Index Home About Blog
Subject: Re: AngryBurgers & Black H*l*c*pt*rs
From: Ian A. York
Date: Mar 30 1996
Newsgroups: alt.folklore.urban

Well, there seems to be the usual feeding frenzy, so on the off chance 
that anyone cares I'm posting here a collection of BSE and prion stuff that 
I happen to have written and collected from one of my mailing lists over 
the past few days.  Mostly I'm just passing on the information, so don't 
write and ask me for more; I probably won't have it.

This being off-topic for afu, I've set followups to sci.med.

By the way, Stephan Zielinski's post is pretty much accurate, as usual.

There are also a number of excellent prion and BSE sites on the web.  Try

http://www.kcc.com.msu.edu/CAI/Pathology/cns_infections
http://www.airtime.co.uk/bse/welcome.htm
http://www.nmia.com/~mdibble/prion.html
http://www.iah.bbsrc.ac.uk/institut/public/3wtse.htm
http://www.cowtown.org/nca4315.html

Table of contents:
1.  Wot's a prion?  by moi.
2.  Handy question-and-answer format BSE thingie, by Mike Painter
          Consultant in Communicable Disease Control,
          Manchester and member of the Spongiform
          Encephalopathy Advisory Committee (SEAC)
3.  The Institute of Food Science & Technology's Position Statement 
    update of 27 March 1996. 

A field guide to the prions ...

This is pretty much off the top of my head, so don't take it as carved in
stone. 

Wot's a prion?  It's the cause of a number of animal diseases which have 
in common a slow course, a lack of an immune response, and 'spongiform 
encephalopathies" - the brain gets holes appearing in it so it looks 
like a sponge under the microscope.  Prions are apparently unique among 
infectious thingies in that they're solely protein - there's no nucleic 
acid (i.e. RNA and DNA) involved.  The word was coined by Stan Prusiner 
and it's short for "proteinaceous infectious" particle, which should 
therefore be "proin" but that didn't sound so good so he changed it to 
prion.  (T).  

There are a bunch of prion disease.  The most common is a sheep disease
called "scrapie".  Bovine and mink and a couple others get 'bovine (or
mink) spongiform ecephalopathies".  In humans, there's Kuru, and there's
Creutzfeldt-Jacob disease, fatal familial insomnia,
Gerstmann-Straussler-Scheinker Syndrome, and some others that don't have
names as far as I can find. 

They're all fatal.

Most importantly, prion protein is a normal component of normal cells.  
All of you are happily churning out prion proteins by the billion right 
now.  Actually, you're churning out prion precursor protein - the normal 
protein is innocuous (although its functiuon is unknown, it's presumably 
required for normal cell function).  When something changes the protein 
to another form then it becomes Evil.  

There are fundamentally three causes of prion protein changes.  (1)  
Spontaneous. No cause known.  There may be a precipitating event or it 
may be a truly random event.  This is very rare - something like 
1/1000000 or less - but is probably the most common cause of prion 
diseases in humans.  (2)  Inherited mutations.  Note that it is, for 
example, fatal FAMILIAL insomnia.  (3)  Infection.  

What seems to happen is that the prion protein can exist in two forms, but
that form 2 (the dangerous one) causes form 1 to convert to form 2.  In
other words, a catalytic feedback reaction.  Hence, the infectious nature.
The familial cases occur because there's a mutation that makes the protein
more likely to assume position 2.  In fact, even spontaneous diseases are
infectious - that is, if someone has CJD from a spontaneous change, the
prion particles from that person are infectious (catalyze the formation of
type 2), even though she was not infected originally.  If you see what I
mean. 

For example, CJD may be sporadic (case 1), familial (case 2) or 
iatrogenic (case 3).  

Recently it was shown that yeast have an analagous process (although it's 
not fatal in yeast) in which a normal yeast protein has two switch 
positions and position 2 converts position 1 to position 2.

It's common for the prions from one species to be able to infect another
species, but it's not inevitable.  Thus scrapie agent (from sheep) can
infect a number of lab rodents; but it's not very infectious at first, and
takes some acclimatization for it to become very infectious in that
species.  Scrapie agent probably originally caused BSE (that's not
certain) and probably originated the mink encephalopathy as well.  On the
other hand, scrapie has been around in sheep for a long time, and there's
never been any epidemiological evidence that scrapie agent would infect
humans. (And people have looked very hard for such a link.) This is one
reason it was originally believed that BSE was unlikely to infect humans. 

One thing about prions is that they're incredibly hardy.  You can't
destroy them with anything, including autoclaving.  (Actually, autoclaving
will eventually destroy them, but it takes a long, long time.) They can
also be present in very high levels, so you can destroy 99% of them and
still be left with billions of infectious particles.  This isn't entirely
unique in proteins - there are some other proteins which can be boiled and
autoclaved and still be functional.  For example, the purification
protocol for the RNase A protein begins "boil a pancreas in sulpheric acid
..." 

The infection process is poorly understood.  In the lab animals infected 
with scrapie agent, it's known that the particles have a blood phase, 
collect in the spleen briefly, then infect the brain and start causing 
gradual problems.  The blood and spleen phase is less easily found in 
some other cases, and apparently in BSE it's very difficult to show this 
at all.  In BSE essentially all the prions are found in the brain and 
spinal cord.  

And that about sums up the current knowledge.  They're a bitch to study -
the process is slow, so you're looking at years for a single experiment
often, and until recently it was difficult to mimic the human processes in
lab rodents.  Until recently, also, there wasn't a great deal of interest
in them - these are very rare sporadic human diseases, and until BSE and
the fear of spread to humans there was little funding for the work. 
(Another argument against directed research?) Also people had to assume
that the first time you used the damn things your whole lab was thereafter
forever a scrapie lab, because you can't disinfect them. 

(You can, actually, disinfect them; but the process is not 100% effective 
- it's more like 99.99 - 99.99999% effective, which can still elave the 
odd prion hanging about.)

There's no BSE in the US or Canada because of stringent import and 
slaughter procedures. 

=========================================================

Here's some BSE info in the popular and convenient question-and-answer 
format.

SPONGIFORM ENCEPHALOPATHY: HUMAN CASES LINKED TO BSE? (5)
=========================================================


Briefing document, forwarded from Mike Painter, with permission.

Martin Wale
Regional Epidemiologist (desig)
Nottingham, England

>From:     Mike Painter
          Consultant in Communicable Disease Control,
          Manchester and member of the Spongiform
          Encephalopathy Advisory Committee (SEAC)

Subject:  CJD/BSE

Date:     22 March 1996

Dear Colleague,

I have put together some thoughts about what has happened which
you might wish to circulate to CCDCs and other interested people
in your area.

I must stress that the views and interpretations are mine and
should not be taken as any form of official comment from
Department of Health, MAFF or SEAC.

As you will be aware SEAC is due to meet again this weekend and I
would hope to be able to communicate with you again after that.

Best wishes.

Mike


1. What exactly has happened?
     The CJD Surveillance Unit in Edinburgh has identified a      
     distinctive brain pathology in some people with CJD that
     appears to be different from anything seen before.

     The key histological feature is the presence of a number of
     multi-centric amyloid plaques present in all sections examined.
     The appearance of these plaques is distinct and has not been
     found in sections taken from people with "classical" CJD.

2. How many cases have there been?
     To date ten.

3. Over what time period?
     The dates of onset of symptoms range from early 1994 to late
     1995.

4. What is the age range?
     The majority are clustering around the mid to late 20s.  Two
     are in their late teens and one is in their early 40s.

5. Is there any geographical clustering?
     Nothing evident but the number of cases is still very small.

6. Have all the cases died?
     No, two are still alive.

7. Is this the forerunner of a massive epidemic?
     Not surprisingly this is impossible to say.  At the moment I
     personally doubt if there will be hundreds of thousands of cases
     but I would be surprised if we didn't see any more than ten.  I
     have no idea what the figure will finally be.

8. Is this new pathology due to eating BSE contaminated beef?
     We really do not know but the fact that this pathology has
     not been described before leads you to the conclusion that a new
     risk factor has appeared.  What that might be is not known but
     taking into account a possible incubation period of, say, 8 - 10
     years the most likely explanation is that it is due to exposure
     to the BSE agent.

9. How could the BSE agent have got into human food?
     Again we cannot be sure.  Muscle tissue has not been shown
     to transmit the BSE agent in any of the transmission studies so
     far reported.  In contrast, high titres of infectivity have been
     demonstrated in brain and spinal cord and the reticuloendothelial
     system.

     One explanation could be that bits of the CNS got into some
     meat products such as burgers or pies.  Whether a case control
     study will ever be able to prove this only time will tell.

10. Does the risk still exist?
     In 1989 a ban was put on CNS, tonsils and spleen from cattle
     aged over 6 months and thymus, intestines and vertebral columns
     of cattle of any age from entering the human or animal food chain
     (this is the Specified Bovine Offals ban or SBO).

     Last year the ban was extended to meat that had been
     mechanically recovered from vertebrae.

     Taking this, plus negative transmission studies from muscle,
     into account it is fair to say that the risk from eating beef in
     1996 has to be many orders of magnitude less than it was
     pre-1989.  Whether that now equates to zero risk is impossible to
     say but it is enough for me not to stop eating beef.

11. Doesn't the appearance of these cases mean that the idea of
    controlling spread by banning SBOs was wrong?
     Not necessarily.  It is clear that enforcement of the SBO    
     ban was initially not as fully implemented as it should have been
     but this has now been addressed.

12. Shouldn't a total ban be put on the consumption of beef?
     There is no evidence of infectivity in those parts of the    
     animal now entering the human food chain.  I would find it
     difficult to defend a total ban on the available evidence.

13. Isn't it better to be safe rather than sorry though?
     We come back to the idea of "zero risk" which is appealing
     but in practice is extremely difficult, if not impossible, to
     achieve. In a crisis it is difficult to avoid responding in a
     purely emotional way but I believe a measured, logical response
     does bring about the most satisfactory outcome.

14. Should people who have eaten meat products like burgers or
    meat pies be worried?
     People are naturally going to be worried and it is
     impossible to give them any absolute reassurance.  All I can say
     is that I think it unlikely that there would have been such a
     degree of contamination prior to the SBO ban that there will have
     been a major risk to an individual.  However, even a very small
     individual risk could still add up to a sizeable population
     attributable risk.

     Since the initial SBO ban the risk of contamination will
     have got progressively less as the ban became effective and the
     number of infected cattle in the country fell.

19. Is it safe to let children eat beef?
     Although transmission studies do not show any infectivity in
     muscle it might still exist below the limits of detectability.
     The fact that children are still growing and, because of their
     age, could have a longer lifetime exposure than adults has raised
     this important query.  At the moment SEAC have not changed their
     advice and there is no recommendation of any restrictions on
     children.  This subject is due for detailed discussion again this
     weekend so watch this space.

20. As 80% of cases of BSE have occurred in dairy cows isn't
    there any risk from drinking milk?
     It has not been possible to transmit the BSE agent from milk
     taken from affected cows so as far as anyone can judge there is
     no risk from milk.

21. Is there a screening test to detect people who may be
    infected?
     No.

22. What about the test being developed by Dr Narang?
     I haven't seen the details of the test's sensitivity and
     specificity so I can't say whether it would be suitable for
     screening for a disease which has a prevalence of 1 in a million.
     A specificity of even 99.95% would still throw up 500 false
     positives for every true case and the effect of that on the 500
     would be catastrophic.

     If and when a suitable screening test does become available
     I have no doubt its application will be looked at as a matter of
     extreme urgency.

23. Is there a screening test to detect people who might be at
    increased risk because of a genetic predisposition?
     No.

24. Is it likely that there might be a risk of humans catching
    scrapie from sheep?
     Scrapie has been in the sheep population for at least two
     hundred years and has never been known to transmit to humans.
     There is absolutely no reason to suppose this has changed.

25. Is it not the case that sheep could have been fed the same
    kind of infected feed that caused the problem in cattle?
     This is a distinct possibility and transmission experiments
     have also shown that it is possible to transmit the agent
     obtained from cattle to sheep.  However, the pattern of scrapie
     in sheep does not seem to have changed recently so there is no
     evidence that they are now a problem to humans.  MAFF are
     continuing to monitor scrapie in flocks and SEAC are kept up to
     date with all information.

26. Why was no action taken before this week?
     CJD is a very rare disease and is monitored by clinicians
     informally reporting cases to the CJD Surveillance Unit in
     Edinburgh.  Confirmation of the diagnosis can often only be made
     by a post mortem examination.  When the different pathology was
     first noted it was not clear whether this was a normal variation
     possibly related to the younger age of the cases.  As more cases
     with the same picture were detected it became clear that this was
     probably not a normal variation.  Because of the importance of
     the findings the doctors involved wanted colleagues to check
     their findings.  Only when this had been done and a consensus
     view emerged that this was new did SEAC advise the Government
     that the information should be made available to the public.

