Dr. M.C. Diffin
mdiffin at crc.ac.uk
Thu Apr 21 22:30:45 EST 1994
In article <766750192snz at chatham.demon.co.uk> ohgs at chatham.demon.co.uk writes:
>In article <2ovkb3$brg at scratchy.reed.edu>
>That is rather my point. I am aware of no repeatable procedure bu which BSE
>can be induced in other cows: prehaps I am wrong. Lots of animals get
>encephalopathies - not least as a consequence of getting old - and to equate
>sick cows and kudu with a proof of an infectious agent is tendencious.
>I have no idea what causes BSE. There have, however, been over 3000 recorded
>cases since the use of animal protein in feeds has stopped; there were cases
>in cows which were not fed concentrates (cross-bred dairy beef); and calves
>are getting it. Perhaps it can be passed mum-to-offspring; or perhaps it is
>inherited. To call it a "prion" is to call it a "thingie" unless one can
>establish the same level of reproducibility that is supposed to be associated
I quite agree that a causative link between BSE and sheep brain ingestion has
not been demonstarted. However, the justification for terming the putative
infectious agent 'prion' is postmortem pathology, not reproducibility of
infection. Don't forget that Gajdusek (in the early days of prion [as we now
call them] reaserch) had great difficulty in developing an animal model and
achieving transmission. Further, the incubation period may be very long and a
diagnosis is only really possible after death.
Apart from the characteristic histopathology, prion related protein (PRP) can
be isolated from the brains of animals which suffered from this class of diseases.
Admittedly this is far from absolute proof for the existence of prions and
their role in the spongiform encephalopathies, but it seems to me the best that
can be done with current information.
JANET: mdiffin at uk.ac.mrc.hgmp PHONE: +44 (0)345 333111 Pager No. 0406653
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