 
>BSE supports a causal association.
>
>In addition, the interval between the most likely period for the 
>initial extended exposure of the population to potentially 
>BSE-contaminated food (1984-1986) and onset of initial new variant 
>CJD cases (1994-1996) is consistent with known incubation periods 
>for CJD.
>
>An experimental study reported in June 1996 showed that three 
>cynomologus macaque monkeys inoculated with brain tissue obtained 
>from cattle with BSE had clinical and neuropathological features 
>strikingly similar to those of new variant CJD (Nature 
>1996;381:743-4).
>
>A study published in 1996 indicated that a Western blot analysis of 
>infecting prions obtained from 10 new variant CJD patients and 
>BSE-infected animals had similar molecular characteristics that were 
>distinct from prions obtained from patients with other types of CJD 
>(Nature 1996;383:685-90).
>
>Interim results of an ongoing experimental study involving 
>inoculation of a panel of inbred mice with the agents causing BSE 
>and new variant CJD substantially increased the strength of the 
>scientific evidence for a causal association between new variant CJD 
>and BSE (Nature 1997;389:498-501).
>
>Two additional groups of inbred mice and a group of cross-bred mice 
>inoculated with brain homogenates from new variant CJD cases were 
>also reported to have had latency periods and lesion profiles 
>consistent with the BSE pattern (Bruce, pers. comm. 2000).
>
>The latency period, neuropathology, and disease-causing PrP isoforms 
>in transgenic mice expressing bovine PrP that were inoculated with 
>new variant CJD, BSE, and scrapie brain extracts provided additional 
>evidence supporting the link between BSE and new variant CJD (Proc 
>Natl Acad Sci 1999;96:15137-42).