27. Is it likely that there will be person to person spread?
     No. People with CJD have never been shown to be able to      
     transmit the agent to other people. There have been instances
     when the agent has been transmitted via surgical instruments used
     for taking brain biopsies but this is not the same as normal day
     to day activity.  There is no reason to suppose that this newly
     described form is any different in this respect.

28. What should I say to a GP who has a worried patient?
     If the person is otherwise fit and well they should be given
     the information stated above and informed that it is very
     unlikely that they will suffer any BSE related disease.  If the
     person is suffering from a neurological condition suggestive of
     CJD then the GP should seek an opinion from a local neurologist.
     Neurologists are aware they can get advice from the clinicians at
     the CJD Surveillance Unit in Edinburgh.

29. Should any special precautions be taken by people working in
    butchers' shops or abattoirs?
     There have been no cases of the "new" CJD amongst abattoir
     workers who you would suppose would be most at-risk. However,
     SEAC has advised that HSE should reconsider safety measures in
     the industry as a matter of course.

30. Aren't farmers at extra risk of CJD?
     It is true that farmers as a group appear to have an excess
     number of cases of CJD. However, there are still only a very
     small number of them and the same excess has been seen in
     countries where there is no BSE.   None of the ten cases of "new"
     CJD is a farmer.

31. Couldn't this increased rate in farmers be due to something
    not connected with BSE such as pesticides?
     It is plain that something must be causing the effect in
     farmers but we do not know what it is.  Pesticides have been
     suggested but once again there is no evidence that they are to
     blame.

32. What exactly is the cause of BSE?
     The debate still goes on to define exactly what the nature
     of the agent is.  A substantial body of opinion holds that it is
     caused by a prion which is a small glycoprotein devoid of nucleic
     acid but which can somehow invoke the production of a special
     kind of protein in the CNS of susceptible people.  There is
     another school of thought that holds that the cause is actually
     some kind of virus.  It is not possible to visualise the agent
     although its handiwork is only too apparent.

33. What about inactivating the BSE/CJD agent?
     This is very difficult because it is resistant to all the
     usual measures including hypochlorite, normal cooking
     temperatures, ultra violet light and weak acids.

====================================================

IFST POSITION STATEMENT ON BSE, UPDATE 27 MARCH 1996
====================================================

Herewith, as promised, the Institute of Food Science & Technology's
Position Statement update of 27 March 1996.

BOVINE SPONGIFORM ENCEPHALOPATHY (BSE)


The Institute of Food Science & Technology, through its Public Affairs
and Technical & Legislative Committees, has authorised the following
Position Statement, dated 27 March 1996, updating the previous
Statement of 6 February 1996, and replacing any previous version :-

Summary

BSE is an extremely serious disease of cattle, the eradication of
which is of primary importance to safeguard herds, and hence future
supply of dairy and bovine meat products for the human and pet food
chains, together with important bovine by-products.

For there to be any risk to humans consuming beef, two conditions
would both have to be fulfilled: that BSE could be transmitted from
cows to humans; and that parts of the animal capable of carrying the
infective agent could enter the human food chain.

As to the first, there is no direct scientific evidence that BSE can
be transmitted from cows to humans, and some research evidence
suggesting that it cannot. Nevertheless, the emergence during the past
two years of ten anomalous cases of Creutzfeldt-Jakob Disease (CJD) in
a previously unrecognised pattern, led, in the absence of other
explanation at present,  to the conjecture  that they were likely to
have been caused by exposure to infected cattle brain or spinal cord
before 1989 (at which time they were banned from the food chain) and
to a judgement that, if  there is any risk to humans, it is extremely
small, and no greater for children, hospital patients, pregnant women
or  people who are immuno-compromised.

As to the second, muscle meat and milk have been shown to be incapable
of carrying the infective agent, and measures have been taken, and
strengthened, to exclude from the food chain certain parts of the
animal, including all those parts shown to be capable of carrying the
infective agent.  These measures require the most stringent
enforcement and heavy penalties for evasion.

Having regard to the present scientific evidence, therefore, and
provided that the above measures are fully implemented, muscle meat of
British beef would appear to be without risk of causing CJD.

As regards animal health, successful measures have been taken, and
strengthened,  to reduce the incidence of BSE in cows and these are
expected to lead to the virtual elimination of the disease.

On the basis of present scientific knowledge, no further measures are
needed. If additional measures are taken, it will be for other than
scientific reasons.

While that sums up the present state of knowledge, scientists always
have to keep open minds. They have to act on existing knowledge while
recognising that further research will bring new information and
knowledge, which may in turn lead to revised conclusions. We welcome
the undertaking to devote substantial extra resources to research in
this field.

Background

Bovine spongiform encephalopathy (BSE) is a fatal brain disease of
cattle which has only come to light in recent years, having been first
recognised in the UK in 1986.  The disease is caused by an
unconventional infectious agent, originally described as a 'slow
virus', a 'self-replicating protein' and more recently as a 'prion'
(PrPsc) an aberrant conformation of normal protein (PrPc). Research is
increasingly supporting Prusiner's hypothesis, whereby  a prion
molecule contacts a normal PrPc molecule in the membrane protein of
the brain, and induces it to refold into the aberrant conformation,
and molecules so formed go on to do the same to other normal PrPc
molecules, thus creating further replicas  from normal protein.

Scrapie in sheep, BSE in cattle and CJD, a rare brain disease in
humans, are all neurodegenerative disorders thought to be transmitted
by such proteinaceous infective agents. These infective agents have
many similar common characteristics.

The incubation period in cattle is very long, commonly 3-5 years (but
the range can be considerably wider), and there were fears that meat
and milk from cattle which were infected with the agent (but not yet
showing clinical signs of the disease) could enter the human food
supply chain and transmit the disease to man. Such fears have been
repeatedly exacerbated by alarmist publicity in the media, by news of
bans on UK beef applied from overseas and by a dearth of easily
assimilated and verified information. The most recent developments
have been wrongly assumed to implicate beef muscle meat.

Independent and UK Government experts considering the problem from
1988 up to the present have judged that the chance of man becoming
infected in some way through meat or milk from BSE infected cattle
were extremely remote, this view being endorsed by the House of
Commons Agriculture Committee in their 1990 report and by the
Southwood Committee set up in 1988 specifically to consider the BSE
problem.  Other experts and perceived experts were not so convinced
and expressed varying degrees of concern.

Even with the latest developments, the Spongiform Encephalopathy
Advisory Committee of independent experts (SEAC), which advises the
Government, and which made recommendations to strengthen the
precautionary measures,  concluded that "If the recommendations are
carried out the Committee considers that the risk from eating beef is
now likely to be extremely small" including for children, hospital
patients, pregnant women and people taking immuno-suppressive drugs.

- --
J Ralph Blanchfield
e-mail: jralphb@easynet.co.uk


-- 
      Ian York   (iayork@panix.com)  <http://www.panix.com/~iayork/>
      "-but as he was a York, I am rather inclined to suppose him a
       very respectable Man." -Jane Austen, The History of England

From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cow Disease  A WEB PAGE
Date: Mon, 25 Mar 1996 11:46:03 +0000

In article <4j3qom$gjj@news.uni-c.dk>, Torsten Brinch <iaotb@inet.uni-
c.dk> writes
>
>The URL is not correct. Please try this one:
>
>http://inet.uni-c.dk/~iaotb/bse.htm
>
>=: Its informative.

Dear Torsten,

I am very sad and dissapointed, having read this page which appears to
be written by your goodself. You always appeared to be honest and
careful that the data you passed on was accurate and essentially true.
Having read some of this URL, I now doubt some of the things you have
said in the past. Your 'report': BSE is a new disease. Is riddled with
inaccuracies (I put it no strongly out of politeness) and innuendo. I
will give a few small examples as a full critique would be too lengthy.

Prior to 1987:

"Scrapie was thought of as a disease that did not affect humans."
Scrapie was KNOWN to be a disease that did not infect humans.
This is one of the few things we can be absolutely sure about.

"Meat & bone meal was fed to cattle to increase their milk yield"
It was included in feed as a cheap source of organic phosphorus and to
replace fishmeal as a high quality protein source. For reasons of
commercial confidentiality, few (if any) farmers in UK were aware that
this was happening as feed ingredients were not disclosed.

"By the direction of MAFF, a change had taken place in the way (M&B
meal) was made in the early 80's."
MAFF did not direct. The new process was allowed to reduce fuel costs
since it was shown to be as effective (bacteriologically) as the old
one. Because animal fats were of low value the solvent extraction phase
was removed. Reducing energy usage was, and is, regarded as important
for energy conservation reasons.

1991
"Fears arose that BSE would also infect the rest of Europe because we
had exported infected animals there."
Fears arose in Europe because thousands of tonnes of British meat & bone
meal had been exported to Europe.
Note that the growth hormone mentioned has long been known as a source
for CJD because it is produced from pooled HUMAN blood.
The 'mad calf syndrome' referred to seems to have been the only one. At
least I have never heard mention of others and at any rate if it occurs
at all, it is at quite exceptionally low levels.

1992
"Only 85% of cattle reported as BSE turned out to be that ..."
Why 'only'? Indicative of the high level of care taken by farmers and
vets to ensure that no animals that might have BSE escaped the disposal
system. Better a few false positives than one should slip through the
net, wouldn't you agree?

1994
"Animal protestors tried to stop the export of calves..."
Because they were being exported to be reared in calf pens, and fed only
on milk. This system is banned in UK for ethical reasons. 

"It is admitted that, of 156 cases of CJD since 1990, 22 are believed to
have given blood."
What has this to do with BSE? I would expect this to be typical
worldwide. Perhaps people should stop accepting blood transfusions or
what?

1995
"In fact, around 90% of the dairy cattle in the UK turned out being in
an infected herd ..."
In fact the London Times today (25/3) quotes that 54% of dairy herds
have had one or more cases.

".. it seemed that the disease was, by 1988 running out of cattle to
involve."
Pure rubbish. Out of a herd of 4,000,000 the average number per year is
16,000 or so. On the face of it infection rate of under 1/2 of one
percent.One can jiggle the numbers around a bit but certainly under 5%
at worst. Basically it's not very infectious even for cattle eating
infected feed. This should hardly surprise anybody, most diseases don't
have very high infection rates. The fact that maternal transmission
doesn't seem to occur to calves is a giveaway of this too.

So what do we have? A lot of panic because it's hard to prove a
negative? Perhaps.

A comment is worthwhile from a friend of mine who has nothing to do with
cattle at all. He asked me why there was so much panic and fear when
10,000 people die in the UK directly due to smoking, yet people still
smoke? Why people drive their cars, and walk along streets when this is
proven to cause death and injury to thousands of people? He said it was
because the risk, however high, was understood. Scare stories bring fear
because of a risk that people can't put into context. The level of the
risk is not important. More people, for example, have been known to have
died of eating inadequately boiled kidney beans than those suspected
might possibly perhaps have got a BSE, yet people still eat kidney
beans. Strange, really.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cow Disease.  What is the truth?
Date: Tue, 26 Mar 1996 18:55:04 +0000

In article <4j6m9l$d6o@mimas.brunel.ac.uk>, Stuart D Neilson
<hssrsdn@brunel.ac.uk> writes
>What is the truth? Who knows? Spongiform encephalopathies 
>can affect all mammals, and in Britain the disease has 
>spread to domestic pets, big cats, ostrich and deer (to 
>name but a few). 

Ostriches is a new one to me. Particularly as they are birds and not
mammals. As far as I am aware no transfer has ever been achieved by
feeding infected matter across species (I am not sure if deer count as
sheep or goats). It can be done with difficulty to special strains of
suceptible mice by injecting infective material directly into their
brains. We should avoid doing this to humans. 

Note particularly that the animal group that has been fed meat and bone
meal throughout at *high levels* is pigs. Not a single case of pigs
getting the disease has ever been reported. (Or chickens either). Guess
which digestive system is most like mans, yup, pigs. Top line boars and
sows DO live a long time, and get the best high protein feed too.

>The most likely source is rendered sheep 
>protein containing the nervous system of sheep with scrapie. 
>Scrapie has been endemic in British flocks for two 
>centuries.

Strange that in those two centuries no cattle ever picked it up although
grazing the same field as sheep, often while they lambed. Strange also
that nobody has been able to transfer scrapie to cattle by *feeding*
scrapie infected material.

>CJD affects not two, but FIFTY people per year in Britain.

Less than one per million people. Ten thousand die directly due to
smoking. How many anr killed and injured on the roads? Perhaps a little
perspective might be in order?

>However, this is the same as other areas studied (one per 
>million of population per year) including vegetarians in 
>India.

So we can't blame the UK deaths on BSE, now can we?

> The mechanism of infection is not known, but may be 
>viral or a prion. Both the suspected viral particle and 
>prions have been found in muscle, milk and urine of affected 
>animals (albeit in very small quantities). 

Wrong. Obviously wrong. If you don't know what is the cause, how can you
detect it? Huh? Duh! This is, in short, a pack of lies. Typical of the
lies^H^H^H misinformation stated as facts. Unfortunately there is NO WAY
of detecting BSE until the animal is visibly affected. Then you kill it
and check a microscope slide of brain tissue. In fact the contrary, all
efforts to show any occurring in milk and muscle (and boy how they have
tried) have been negative. And this is on highly suceptible mice getting
a brain injection. Please try to keep to the facts.

>The number of CJD 
>cases is not statistically in excess of the number prior to 
>the BSE epidemic in British cattle. Scientific evidence can 
>therefore not rule out infection from meat, nor confirm 
>infection at present - 

Oh dear, you try my patience. Of COURSE it shows that there is NO
clinical disease due to other causes *at the moment*. This is one of the
few things that we DO know. Without a test, we can't say more. This is
the problem, fear of the unknown.

>the lack of cases is not sufficient 
>cause to blame "the scientists", although the public 
>presentation of scientific evidence has been woefully 
>indequate.

The information is there. The problem is that no-one is prepared to
believe it for all sorts of reasons. Perhaps it's too complicated for
you to understand? Proving negatives is notoriously difficult.

>The risk from BSE infected meat is probably very small, 

If that is your view given what you said earlier, I guess you are much
less worried now.

>but 
>that is no longer the question. Economics and the 
>international reputation of British farming will determine 
>policy more than science (as it has so far!) - not 
>forgetting also the need to calm a worried population of 
>beef eaters whose shopping habits are bound to change.

Not me. I'm eating lots of cheap steaks and beef. Hey, it's all less
than 20 months old, no animal under 30 months has ever shown clinical
disease, it's as safe as houses in my opinion, even in the worst case.
If a load of ill-informed and press scare-mongered people don't want it,
I'll pick up the cheap quality meat. Yes sir!

>The BSE epidemic in cattle is by no means over - currently 
>around 300-400 BSE infected cattle a week are identified, as 
>compared with 1,000 per week before the feed ban took 
>effect. 

I think you will find it's down to a quarter of the peak (three years
ago), and falling fast.

>Nobody can yet guarantee that beef products 
>(including gelatine, glycerine, tallow, salts, stearine etc, 
>used in food products, desserts, snacks, yoghurt, soap, 
>shampoo and medicines) are safe to eat and use.

Nobody can guarantee that a meteorite will kill you in the next ten
minutes either. However you are going a bit over the top. Unless you eat
shampoo, soap or candles that is. You're not scared of the dark, are
you?

>And yes, the incubation time is 5-15 years in cattle, 

Pretty clever to work out 15 years, we haven't got there yet. One ought
to try to stick to the facts, hard I know.

>although most are slaughtered before the possibility of 
>symptoms. We probably eat two infected cattle for each 
>symptomatic animal removed from the food chain. 

Eh? We almost certainly don't. All quality beef is under 20 months and
they haven't seen a whiff of meat and bone meal since 1989, oops they
weren't even concieved then. So how do they get infected? By rumour? 

>Animal 
>derived protein is still being fed to other animals 
>(including sheep and chicken) - including beef protein.

Not so. Sheepfeed has been meat & bone meal free since 1989. They
probably never had any anyway, who can afford to feed sheep expensive
stuff like that?

>So, although the risk is probably small, there is plenty of 
>rational basis to be scared witless.

No. But there are plenty of IRRATIONAL reasons if you like being
witless.

Have a good day.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cow Disease.  What is the truth?
Date: Mon, 1 Apr 1996 08:32:52 +0100

In article <4jnp8h$mo3@homer.alpha.net>, "Ingrid K. Buxton"
<buxtoni@mixcom.com> writes
>
>... you have hit exactly on the problem with scientific
>investigation... nothing can be proven in the affirmative, ie, is the
>meat safe?, because you can never know if you have the correct
>questions to ask in the first place... I would not trust US to tell me
>if our beef supply was contaminated.. I would only trust another
>country... why dont they have a science exchange program to certify
>whether or not the meat supply is safe?

Nothing is safe. Even water has an LD50, and so does oxygen. Beans
contain many natural toxins and estrogens, cabbages contain carcinogenic
mustard oil etc etc. So if you ask any honest scientist if anything is
absolutely safe, he must always say no. The trouble is that people in
general do not understand this at all. So if a truthful scientist says
no, he is effectively misleading you. Not simple, is it? Whatever you
say, you are effectively not telling the truth.

It's also important to realise that scientists are ordinary people, with
their own aims, foibles, beliefs and failings. Given two items of
information, they may well not agree for other reasons. A vegetarian
scientist might well play up the safety of vegetables and risks of
eating meat, whilst a non-vegetarian may do the reverse. This is why
scientists take very little note of non-peer reviewed publications. When
you have a group of experts in the field agreeing, you are going to be
on very much safer ground. It is also important to note that one expert
may not agree with others. For example Prof Lacey, a british
microbiologist, has been scaremongering since this affair first started
and got a lot of press. For example he said that it would almost
certainly be passed from cow to calf and eradication of the disease by
insituting a feed ban was doomed to failure. The experts disagreed.
Lacey has been proven wrong, but this mode of infection is still
erroniously considered significant.

One oddity that I have noticed in our society for the last few years is
for people to belive obviously biassed laymen, but to disbelieve
experts. So people will belive some vegetarian crank, but disbelive
someone who has been working scientifically in the field for years.
This, IMHO, is absurd. It must be the evangelism of it that sways
people, it's certainly not the logic.


------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cow Disease.  What is the truth?
Date: Mon, 1 Apr 1996 14:56:55 +0100

In article <4jgpql$7us@mimas.brunel.ac.uk>, Stuart D Neilson
<hssrsdn@brunel.ac.uk> writes
>Oz writes:
>"Ostriches is a new one to me. Particularly as they are 
>birds and not mammals. As far as I am aware no transfer has 
>ever been achieved by feeding infected matter across 
>species... It can be done with difficulty to special strains 
>of mice by direct injection to the brain. We should avoid 
>doing this to humans."
>
>You are correct about one thing - information is available, 
>if we are prepared to believe it:

It does pay to read the papers though before misreporting them.

>Transmission of spongiform encephalopathies between species 
>has been demonstrated experimentally by direct injection of 
>brain homogenate to the brain, by oral ingestion and by 
>introduction to the tear duct in experiments dating back to 
>1968. 

But nobody worried about scrapie as a possible danger to health since an
experiment lasting 200 years had shown it not to be a problem. On the
other hand HUMAN transplants were known to offer a significant risk. So
what does this suggest to us?

>For instance "[the BSE agent] has now been 
>experimentally transmitted to sheep, goats, pigs, mice, mink 
>and marmoset monkey" - WJ Patterson and S Dealler (1995) BSE 
>and the public health. Journal of Public Medicine 
>17(3):261-268.

They also say "However, it is also concievable that the epidemic
developed from unrecognised BSE infection in British cattle." and go on
to indicate how the epidemic would have occured. This is in keeping with
all the natural epidemics we know about, kuru, scrapie, wasting disease
of mule deer and elk, and transmissable mink encephalopathy. All cause
by cannibalism. This would mean that consumption of BSE animals has been
occuring, probably for centuries, without increasing CJD above the level
found in vegetarian societies.


>Ostriches (fed with animal protein supplements) have 
>developed spongiform encephalopathy. 

You conveniently omit to mention that the Ostriches concerned were from
two WEST GERMAN zoos, the first dying in 1986. "A conclusive diagnosis
could not be made and toxic or nutritional aetiology could not be
discounted." It would be most unlikely in the extreme that these animals
would have been fed british animal feed, to say the very least.

>"Since 1986, 
>scrapie-like spongiform encephalopathy has been diagnosed in 
>19 captive wild animals of eight species at zoos in the 
>British Isles... nyala, eland, greater kudu, gemsbok, 
>Arabian oryx, scimitar-horned oryx, cheetah and puma. Three 
>cases of spongiform encephalopathy of unknown aetiology have 
>been reported in ostriches" - JK Kirkwood and AA Cunningham 
>(1994) Epidemiologic observations on spongiform 
>encephalopathies in captive wild animals in the British 
>Isles. Veterinary Record 153(13):296-303.

This reference is worth reading, since it is so often misinterpreted.

Most (including several herbivors) come from one zoo where the carnivors
were fed on knacker meat, including heads of cows and horses. They also
appeared to dispose of dead kudu etc by tossing them in the carnivore
enclosure. On top of that the knacker meat for the carnivors was carried
through the enclosure containing the herbivors and 'some contamination
could have occurred'. Two feral cats that scavenged the carnivor
enclosure got TE too and I personally wonder how many scavenging feral
cats were caught by the big cats. There is also a case to be made that
at least one family of herbivors may have had a genetic predisposition
similar to the one shown by scrapie sheep breeds.

In short it shows little except that there are a lot of possible routes
for cannibalism to occur if you aren't careful. It would certainly be
foolhardy to draw any conclusions from it. It's an excellent peice of
work.

Personally, I suspect that at least some of the herbivors, many of which
ate commercial cattle feed daily, did in fact catch the TE from the
infected feed in the same way that domestic cattle did.

>The pig is most certainly not immune, either to transmission 
>by direct injection to the brain or to transmission by oral 
>ingestion. Eg: M Dawson, GAH Wells et al (1990) Primary 
>parenteral transmission of BSE to the pig. Veterinary Record 
>127(13):338-338.

You should READ the paper. They managed to infect some of their pigs by
'extremely high exposure' of hightly infective BSE extract. They did it
by three SIMULTANEOUS doses given inside the body cavity, directly into
the bloodstream AND by direct injection into the brain. Note: NOT 'or'.

>As I stated before, the infectious agent has not been 
>identified. 
>A number of candidate infectious agents have 
>been identified. Infected brain tissue can infect other 
>animals, but transmission has not been demonstrated with 
>isolated candidate infectious agents. Two candidate 
>infectious agents (prions and "viroids") are ubiquitous in 
>the tissue of affected animals, 

All the references I have state the opposite. "No infectivity has been
found in muscle, milk, udder, placenta, liver, kidney, blood, bone
marrow, spleen, lymph nodes, semen and a range of other tissues from
cows confirmed to have BSE". SEAC Sept '94. A similar, but much longer
list, as published by CEE Directorate-General for Agriculture in '94.
(EC body).

>but the highest 
>concentration is in the brain and CNS.

Certainly. That's what everyone is saying, isn't it?

Currently there is only one country I know of where brain and other
suspected infectious material is kept out of the human food chain, and
where an extremely effective detection and disposal system is in
operation for trapping infected animals, and that is Britain. 

In other countries a draconian slaughter policy that is totally
inappropriate for a disease that doesn't spread from animal to animal is
in operation, if they have any policy all. This almost certainly results
in severe financial hardship to the farmer concerned giving him an
excellent reason to cover up any cases he comes across. This does not
fill me with confidence to buy beef from other countries, particularly
when large tonnages of infected meat and bone meal were exported
elsewhere from britain.

It may turn out that there was a very small risk in the late 1980's, or
again maybe none at all. We will have to wait to find out. What I,
personally, am sure is that with the stringent controls now in place
British beef is the safest in the world as far as BSE is concerned.
Everyone must make their own mind up about the risks, and weigh up the
evidence themselves, but that's my personal view.

It would be ironic if, in a few years time, British Beef commanded a
premium because it was the only beef that one could be sure was BSE
safe. Poetic justice indeed!

It is interesting to note that Sainsbury's, one of Britain's most
respected and largest supermarket chains (that specialises in quality
meat in particular), announced it was selling beef at half price. They
were sold out completely in a day and had many unhappy customers who had
to go away empty handed. Perhaps the ordinary British person is not
quite so easily swayed by scare mongering stories in the press as one
might believe from the media.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cow Disease.  What is the truth?
Date: Mon, 1 Apr 1996 15:13:15 +0100

In article <eu64tr8x9l3.fsf@ferguson.cogsci.ed.ac.uk>, Janet
<janet@cogsci.ed.ac.uk> writes
>In article <qjdnXCAI2DWxEw7y@upthorpe.demon.co.uk> Oz <Oz@upthorpe.demon.co.uk> 
>writes:
>
>   >although most are slaughtered before the possibility of 
>   >symptoms. We probably eat two infected cattle for each 
>   >symptomatic animal removed from the food chain. 
>
>   Eh? We almost certainly don't. All quality beef is under 20 months and
>   they haven't seen a whiff of meat and bone meal since 1989, oops they
>   weren't even concieved then. So how do they get infected? By rumour? 
>
>Is it possible that these young cows inherited it from their mothers?

Transmission from cow to calf seems to be quite insignificant, possibly
zero. I haven't seen an up to date report on it. Certainly cases would
not be falling so fast (1995 was 40% down from 1994) if there was any
significant maternal transmission.

It's a bit ironic that this scare has occured now, when the disease in
cattle is well under control and heading towards extinction and all
material that there is a chance might be infective is removed from the
food chain regardless. Before there was the suggestion that we were
closing the stable door after the horse had bolted, even if we were not
sure there had been a horse in the stable anyway. To panic now seems to
me to be most strange with the controls in place. Still, everyone must
decide for themselves.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science
Subject: Re: Slaughter of 11 million cows
Date: Mon, 1 Apr 1996 17:57:11 +0100

In article <rrg.150.147C1C00@aber.ac.uk>, Roy Goodacre <rrg@aber.ac.uk>
writes
>In article <Klfv1CADW7WxEw$3@upthorpe.demon.co.uk> Oz <Oz@upthorpe.demon.co.uk> 
>writes:
>
>|*****IMPORTANT*******
>|BSE is not infectious between cattle. So if one animal in a herd has had
>|it, it does not mean that they all will have caught it. This is not
>|uncommon with diseases, many have a definite infection route and cannot
>|be caught any other way. This is rather common even amongst human
>|diseases.
>
>If this is true then why is the occurence of the disease exponential rather 
>than level.  One theory was that BSE has arsien from cattle being fed with 
>scrapie infected sheep.  MAFF banned this practice in 1988 so we should have 
>seen the disease leveling if this theory were true, but it hasn't.

Eh? But it has. Cases are currently down to 1/3 of the peak, numbers
affected in 1995 are 40% below 1994. Surely you knew that?

>It has been proven that infective material from the brain of confirmed BSE cow 
>when injected into a healthy cow will cause that cow to get BSE.  There are 
>also recorded cases of calves with BSE from mothers who also have BSE - this 
>shows vertical spread,

It shows mothers have daughters who are also milking in the herd and
both could have eaten infective material. I haven't seen any figures
that allow one to separate out any small vertical transmission but it's
clearly not significant or the effects would have been very clear by
now, and it isn't.

> unfortunately the placenta was not analysed for 
>infectivity.

Eh? Of course the placenta has been tested for infectivity. Do you think
the people working in the field are stupid? A whole bundle of other
tissues have also been tested. Some you might find interesting that gave
negative results are, milk, udder, placenta, muscle. The full list of
negatives is very long. 

Refs: 
Veterinary Record 1993: 132, 545-547 Middleton & Barlow
CEE Directorate General For Agriculture. Proc. BSE vet group 1994.
SEAC 1994 report.

>|>It must surely be time for culling to start.
>
>|Bearing in mind that only a tiny, miniscule minority of cattle are
>|infected, do you really propose killing several million innocent
>|uninfected cattle for no reason? Do you have a blood lust? There *might*
>|have been a risk in the mid 80's, but the risk now is not one you should
>|worry about IMHO. This has all the feel of a Witch hunt. Can you prove
>|you are a witch; no: so burn.
>
>I would not call 161,663 recorded cases in the UK up-to-date a miniscule 
>number.
>
>I do not have blood lust.
>
>Indeed culling will not stop it.  Since these prions are very restive to 
>heat and UV they are fairly difficult to kill (or at least lose their 
>infectivity, since I'm sure we can argue about whether they are alive or not). 
> There is recorded a case where a herd of sheep with scrapie were culled and a 
>year or so latter fresh sheep raised on the same land - within 5 years the 
>scrapie had reappearred.  So it is plausible the same thing will happen with 
>cattle.

The fall in the number of cases makes this unlikely at present.
Management of sheep is important for scrapie as I have pointed out on
another thread, so this in itself doesn't necessarily mean much.

>|>I did hear that the UK government were thinking of doing a U turn (how 
>|>unusual!) and introduce selective culling.  However, rather than this being 
>|>because of the scientists say-so it is because the farmers have asked for it 
>|>so that some confidence in the UK beef market can be restored.
>
>|How do you remove an irrational fear of the unknown?
>
>You can't, but if UK government get the go ahead from their talks in 
>Luxembourg today it might do.
>
>Incidently it was announced that beef sales were back to normal in most 
>supermarkets this weekend, and Sainsburys even ran out of beef.

It looks like the majority of British people are less suceptible to mad
media disease than was predicted. By the media of course.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science
Subject: Re: Slaughter of 11 million cows
Date: Mon, 1 Apr 1996 22:02:11 +0100

In article <gjs.3385.630E8280@aber.ac.uk>, Gaz <gjs@aber.ac.uk> writes
>>From: Oz <Oz@upthorpe.demon.co.uk>
>>In article <rrg.130.22D3D180@aber.ac.uk>, Roy Goodacre <rrg@aber.ac.uk>
>>writes
>>>
>>>You are correct in your assumption that 'time will tell'.  However the 
>>>incubation is long 10-30 years (and as yet not truely specified), the fact 
>>>that under 42 year olds have contract CJD is very significant; especially 
>>>since it has been seen in teenagers for the *first time* in the UK.  
>
>>Strange, I thought it had happened with growth hormone (human), the
>>preparation given to haemophioliacs (ex human), transplants, dentists
>>......
>
>True, but the method of infection (injection) is different, and known to 
>produce much quicker results than eating the agent. Even so, clinical symptoms
>took 5-15 years. so it seems safe to assume that the "illness" from eating BSE
>meat (if it exists...) will take longer than this 5-15 year period.

I don't have references on this. However my memory of the cases is that
the disease appeared very much more quickly. In particular I seem to
remember that children treated with infected growth hormone died in
their late teens or early twenties. This is what puzzles me in the
statement that deaths from CJD have *only* occured in elderly people. I
would be interested to know if the symptoms in these young cases was
similar to the ones recently reported.

It is also unclear from the references I have to hand if the incubation
period refers to the delay from a single dose of infected brain extract,
or whether the animals had been fed for an extended period. If the
latter (which is implied in at least one paper) it may simply reflect
the difficulty of infecting an animal via an oral route. Certainly it
seems to be very much harder to do it orally than by direct brain
injection. Many cattle that did eat infected feed do not seem to have
developed the disease, and may well not be infected. 

>>*****IMPORTANT*******
>>BSE is not infectious between cattle. So if one animal in a herd has had
>>it, it does not mean that they all will have caught it. This is not
>>uncommon with diseases, many have a definite infection route and cannot
>>be caught any other way. This is rather common even amongst human
>>diseases.
>
>No. This is just an educated guess and not at all proven. Some tentative 
>evidance exists that suggests that these agents (not just BSE) can infact be 
>passed to others in the herd/flock/group by some method.

I cannot agree with you here. If this was the case then we would not see
a decline in cases. There are certainly mechanisms that it can happen, I
have already suggested why scrapie might be largely only a disease of
british sheep. This does not seem to apply to cows to any noticeable
extent. The epidemiology already bears this out.

>>>It must surely be time for culling to start.
>
>>Bearing in mind that only a tiny, miniscule minority of cattle are
>>infected, do you really propose killing several million innocent
>>uninfected cattle for no reason? Do you have a blood lust? There *might*
>>have been a risk in the mid 80's, but the risk now is not one you should
>>worry about IMHO. This has all the feel of a Witch hunt. Can you prove
>>you are a witch; no: so burn.
>
>But when records of bloodlines and stock movements are not kept, how are you 
>supposed to know which are infected and which are not. By the time clinical 
>symptoms are shown it is too late....

Eh? Stock movements have been kept, and are regularly inspected, by MAFF
ever since the early foot and mouth epidemics. Woe betide a farmer that
doesn't keep them too. The brits have a suicidal tendency to following
to the rules, unlike many countries. Certainly in dairy herds all the
bloodlines are known, and also in most beef units too where they breed
their own stock. Unique ear tag numbers are also checked and recorded in
markets too. Animals are certainly traceable.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science
Subject: Re: BSE: IFST Position Statement Update, 27 March 1996
Date: Mon, 1 Apr 1996 22:22:09 +0100

In article <gjs.3386.6326EB40@aber.ac.uk>, Gaz <gjs@aber.ac.uk> writes
>>From: Oz <Oz@upthorpe.demon.co.uk>
>>>In article <3159f091.23743473@news.easynet.co.uk>, J Ralph Blanchfield
>><jralphb@easynet.co.uk> writes
>
>>>As to the second, muscle meat and milk have been shown to be incapable
>>>of carrying the infective agent,
>
>Oh, and what was this proof? 

Ref: SEAC HMSO Sept '94.

>>> and measures have been taken, and
>>>strengthened, to exclude from the food chain certain parts of the
>>>animal, including all those parts shown to be capable of carrying the
>>>infective agent.  These measures require the most stringent
>>>enforcement and heavy penalties for evasion.
>
>Which up to now have been a joke. Thousands of BSE infected cattle get into 
>the meat supply, 

How do YOU know? 

>and checks comfirm that in addition a massive proportion of 
>slaughter-houses fail to abide by the goverments (limited) measures.

No. A small minority. They were found by regular govt random checks. I
don't think you could possibly describe the measures as 'limited'. What
would you suggest ought to be done further, and why?

>>A point not well appreciated is that NO ruminants have eaten any meat &
>>bone meal since 1989 (1990 if you want to be certain).
>
>Hmmmm. What about non-ruminants. An awfull lot of them get eaten by people.

None as of now. No cases have ever been found in the pig or poultry
population. It would be helpful to stick to facts rather than innuendo.

>>>Placental transmission has been identified as
>>>a likely route in sheep. 
>
>But the potentialfor it an cattle has been largely ignored. Indirect evidance 
>would in fact tend to support it.....

No infective agent has ever been found in placental tissue. Same
reference as above. More innuendo unsupported by facts.

>Worried?
>
>I am. Why hasn't the research been carried out...

What research is that?

>>>      to prohibit the feeding of material containing animal protein
>>>derived from ruminants to cattle and other ruminants;
>
>>Note that this occurred in July 1988. Even allowing a year for odd local
>>stocks to be used we should be pretty certain that animals born after
>>1st Jan 1990 never ate any infective material.
>
>So why are they still going down with BSE? Goverment figures suggest that the 
>incidence of BSE is on the decline. Farmers will tell you that the incidence 
>is still on the up. 

Rubbish. You don't know what you are talking about. I doubt you know any
UK farmers who have had BSE in their herd. More innuendo, actually
downright untruths here. 

>Mainly because the goverment payment to farmers for the 
>slaughter of a BSE cow is so low (why is this....) 

Eh? It's quite acceptable. Your information is incorrect. Again.

>that many send them to 
>market at the very first sign of BSE. Thus they are never shown in the 
>"official" stats.

You have obviously never sent animals to market. The buyers are shrewd
and knowlegeable people. So is the RSPCA man, and the govt vets. No
chance. Dream on.

>>>The banning of ruminant material from animal feedstuffs from July 1988
>>>has led, after a time lag (due in part to farmers using up their
>>>stocks of cattle feed after July 1988, but due mainly to the
>>>incubation period)  to a dramatic decline in new cases (30 percent
>>>drop from 1993 to 1994, over 40 percent drop from 1994 to 1995, and,
>>>up to 20 March 1996, a further 27.5 percent drop compared with the
>>>same period in 1995). 
>
>No. See above. Most dairy farmers will tell you that BSE is at levels thay 
>have never seen before in the past. Goverment methods of finding and recording 
>these BSE figures are in error, if the farmers are to be believed.

Nonsense. You clearly don't know any british farmers. You are dreaming
again. 

>Why was compensation reduced in 1994? If you really want to find BSE infected 
>cattle the smart thing to do would be to make the compensation higher than the 
>market price for the cow.


I think you are trolling. 

Since this is a serious subject, that has all the capability of
bankrupting large numbers of your fellow coutrymen, causing a serious
number of suicides amongst farmers and their staff and costing everyone
in britain thousands of pounds it is in very bad taste. I can only
assume that you are a student at Aberystwyth Univerity who thinks
spreading untruths and innuendo is a good prank.

You might try to grow up.


------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cows - why the fuss?
Date: Thu, 4 Apr 1996 08:18:03 +0100

In article <4jtbp7$36m@unpsun3.cc.unp.ac.za>, Eric de la Harpe
<delaharpe@ageng.unp.ac.za> writes
>Someone help me.
>
>So they find a link between mad cows and some deadly disease in humans. 

No, no, no. They find what appears to be a new strain of CJD which they
cannot rule out as not being due to BSE. (A bit convoluted, I know but
this area works like that). Since then cases have been found elsewhere
which makes it less likely to be due to British BSE.

>Surely, if you cook the meat, you kill off the organisms?  

'Fraid not. It is rather resistant to heat.

>Apparently the 
>organisms are not found in the meat anyway.  

Muscle, milk, liver and most organs don't appear to be infective when
extract is injected directly into the brains of suceptable mice. They
have tried very, very hard to find infectivity here without success.
Brain and spinal cord is infectious, not much else.

>I've heard that the disease 
>can only be caught through contact with the LIVE animal.  

No. The disease doesn't seem to be transmitted at all by contact (cow to
cow) and if it exists at all from mother to calf it is insignificant.
Absolutely nobody is suggesting that it can be transferred to man by
contact, even Prof Lacey.

>What proportion 
>of the UK herd is infected? 1%? 0.1%? 0.00001%?

The figure keeps dropping. I believe the cases at the moment (last year)
comprise something like 0.01%. That's still a lot of animals though, if
you want to scare-monger.

>I wouldn't hesitate to eat British beef.  I take much greater risks 
>driving to work every day and by not locking my doors at all times.  What 
>are my chances of being affected?

No-one knows, thats the problem. One can probably be pretty sure that
it's low or abbatoir workers and feed-mill workers would have gone down
in noticeable numbers by now. CJD runs normally at about 1 per million
per year, and so far the UK has shown NO increase at all. You are quite
right to worry about driving as a much, much, much, much higer risk.

Anyway, with all the controls the UK has enforced in 1988, and the way-
over-the-top extra ones this year, I AM personally confident of eating
British beef, and am doing so. It is almost certainly the safest in the
world as far as BSE in concerned. I am NOT, however, going to eat
continental beef, or Argentinian beef. They have no controls I can
believe in. I think British beef is now hypersafe, and good value!

>Why the fuss with British beef?  Are all other herds immune?

Well, that's a nice way of putting it.

>SURELY, SURELY, SURELY this is not about a disease? it's 
>economic politics.  What a mean and very nasty way to knock out the 
>opposition.  Am I right?

Many British farmers would whole heartedly agree with you here. Like so
many of these things it has backfired. The British have always eaten
large quantities of imported foodstuffs, particularly from France and
Holland. It is a little galling for them to complain about the little
agricultural produce we send to them.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cows - why the fuss?
Date: Thu, 4 Apr 1996 08:39:10 +0100

In article <828560626snz@zhochaka.demon.co.uk>, "David G. Bell"
<dbell@zhochaka.demon.co.uk> writes
>
>There was a change in the time-temperature limits imposed on rendering 
>processes, still sufficient to kill micro-organisms but not, apparently, 
>the agent that causes BSE.  This reduced the processing costs.  Are you 
>sure which standard you are referring to?
>
>If anything is to blame, it is the pressure to provide cheap foodstuffs,

Being sensible, there are no villains only victims. 

Nobody actually cut corners or attempted anything devious. The country
wanted energy conservation, the rendering mills (which had been working
without problem for decades) went on to a new sterilisation system which
is approved worldwide, the feed compounders continued to add meat and
bone meal for better animal nutrition, farmers continued to feed their
branded material all as it had been for years. The UK did nothing
strange that is not done in many other countries. All the above have now
already suffered greviously.

>leading to potentially dangerous cutting of corners all through the 
>chain from farm to kitchen.  

Eh? What evidence have you for this? OK, supermarket beef is not hung,
so it doesn't taste too good, but what else?

>My business has dropped from 3 full-time 
>staff to 1, and farm finances, if you compare prices in terms of tonnes 
>of wheat, are beginning to make the idea of becoming a farmer look 
>ridiculous.

Yup. I saw a figure quoted recently for the real value of wheat between
the wars. It was uk# 300/ton! Makes your eyes water! Mind you even in
the 70's you could buy a decent tractor for 50T wheat, now it costs you
over 200T, and that's in the EU!

>You might not lose your money so quickly in farming, but slow horses and 
>fast women probably give you more pleasure.

You should have said that 20 years ago, it's a bit late now!

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: : Mad Cow disease, BSE; Justice is served.
Date: Thu, 4 Apr 1996 11:13:15 +0100

In article <DpAu3s.770@cix.compulink.co.uk>, "\"Stephen Rawlings\""
<srawlings@cix.compulink.co.uk> writes
>>>I believe it's a nice smelling pelletised feed in it's
>neat form. You may even put low grade stuff on your organic garden as
>meat & bone meal.<<
>
>Which is worrying as I have seen the theory expressed that a likely form 
>of transmission of the BSE agent to cattle that have subsequently become 
>affected, is by a nasal route rather than digestive.

I have just been looking through 300 (!) abstracts of BSE/TE related
papers. I noticed that some did mention nasal inocculation as an
infection route that they tried, but (not unsurprisingly) I don't
remember the details, and these are important. The vast majority of
researchers inocculated by several routes SUMULTANEOUSLY, typically
infective extract straight into the brain, the blood, the stomach and
the body cavity. Indeed many of the papers quoted as showing
transmission by a particular route are misquoted for this reason.

Although the lymphatic system seems to be infective in scrapie, it
doesn't seem to be in BSE (although it is one of the condemned offals)
which is odd. So a nasal route (in cattle) is an interesting idea,
particularly as the scent receptors are a bit of brain that is more-or-
less external. Just out of interest the lengths that have been gone to
in order to locate all potential sources of infective material have
their bizarre side. Retinas from infected cows (I kid you not) have been
tested and shown to be infective, which isn't surprising as it's part of
the brain, but still!

If the nasal route was a human infective route then workers at the meat
& bonemeal plants could be expected to have caught the disease in a big
way since these places are notoriously dusty. They don't appear to have,
at least so far and it's been over seven years now.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cows - why the fuss?
Date: Thu, 4 Apr 1996 20:43:11 +0100

In article <DpCLJw.H5o@mv.mv.com>, "T. Ricker" <spheres@mv.mv.com>
writes
>
>I disagree with the statement that British beef is the safest in the 
>world as far as BSE is concerned.  

Well, you might reconsider this after you have thought over my reply.

>The media has conveniently forgotten 
>to tell the rest of the world that BSE has occurred in other parts of 
>Europe.  Thanks to Clari news releases via the 'net, I heard this week 
>that a herd in France was found to have a case of BSE, which was 
>something like the 16th herd in France to have had a case of BSE. The 
>difference is in the approach the governments take when a case is 
>discovered.  In France, I believe they destroy the entire herd.  This is 
>a very aggressive approach, certainly, but then the world has not 
>(rightly or wrongly) stopped eating French beef.  Had Britain had a 
>similar approach, or had they taken steps to cut the media hype off 
>before it aired, perhaps consumers would not have been so quick to pass 
>judgement.

It was condidered by MAFF in 1988 when this all came up. You should note
that Britain's main method of dealing with ***infective*** stock
diseases has always been full herd slaughter. We probably have the most
experience of handling it in the world. It was rejected because the
disease is not infective. It was *also* rejected because there was
always the worry that such drastic action might result in cases being
hidden and thus allow infective material into the food chain. The
comments that have been bandied about in the press when they though that
was the position confirm this. It is quite unlike foot and mouth and
other serious cattle infections as most herds only ever had one or two
cases a year even at the peak, and with the decline many have been free
for one or two years. The full (even slightly generous) payment that was
decided upon has been very effective in ensuring infected cattle never
reach the food chain, even from the small minority of 'self-seeking'
british farmers. 

That, together with the draconian removal of offals, means that even
infected cows wouldn't transmit material into the human food chain in
any case. This is not very well understood. The SEAC committee in 1988
were quite aware that they were working with limited information and as
a result proposed a belt and braces procedure which was really thorough.
As it has turned out they went a fair bit over the top, now much more
information is available, however the procedures remain in force.

Actually the ministry took a sensible, effective and shrewed route. They
are not stupid.

Nowhere else in the world do they remove defined offals, AND ensure that
it pays a farmer (admittedly not much) to send his animals suspected of
BSE for inspection and incineration. As a result only British killed
beef has this double protection. 

<snip>
>and animals without cutting corners like feeding sheep guts to 
>herbivores.  

Sigh. 
I have answered this so many times I can't be bothered to do it again.


------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cow Disease.  What is the truth?
Date: Thu, 4 Apr 1996 22:40:54 +0100

In article <040596080332Rnf0.78@zephyr.manawatu.planet.co.nz>, Stuart
Brown <stuart@zephyr.manawatu.planet.co.nz> writes
>Oz <Oz@upthorpe.demon.co.uk> writes:
>
>You made some very good points.
>
>>It is interesting to note that Sainsbury's, one of Britain's most
>>respected and largest supermarket chains (that specialises in quality
>>meat in particular), announced it was selling beef at half price. They
>>were sold out completely in a day and had many unhappy customers who had
>>to go away empty handed. Perhaps the ordinary British person is not
>>quite so easily swayed by scare mongering stories in the press as one
>>might believe from the media.
>
>I wonder where that half price beef came from?

Very fine young animals. Sainsbury's were oringinally a chain of
butchers, and they offer probably the best meat available from a
supermarket. I expect the main reason was that they had a lot of meat
hanging because they are reputed to actually hang their meat properly.
As a result they needed to keep it moving. This was a problem other
supermarkets don't have, because they don't bother to hang it.

No, I don't have shares in Sainsbury's!

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science
Subject: Re: Slaughter of 11 million cows
Date: Fri, 5 Apr 1996 08:06:06 +0100

In article <hlr.393.03C98547@aber.ac.uk>, hlr@aber.ac.uk writes
>
>NOTE THIS IS ME SPEAKING AS ME, NOT AS A SCIENTIST :-)
>
>If these records are so well kept why did the 10 o'clock news last night show 
>a farmer checking the teeth of his cow to find out how old it was? Not exactly 
>the best way of reassuring us that no cattle over a certain age are entering 
>the food chain is it?

Sigh. Dear oh dear.

As I understand it, in order to be absolutely sure that no evil farmer
is trying to pull a fast one they are going to use cattle dentition to
assess age. After all, he might spend a week or two re-writing his
records, artificially ageing them etc etc (I have said HM Govt was going
over the top, haven't I?) so as to fiddle the books. <NB this is called
sarcasm>.

Unfortunately some cattle show this dentition change at 20 weeks.

The only groups of animals who would be tedious to track would be the
rather small number on 'finishing' farms where they are bought in as
stores (12-15 months) from a market because they may have gone through
two or three hands in the meantime. For the majority of herds where the
animal had remained on one farm from birth, or arrived aged two or three
weeks, it's not a problem. 

You should already be aware of this. Unless Aberystwith is breaking the
regulations. I presume the agricultural college is still part of your
'university'? I presume they actually have animals?

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science
Subject: Re: BSE: IFST Position Statement Update, 27 March 1996
Date: Fri, 5 Apr 1996 09:13:19 +0100

In article <gjs.3386.6326EB40@aber.ac.uk>, Gaz <gjs@aber.ac.uk> writes
>>From: Oz <Oz@upthorpe.demon.co.uk>
>>>In article <3159f091.23743473@news.easynet.co.uk>, J Ralph Blanchfield
>><jralphb@easynet.co.uk> writes
>
>>>As to the second, muscle meat and milk have been shown to be incapable
>>>of carrying the infective agent,
>
>Oh, and what was this proof? 

Actually there have been quite a few studies I have come across, but
since I am an individual and not an academic or organisation I don't
have access to cross-referenced libraries (as you do) I have not the
time to look out a long list. A manual look threw up the following:

Middleton & Barlow, 1993 Vet Rec 132, 545-547 Feeding study.

Neuropathogenesis Unit, Edinburgh, Vet Rec, 1995 136 23-592
(Intracerebral)

Doubtless you can find more yourself, if so please let me know and I
will try to obtain copies, although it's difficult for me.

>>> and measures have been taken, and
>>>strengthened, to exclude from the food chain certain parts of the
>>>animal, including all those parts shown to be capable of carrying the
>>>infective agent.  These measures require the most stringent
>>>enforcement and heavy penalties for evasion.
>
>Which up to now have been a joke. Thousands of BSE infected cattle get into 
>the meat supply, 

Evidence please.

>and checks comfirm that in addition a massive proportion of 
>slaughter-houses fail to abide by the goverments (limited) measures.

Evidence please. 
As I understand it a small number of tiny abbatoirs got a bit careless.
The inspectors found them, the govt. published the information. One (at
least) is being prosecuted. How transparent do you want it? You get the
truth, you blow it up, you complain of lies and deception. Do YOU
habitually lie and misrepresent? Oh. Well actually most people don't.

>>A point not well appreciated is that NO ruminants have eaten any meat &
>>bone meal since 1989 (1990 if you want to be certain).
>
>Hmmmm. What about non-ruminants. An awfull lot of them get eaten by people.

Not at present, but they were. 
There is still no evidence of any transmission by feed to pigs and
poultry. Please don't quote laboratory transmission to pigs by massive
infected brain extract, it's not a customary method of feeding pigs.
Also please note that clinically infected cows are incinerated, and all
brain and spinal cord (the only material found to be infective from
cattle) from ALL cattle is removed from the food chain, infected or not.
Anyway, at present no cattle M&B meal is being fed to anything. A
serious of a disposal problem.

Pretty rock solid, yes?

>>>Placental transmission has been identified as
>>>a likely route in sheep. 
>
>But the potentialfor it an cattle has been largely ignored. 

AARRGGH! It was the main worry in 1988. So far evidence has shown it to
be nil, or insignificant. We are now many years down the road, if it
were to be a problem it would have surfaced by now. At worst it will
result in a very, very low level of disease indeed for another
generation of cows.

>Indirect evidance 
>would in fact tend to support it.....

No, I am tired of pointing this out. Direct evidence shows quite the
reverse.

>Worried?
>
>I am. Why hasn't the research been carried out...

AARRGGHH! Over 300 papers published, most if not all of the things you
have worried about have been investigated. Please go to your univeritly
library and look them up! You are in the privilaged position of being
able to do so, take advantage of it.

>>>      to prohibit the feeding of material containing animal protein
>>>derived from ruminants to cattle and other ruminants;
>
>>Note that this occurred in July 1988. Even allowing a year for odd local
>>stocks to be used we should be pretty certain that animals born after
>>1st Jan 1990 never ate any infective material.

>So why are they still going down with BSE? 

You DO understand the epidemiology? You DO know how long a cow lives in
a dairy herd? So why ask this stupid question. Yet again.

-----

Oh-hum, sorry folks. I wasn't expecting a long visit here, so I omitted
to reset the defaults for this group. As a result I may have answered
several posts twice (I *hope* not three times). I have reset the
defaults to more sensible figures.

My apologies for any inconvenience caused.

<Embarrassement!>

-----

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science,sci.bio.microbiology
Subject: Re: BSE: the internet discussions
Date: Fri, 5 Apr 1996 09:48:38 +0100

In article <4k1i6f$4d5@irk.zetnet.co.uk>, Malcolm Goodall
<easterly@zetnet.co.uk> writes

>Lets hear where the vested interests lie,  instead of the cant!

Firstly I abhor the suggestion that if anyone has an interest in
something he/she cannot be trusted and is lying for gain. There is such
a thing as ethics and honesty and the vast majority of people do behave
ethically IMHO. If you believe 'vested interest' results in you being a
liar then you must disregard all information from pressure groups,
religions, politicians and other enthusiasts or organisations. A rather
sad way to live, I would suggest. Having said that I would agree that
caution is always appropriate and you should weigh the actual evidence
and arguments. I am all for that. Harder work though, I must admit.

Oz: MA (Cantab), sometime computer person, earns part of his income from
a UK dairy herd and has been interested in TE's as an informed layman
since about 1970 because it was interesting. Has a family of two young
children. Not an academic, earns his own living.  :-) Believes in the
scentific method, can't stand misinformation. Tries to keep learning,
note my .sig

It's odd that others have not been asked the same question. However I am
rather used to the problem of 'received knowledge' where facts are
regarded as suspect and hearsay is regarded as fact. Science has had to
fight this since witches were burnt at the stake, and humankind hasn't
changed so much since.

Happy?


------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.environment,uk.environment,alt.sustainable.agriculture,
	sci.agriculture,scot.environment,misc.consumers,alt.politics.greens,
	alt.org.earth-first,alt.save.the.earth
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: Fri, 5 Apr 1996 10:12:19 +0100

In article <jscanlon-0404962241520001@sp77.linex.com>, Jim Scanlon
<jscanlon@linex.com> writes
>
>It seems to me that this disease might have been and is being, under reported.

There was the *suspicion* that it might have been under-reported in the
first year or so (sort of 1989ish) when HM Govt only paid 50% of the
'value' (about 5000% of what the animal was really worth as it was
unsaleable except as knacker meat). The payment was raised to 100% to be
sure and I believe (from memory) that there was NO sudden increase in
reported cases as might have been expected were there to have been
significant under-reporting. This strongly suggests that reporting was
near 100% even at 50%.

Since most commercial herds have had one or more cases over the last
seven years (mostly '89-91) and there was little (or no) financial loss
from declaring BSE animals I would expect near 100% reporting to be
right. HM Govt vets/officials were smart enough to realise that they
could be pretty well certain to catch all the cases, protect the
population and kill off the disease as it progressed in the expected
epidemiological decline (which it has) using theis method. A quiet,
effective and sensible approach in the absence of too much media
hysteria.

Please note that on the continent, and in Canada this is not the case.
Whole herd slaughter is the rule here, inappropriate to a non-infectious
disease, and there is a BIG temptation to hide cases in this situation.

It is also noteworthy that only in Britain are all potentially infective
organs (many unproven, only suspect) are removed from the food chain and
no meat and bone meal fed to ruminants and all clinical cases destroyed
completely. Actually at the moment no ruminant M&B meal is fed to
anything. As a result we are in the slightly odd position that it's
probably safer to eat British beef than any other!

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cow Disease.  What is the truth?
Date: Fri, 5 Apr 1996 17:18:40 +0100

In article <4k2f3n$8oa@homer.alpha.net>, "Ingrid K. Buxton"
<buxtoni@mixcom.com> writes
>janet@cogsci.ed.ac.uk (Janet) wrote:
>
>>Is it possible that these young cows inherited it from their mothers?
>... yes, possibly through the milk... Ingrid

No, no, no. Despite huge efforts in injecting milk from cows that have
died of BSE directly into the brains of specially senstive mice they
have been unable to find any infectivity in milk. Or muscle either, or
indeed most organs come to that. As an example reference:

Neuropathogenesis Unit, Edinburgh, Vet Rec, 1995 136 23-592
(Intracerebral)

I am impressed by the SEAC reccommendations which in 1988 were a
remarkable example of top scientists in their field coming up with a
belt and braces failsafe package. It's quite remarkable, IMHO, that even
today, 8 years later and with much more research information available
they still look about as conservative and sensible as you can wish.
Maybe rather more rigorous than one would set in motion today, but very
close, and even safer of course. Their work really should be applauded.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"


From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science
Subject: Re: BSE prions outside the brain
Date: Sat, 6 Apr 1996 07:25:04 +0100

In article <952@purr.demon.co.uk>, Jack Campin <jack@purr.demon.co.uk>
writes

>>J Ralph Blanchfield <jralphb@easynet.co.uk> writes
>> muscle meat and milk have been shown to be incapable
>> of carrying the infective agent,
>
>The abnormal prion proteins are expressed in all nervous tissue, are
>they not?

I can't remember seeing any statement or abstract that states this. Do
you have a reference? However if so wouldn't we see parts of the body
that are weak in infected animals (legs for example) were this the case?
What you actually see is a discoordinated animal that has no problem
with weak limbs at all. So it would, on reflection, seem likely that
peripheral nerves are not effected.

It is not so uncommon to find diseases that only attack either the
central nervous system (brain and spinal cord) or the peripheral one.
Polio being the most obvious, presumably whatever Stephen Hawking has
takes out the peripheral nervous system, but clearly leave the brain
intact. Perhaps we have a neurologist in the group to comment on this?

>Muscles contained nerve tissue last time I looked at an anatomy text.

Certainly. However they have not been able to transmit BSE to suceptable
mice by injection muscle from terminally BSE infected animals directly
into the brain.


------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"


From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.environment,uk.environment,sci.agriculture
Subject: Re: : Mad Cow disease, BSE; Justice is served.
Date: Sat, 6 Apr 1996 18:36:54 +0100

In article <4k5qgr$kc6@tribune.concentric.net>, Emmett Jordan
<wpcc88a@prodigy.com> writes
>To Laz et al:
>Apparently by your definition one third of Wisconsin's dairy farmers are 
>the dumbest kids on the block: they have been feeding their dairy cattle
>offal-derived feed.

Well. I for one am very pleased to know that they haven't. I wouldn't 
wish BSE on any farm, anywhere. 

Just bear in mind, however, that it's easily done. We too feed our cows 
and heifers only straight feeds (for over 15 years). Except for young 
calves to two to six months because my herdsman wanted them to have 
only the best. We bought in a top quality propriety calf weaner pellet, 
like all feeds in the UK until very recently the only analysis on it was 
protein, fibre, oil, ash. Well, now we know at least one of the 
ingredients. Unfortunately.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.environment,alt.sustainable.agriculture,sci.agriculture,
	misc.consumers,alt.politics.greens,alt.org.earth-first,alt.save.the.earth
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: Sat, 6 Apr 1996 18:42:01 +0100

In article <jnmeade.828799999@blue.weeg.uiowa.edu>, "J. Meade"
<jnmeade@blue.weeg.uiowa.edu> writes
>Ursula,
>
>Thanks for posting the facts.  Concern is one thing; fearmongering
>such as you exposed is counterproductive.

Regrettably, in this appalling blood mediafest, it is the norm. The fact 
that this misinformation, at least some of which MUST be deliberate, has 
already cost 40,000 Dutch (ex UK) calves the death penalty and will 
undoubtedly result in premature slaughter of many more, is so 
reprehensible that I don't have words to express it.

What is even more astonishing is that some seems to come from those that 
claim to love animals.

What a distorted view some people have of the world. (I am being polite)

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cow Disease. What is the truth?
Date: Sun, 7 Apr 1996 07:34:26 +0100

In article <4k6r27$lth@homer.alpha.net>, "Ingrid K. Buxton"
<buxtoni@mixcom.com> writes
>jnmeade@blue.weeg.uiowa.edu (J. Meade) wrote:
>
>>buxtoni@mixcom.com (Ingrid K. Buxton) writes:
>>Can you cite the studies/evidence that lead you to say BSE can be
>>transmitted through milk?
>>Jim - Farmer - Iowa City, IA, 
>>jnmeade@blue.weeg.uiowa.edu
>
>"TSE infectivity is present in most tissues tested 

The scientific evidence is to the contrary as far as BSE is concerned. I
have posted the references.

>" Over 18,000 cases have been developed BSE although they were born
>after the ban of oral infectious material being present in their food.
>It is still unclear whether the cattle become infected directly from
>the food that they eat 

Refs please. Without further info your statement is meaningless.

The ban occurred in 1988, it is generally regarded as being effective in
1989. However due to the lack of labelling on UK feedstuffs there was no
way of knowing what had M&B meal in and what did not. Expensive calf
weaner was almost certainly carried over in some farms. Also 'tower'
type feed bins empty from the TOP. This is hard for people to
understand, but true. So if dairy feed is ordered when there is still a
few tons in the bin (absolutely normal) the last few tons stays there.
As an example we had to do some work on one of our bins last Autumn and
my staff were absolutely astonished (despite me telling them this is how
it worked for 20-odd years) to find the 'empty' bin actually contained
some four tonnes of mix that contained 30% sugar beet pulp, a mix that
we hadn't used for 18 months. Since they had to shovel it out they now
believe me! Herdsmen are paranoid about running out of feed, for VERY
good reason. It's therefore hard to draw too many conclusions, and I
would have said that 18,000, or more than 10% would not be supported by
any UK dairy farmers I know. All the ones I have talked to have had none
born after 1989. There may be some, but the incidence is very small.

>or from 
>-->asymptomatic mothers<--- that have done this.The possibility that
>an environmental factor other than the BSE infective agent may be
>involved with the transmission of BSE has been suggested due
>to the relatively low incidence of disease on 'organic' farms and
>organosphorus insecticide use has been suggested as being involved.

I shot this one down a week or two ago. Conclusively. Evidence shows it
to be wrong.

>http://www.airtime.co.uk/bse/tse.htm#cjd

From what another poster has said this source is essentially a collation
of lies and rumour. Anyone can make up their own page and put whatever
they like in it.


------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cow Disease. What is the truth?
Date: Sun, 7 Apr 1996 07:40:51 +0100

In article <4k6rbk$lth@homer.alpha.net>, "Ingrid K. Buxton"
<buxtoni@mixcom.com> writes
>jnmeade@blue.weeg.uiowa.edu (J. Meade) wrote:
>>Can you cite the studies/evidence that lead you to say BSE can be
>>transmitted through milk?
>>Jim - Farmer - Iowa City, IA, 
>>jnmeade@blue.weeg.uiowa.edu
>The following material was prepared by Michael Hansen, PhD., from
>testimony that the Consumer Policy Institute (an affiliate of
>Consumer's Union) submitted March 31, 1993 to the Veterinary Medicine
>Advisory Committee of FDA on the subject of potential animal and human
>health effects of rbGH (recombinant bovine growth hormone) use. 

Right. Anyone can post any 'evidence' to these sorts of committee,
doesn't make it right. Obviously the vet's didn't agree either or much
more would have been done in the US from 1993.

><snip, snip>
>Ominously, in a Reuters news report from March 12, 1993, there is a
>story of an old dairy farmer in England who recently died from
>Creutzfeldt-Jakob disease (CJD), the human form of spongiform
>encephalopathy; the farmer had a herd of BSE-infected cattle that had
>to be destroyed in 1989 and had been drinking milk from the herd for
>at least seven years. 

Old news. With about 55 cases of CJD annually (like all countries about
1:1,000,000) there have been about 500 cases since 1986. The last time I
heard the highest risk group was taxi drivers (!). Farmers have about
average incidence. You would expect several cases of farmers getting it
out of 500 cases in normal circumstances. Since most UK herds have had a
case of BSE, and they and their staff usually drink the milk unprocessed
(and jolly nice it is too) this is meaningless.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.environment,uk.environment,alt.sustainable.agriculture,
	sci.agriculture,scot.environment,misc.consumers,alt.politics.greens,
	alt.org.earth-first,alt.save.the.earth
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: Sun, 7 Apr 1996 07:45:39 +0100

In article <4k2rln$1bd@main.freenet.hamilton.on.ca>, Scott Nudds
<af329@freenet.hamilton.on.ca> writes
>Oz (Oz@upthorpe.demon.co.uk) wrote:
>: Indeed the almost indecent hast of the British Government
>: to make public a preliminary paper on young cases caused the world-wide
>: scare.
>
>  I've known of the suspected connection for about 2 years.  But at that 
>time, the suspected # of cases in human's was 2.  Now what is it?  
>Slightly over 10?  If there is any blame here it is with witholding 
>information from the public, not premature release.

Since then the varient has been found in other countries. Notably a
vegetarian from Germany. Caution is still needed, ten cases since (I
believe 1990) one of whome had lived in Australia for twelve years. It
is certainly not clear.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"


From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.environment,uk.environment,alt.sustainable.agriculture,
	sci.agriculture,scot.environment,misc.consumers,alt.politics.greens,
	alt.org.earth-first,alt.save.the.earth
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: Mon, 8 Apr 1996 14:19:55 +0100

In article <Pine.SOL.3.91.960408022527.5999A-100000@james.freenet.hamilt
on.on.ca>, Scott Nudds <af329@freenet.hamilton.on.ca> writes

>On Sun, 7 Apr 1996, Jim Scanlon wrote:
>> There have been several case in cats attributed to contaminated pet food,
>> but none, as far as I am aware of dogs. But....there are similar diseases
>> know to infect hamsters, mice, mink, (mule deer yes, mule deer) cats,
>> sheep and humans.
>
>  Has there been a definite link between these diseases and prions?  Or 
>is the link assumed from the fact that no other agent has been found?

Basically the evidence for the disease being carried by a protein and 
not a DNA or RNA virus seems to be because:

1) It is extremely resistant to heat. Unlike DNA/RNA
2) It resists DNA and RNA denaturing enzymes.
3) It passes through filters that would trap DNA/RNA
4) Purified protein material is still infectious.

I haven't read most of the papers I have come across, this is based on 
abstracts remembered. The general impression is that most people in the 
field now believe the prion infective agent, which certainly wasn't true 
a few years ago.

>> Sorry about your dog.

Yuh. Me too. Always terribly sad when your dog dies, I have had to watch 
two go. The problem I always find is that you tend to keep them going 
well past the point when recovery is impossible, and long into the time 
when they have ceased to enjoy life at all. A very difficult ethical 
problem, I have found.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cow Disease. What is the truth?
Date: Mon, 8 Apr 1996 17:59:52 +0100

In article <Pine.SUN.3.91.960408073404.16825A-100000@eli>, "David D.
Kee" <dkee@ag.auburn.edu> writes
>I have a question on BSE, the human connection and the ban on british beef?
>
>The scenario as I understand it.
>
>1) Cattle first got the disease by consuming bone and protein meal made 
>from infected sheep.

That is what most people think.

>2) There is a possibility that man gets a similar disease from consuming 
>infected, albeit symptomless, beef.

That is the worry, all the evidence (and there has been a lot produced
since 1988) is to the contrary. One could go on at length .....

>Question:  Would it not be more probable that man gets the disease by 
>consuming infected, albeit symptomless, mutton and lamb?

So one might have thought. Particularly as the brains will have been 
consumed too. However scrapie has been a disease of British sheep for 
some 200 years and the evidence shows that the incidence of CJD in UK is 
the same as elsewhere including vegetarian countries such as India.

It is also important to note that it is STILL the same incidence as it 
is elsewhere. There is STILL no epidemiological evidence for any 
increase in CJD in the UK. It remains at about one per million
population per year, same as elsewhere.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science
Subject: Re: BSE: the internet discussions
Date: Tue, 9 Apr 1996 07:39:26 +0100

In article <4kc768$jcq@irk.zetnet.co.uk>, Malcolm Goodall
<easterly@zetnet.co.uk> writes

>As regards your membership I can't help but think that Food Scientists 
>and Technologists  must work for some company or other - apart from the
>acedemics who you dont like anyway, and who do you "consult" with? 

If you concentrate on the arguments and academic papers on the subject, 
then you won't need to worry so much about phantom fears of a cover up. 
If this group is anything like the other tech ones on the net it's a 
waste of time trying to put up a fake argument, because someone will 
know more than you and come down on errors like a ton of bricks. 

>Basically I am complaining about  statements made by you and others which
>only give one side of the story, and denigrate others who oppose them.

I haven't denigrated anyone. I have gone way out of my way to obtain the 
papers discussed AND READ THEM. These are peer reviewed papers, and if 
you have ever tried to get a paper peer reviewed you will know how they 
stop fallacious arguments or bad experimental technique. On the other 
hand *anyone* can post any rubbish they like on their own URL. And DO!
     ^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^

>I belive research time has been wasted since the 1980's - but in
>who's interest is it to fund research - the Food Industry, MAFF, NFU,
>the Government? I doubt it.

With over 300 papers quoted, mostly in peer reviewed publications, you
regard this as 'not much research"???

I make no comment on the partial posting from a SEAC member which is
quoted in full elsewhere. He has more information than I, and is an
expert in the field, which I am not. I don't therefore disagree with his
statement, but DO note that (as he admits) some is opinion at this
stage. I have no objection to *considered* opinion, indeed until yet
more information becomes available it is all one can, and should, offer.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cow Disease. What is the truth?
Date: Thu, 11 Apr 1996 14:32:24 +0100

In article <4ki00b$6hc@homer.alpha.net>, "Ingrid K. Buxton"
<buxtoni@mixcom.com> writes
>Oz <Oz@upthorpe.demon.co.uk> wrote:
>
>>It is virtually certain that BSE is not a virus, but a prion.
NOTE----^^^^^^^^^
> 
>... only a non-scientist would make such a statement.. there is no
>such thing as certainty... and the debate within the virolological
>world is precisely over this... and will continue until the mechanism
>of how a protein can be infectious is known and demonstrated ... that
>is, they will have to make the prion protein in vitro (in a cell free
>system), inject it into animal and cause disease... 

Certainly brain extract, made cell-free, treated with DNAases, RNAases,
further heat treated so as to convince the vast majority of virologists
that there can be no nucleic acids present has still been shown to be
infective. This may not make you completely sure, but should make you
pretty convinced.

>> Generally this is not important unless it results in burning innocents as 
>witches.
>.. how is this germane to the DISCUSSION? ... discussion, you see, is
>what newsgroups are about, 

They certainly should be.

>not propaganda .... and certainly not
>thinly veiled attempts at sarcastic degredation...... 

No sarcasm involved.

>try to separate
>your wallet from this discussion, heh?

That comment should be beneath you. If you look back over my postings I
have never resorted to denying the truth, nor distorting it. I have
certainly a bigger interest than many here, and I have never denied it.
However you should bear in mind that the interest in understanding and
assessing the risks is for me much more personal. I drink my own milk
untreated, and so do my children. My staff (who are personal friends) do
also and they calve down cows, inject them as required and are at far
higher risk than you are. I can assure you that if I had any significant
worry then no one here would drink the milk or expose themselves to real
chance of infection. To suggest otherwise is to suggest that I value
cash over my family and friends, and that is not at all a nice thing to
suggest. It is in any case quite wrong. I hope you can see that clearly.

Some bedtime reading:
Biochemical and Biophysical Research Communications
1995 207 2 621-629 0V00000 En 31 ref.
MRC Neurochemical Pathology Unit, Newcastle General Hospital, 
Westgate Road, Newcastle upon Tyne, NE4 6BE, UK.
LL820
In a mass spectrometry assay, synthetic peptides containing 3 or 4
copies of an octapeptide repeat sequence (PHGGGWGQ) of highly conserved
N-terminal domain of mammalian prion protein (PrP), preferentially bound 
copper over other metals. The same binding preference was demonstrated
with peptides containing an N-terminal repeat domain of the hexapeptide
(NPGYPH) of chicken PrP. Concentration dependent binding of copper to
the mammalian tetra repeat PrP peptide was demonstrated in gel
filtration chromatography. It is suggested that PrP could be a copper
binding protein in vivo.



Journal of General Virology
1995 76 10 2567-2576 0V00000 En 76 ref.
Robert Koch-Institut, Bundesinstitut fur Infektionskrankheiten und nicht 
ubertragbare Krankheiten, FG 123, Nordufer 20, 13353 Berlin, Germany.
LL820\WW000\VV200
SAF-protein, an amyloid, is the main constituent of scrapie-associated 
fibrils (SAF) and a specific marker for transmissible spongiform 
encephalopathies (TSE). Using an improved extraction method and 
Western blot detection, the disease-specific amyloid was found in
various 
parts of the central nervous system of hamsters orally infected with 
scrapie, of squirrel monkeys orally infected with kuru, sporadic 
Creutzfeldt-Jakob disease (CJD) and scrapie, of human patients with 
sporadic CJD, of sheep with natural scrapie and of a cow with bovine 
spongiform encephalopathy (BSE). In human CJD samples, the 
concentration of TSE-specific amyloid was estimated to be 1000- to 
10<thin>000-fold lower than in the central nervous system of hamsters 
with scrapie. The extraction method has a yield of 70% and allows 
Western blot detection of the TSE-specific amyloid in samples 
representing 1-10 <micro>g of brain tissue from intracerebrally infected 
hamsters, as well as individual spleens from hamsters with terminal 
scrapie infected by the intracerebral, oral or intraperitoneal route. A
20-
100 mg sample of material is sufficient for the extraction of the 
pathological protein from different rodent, monkey, ovine, bovine and 
human tissues. The results reported here show the potential of the 
method for the routine diagnosis of TSE as well as for the detailed 
analysis of distribution patterns of the TSE-specific amyloid in 
experimental approaches to the investigation of these diseases.

Micron
1995 26 3 277-298 0V00000 En 155 ref.LL860
The pathology of spongiform encephalopathies, including scrapie, BSE, 
and Creutzfeldt-Jakob disease is reviewed. It is concluded that a prion 
protein is released from the surface of neurons and neurites, diffuses 
through the extracellular space around infected cells where it 
accumulates and finally becomes aggregated as amyloid fibrils. It is
likely 
that the accumulation of prion protein within the extracellular space is 
instrumental in causing nerve cell dysfunction and, ultimately, 
neurological disease.

Journal of Veterinary Diagnostic Investigation
1995 7 2 245-247 0V00000 En 15 ref.
National Veterinary Services Laboratories, Veterinary Services, Animal 
and Plant Health Inspection Service, US Department of Agriculture, 
Ames, IA 50010, USA.
LL820\LL880
A Suffolk sheep PrP gene subunit was expressed with a baculovirus 
transfer plasmid and the resulting immunoreactive protein was 
described and evaluated immunohistochemically against proteinase 
K(PK)-resistant PrP found in naturally scrapie infected sheep. This 
appears to be the first report to describe the expression of a PrP
subunit 
fusion protein and its application in the production of diagnostically 
useful antisera.

Enough? Unfortunately I cannot find the references for the degradation
of infective material such as to make RNA or DNA based infective
material very unlikely. However since you have doubtless got a good
library, you should be able to look it up. From memory it was published
about four years ago, although I expect it has been duplicated since.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cow Disease. What is the truth?
Date: Fri, 12 Apr 1996 19:00:15 +0100

In article <VfLbx0O5IIyF084yn@teleport.com>, Larry Caldwell
<larryc@teleport.com> writes:

>By the way, what does "hang meat properly" mean to a Brit?  Around here
>it means about 3 days in the cooler to let the rigor mortis go out of
>the meat.

For supermarkets that's about right in most cases. For the old fashioned
butcher, three weeks is about typical.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: mad cow
Date: Fri, 12 Apr 1996 19:04:40 +0100

In article <SCAG.4AC3@choice.southern.co.nz>,
stuart@choice.southern.co.nz writes
>JM>Internet: jnmeade@blue.weeg.uiowa.edu
>
>JM>Nope.  This is about the time to get in the beef business.  Probably
>JM>next spring will be very good.  Grain will probably be cheaper and the
>JM>hysteria over BSE will have blown away.
>JM>--
>
>JM>Jim - Farmer - Iowa City, IA,
>JM>jnmeade@blue.weeg.uiowa.edu
>
>
>Maybe  ......with an incubation period of 5-15 years I think it is going
>to be a little longer before peoples hysteria to blow away.

Considering that if BSE can be transmitted to humans and if any
infective cattle went into the human food chain and if infective brain
was eaten in UK then it would have happened in 1986/7. That means we are
already 10 years down the line. If it was likely to be a serious problem
then we probably ought to have seen a few hundred cases by now.

We haven't so it's looking good for humans in Britain so far. Long may
it continue.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.environment,uk.environment,sci.agriculture
Subject: Re: : Mad Cow disease, BSE; Justice is served.
Date: Sat, 13 Apr 1996 08:13:28 +0100

In article <aquilla.1179447721E@emba-news.emba.uvm.edu>, Tracy Aquilla 
<aquilla@salus.med.uvm.edu> writes

>This illustrates an interesting point. How is it that the cattle are
>(supposedly) getting this disease from eating meat and bone meal made from
>sheep, but humans only get it from eating infected beef, and not from eating
>infected sheep? I realise that at this point the facts are lacking and this
>is just an hypothesis, but it seems to me a better hypothesis might be that
>IF humans can become infected by eating infected beef, then humans could
>also become infected by eating infected sheep. Does that make any sense? If
>this is the case and sheep are the true reservoir of the disease, why not
>slaughter the sheep herd and be done with the disease?

Ah, but we KNOW that scrapie doesn't cause any increase in CJD when we 
eat the sheep. Scrapie was first identified in Britain in 1720! So on 
your argument it is unlikely that eating infected beef will result in a 
human disease. What evidence do we have for this so far? Why, no 
increase in CJD in people living in the UK, who may well have been 
exposed 1986/7/8, or ten years ago.

However, lets be quite sure. Let's make certain that no animals with 
clinical disease will enter the food chain by making it a notifiable 
disease and paying farmers full compensation.

Then lets remove the source of infection by banning meat and bone meal 
from ruminant rations.

Then let's assume that all the above fails occasionally for reasons of 
human frailty and prevent a whole bunch of organs that might possibly be 
infective from entering the food chain even for healthy cattle.

Then lets set research in motion to find out a bit more. 1988 SEAC 
approach.

Now what has research shown to 1996?
1) Only brain and spinal cord is infective in terminally ill cows by 
techniques below.
2) It's ever so hard to infect other species with BSE except by massive 
doses of extracted clinically infected BSE brain directly into the 
brains of animals. Some oral routes for some animals have been found but 
the doses have been just huge. Most of the work is done by injecting 
into the brains of specific suceptible strains of inbred mice lines.
3) Calves have been infected orally with a massive dose of extracted 
brain and killed off at regular intervals. So far (I think they are 
about two years down the line) even their brains have not been shown to 
be infective. So the possible worry of animals not showing clinical 
disease but still having infected brains (which aren't eaten anyway) is 
receding.
4) Despite statements to the contrary in 1988 by some "experts" (like 
Prof Lacey) the BSE epidemic has indeed declined as predicted by the 
MAFF epidemiologists.
5) Now people are looking the 'strange young CJD' that caused the scare 
doesn't seem to be so unusual as was thought. A preserved brain from the 
1950's shows the symptoms too for example. Well before any BSE.

Any bets as to what our view of all this will be in 2005?


------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: Sat, 13 Apr 1996 08:33:53 +0100

In article <829341165snz@zhochaka.demon.co.uk>, "David G. Bell"
<dbell@zhochaka.demon.co.uk> writes
>
>After all, scrapie has been around for a long time, and people have been 
>eating mutton without any obvious problems.  Cows, on the other hand, 
>haven't evolved on a meat-rich diet.

Actually all the TE's naturally found seem to be very species specific.
They only seem to increase by cannibalism, although there is no doubt
that some of the cases have a very strong genetic link that probably is
how the spontaneous cases arrive in the first place.

The worry was that scrapie may have jumped the species barrier and
infected cattle, producing BSE. That was why the concern about BSE came
about, if anyone can cast their mind back to 1988. However research in
the USA has now shown that cattle infected with scrapie (injection into
the brain etc) show a *different* pathology to that of BSE. So it's now
unlikely that this was how BSE came about. *Now* people are saying (see
recent New Scientist article, complete with the usual NS scaremongering)
that BSE probably always existed as a very low (1:million) level
sporadic disease of cattle and the recycling through M&B meal is the
likely cause of the epidemic. In other words no crossing of the species
barrier and it's just another species-specific TE behaving just like all
the others. Those of you who have been on this group for a while will
remember that I have always said this was the most probable scenario.
Well surprise, surprise.

NB Scrapie was first described as a sheep disease in 1720.
I expect the sheepdogs live off them in some places.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"


From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: alt.agriculture.misc,rec.food.cooking,alt.sustainable.agriculture,
	sci.environment,uk.environment,sci.bio.food-science
Subject: BSE panic ends.
Date: Mon, 15 Apr 1996 12:32:37 +0100

The European Agriculture Commissioner, Frank Fischler stated to Reuters 
yesterday that there was no health risk in eating British beef, and that 
the ban had been imposed for political reasons to support the European 
beef market. He said he would not hesitate to eat beef in Britain and he 
saw no medical reason not to do so. He said the ban had been imposed to 
make sure the beef market in Europe did not collapse as it had in 
Britain and not for public safety reasons.

His press spokesman insisted that it was not Herr Fischler who imposed 
the ban, but the council of ministers.

Ho-hum. Now you can sort out those who have been perpetrating scare 
stories, from those more level-headed people who have been trying to 
pass you accurate information.

I expect, however, that many cattle will still die before their time to 
assuage the loss of face of those in the council of ministers. In 
particular I predict that the 30 month rule (plucked out of the air as 
far as I can tell) will continue and the slaughter of Dutch calves also. 
I hope this blood makes the ministers feel happy.

Please note carefully that this has been crossposted to a large number
of groups. You should edit your groups appropriately before posting a
reply. Note also that I only subscribe to sci.agriculture and
sci.bio.food-science.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: BSE - I think it's time to calm down
Date: Mon, 15 Apr 1996 12:46:54 +0100

In article <Pine.SUN.3.91.960415093900.23569B-100000@langs>, Stephanie
Malone Thorson <smt2@st-andrews.ac.uk> writes
>On Sat, 6 Apr 1996, Ingrid K. Buxton wrote:
>
>> Oz <Oz@upthorpe.demon.co.uk> wrote:
>> >Very emotionally put.
>> .. exasperation is more like it... 
>> >However, I am unable to exactly follow why this should result in the
>> >slaughter of 60,000 innocent calves. Or are we perhaps talking scapegoat
>> >here?
>> .. if they were born to potentially infected mothers, the possibility
>> of vertical transmission should be considered... Ingrid
>
>I would point out here that the only clinical trials currently underway to
>determine if there *is* vertical transmission of BSE will not be complete
>until November 1996, and the results will not be available until early
>1997.  Surely the slaughter of potentially infected (but also potentially
>*healthy*) animals can wait until we have better evidence in hand,
>especially since there is no evidence to date that BSE can be communicated
>between animals. 

Actually an examination of the records of 300 HERDS with BSE was
undertaken, and it's this that I am using to base my evidence on. As
well as local experience, of course. So there is rather strong evidence
against maternal transmission available already in fact.

There is also the evidence that the placenta in BSE affected cows is not
infective. I believe that in scrapie, however, it is.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"


From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science
Subject: Re: Subject: Re: BSE: IFST Position Statement Update, 27 March 1996
Date: Wed, 17 Apr 1996 21:01:05 +0100

In article <gjs.3395.B0843500@aber.ac.uk>, Gaz <gjs@aber.ac.uk> writes
>
>I could indeed quote several groups who believe this view is wrong, but what 
>is the point, at the present time, (it is clear to me that) conflicting 
>evidence exists. 

It does?

>(For example: From Scrapie work (by Groschup MH, Weiland F 
>and Pfaff E. FederalResearch Center for Virus Diseases of Animals, Paul Erlich
>Str 28, 72072 Tubingen, Germany, presented at a Prion meeting at Goettingen, 
>November 1995) "Although no sensitivity for the mouse assay was known, it was 
>found that peripheral nerves may contain >10 thousand IU per gram. The most 
>important factor here is that this represents one tenth of the amount found in
>the brain (by Hadlow) in sheep. The question must arise as to the absolute 
>amount of infectivity that this represent to be present in peripheral nerves 
>(i.e. taking the senstivity of the mouse assay into account) and from that the 
>amount of BSE infectivity present in the peripheral nerves of cattle that are 
>being eaten in the UK")

Well this to my mind confirms the experiments. They can find infection 
in the peripheral nervous system of scrapie sheep (ie the tests and 
techniques are good enough to detect it). But NOT in bovine peripheral 
nervous systems. This is excellent news. The evidence is increasing that 
BSE is a classical TE of cattle and did not jump the species barrier 
from scrapie'd sheep. The disease in sheep is rather different from BSE 
as you have pointed out, infectious material is fairly liberally 
scattered throughout the organs (the placenta for example) which is not 
the case in BSE where only the CNS seems to be involved. Thank you for 
bringing this up.


>In addition Georgsson G and Sigurdarson S. (Institute for Experimental 
>Pathology, Univ of Iceland, Keldur, Reykjavik, Iceland) have said that 
>scrapie seemed to remain endemic in an area of the country (Iceland) even if 
>the sheep were removed. Could this happen with BSE????

Well, one has to say that it looks unlikely at present. Firstly we ought 
to be seeing epidemiological evidence by now, and we don't seem to be. 
Secondly the placenta in BSE does not seem to be infective, unlike 
scrapie. Thirdly, as I have pointed out before, sheep typically lamb in 
high density (in UK, maybe Iceland too) on the same field annually so 
coupled with infective placenta (and I believe also amniotic fluid) and 
a rather undegradable PrP, infection from the soil is in scrapie not out 
of the question. So there is good reason to hope and expect this not to 
be a problem in BSE.

>I am not saying the above will be true for BSE as well, only that info from 
>all areas should be considered, especially as we actually know so little about
>BSE.

They were considered at the time BSE came to prominence, it was all over 
the agricultural press. Luckily hasty decisions were not taken, which 
would have been very expensive, quite unnecessary and resulted in many 
more cattle slaughterings than were needed.

>The BBSRC
>
>>>>> and measures have been taken, and
>>>>>strengthened, to exclude from the food chain certain parts of the
>>>>>animal, including all those parts shown to be capable of carrying the
>>>>>infective agent.  These measures require the most stringent
>>>>>enforcement and heavy penalties for evasion.
>>
>>>Which up to now have been a joke. Thousands of BSE infected cattle get into 
>>>the meat supply, 
>>Evidence please. 
>>As I understand it a small number of tiny abbatoirs got a bit careless.
>>The inspectors found them, the govt. published the information. One (at
>>least) is being prosecuted. How transparent do you want it? You get the
>>truth, you blow it up, you complain of lies and deception. Do YOU
>>habitually lie and misrepresent? Oh. Well actually most people don't.
>
>You don't need evidence, to me it seems clear that this has to be happening. 
>Reported BSE cases showing clinical signs get removed from the food chain, we 
>both agree on that. Everybody also agrees that the disease is slow, taking 
>years to progress to the stage where clinical signs are clear. Thousands (in 
>fact tens of thousands) of cattle have been reported as BSE infected, older 
>cattle, cattle to be kept on in the herd. How many younger cattle carry BSE 
>within them without showing clinical signs and go to our tables. 
>
>None, hmmmm

Well no, not none. An animal showing the early signs is quite unsaleable 
since any buyer at a market would notice something amiss, they know 
their stuff. We are talking about pre-clinical. Now the work on the 
animals deliberately infected (with 100 times the dose known to 
guarantee disease) have shown no infectivity as they have been 
slaughtered and tested so far (except for at one age, very early on from 
the stomach, probably direct contamination). I believe they are over 30 
months (oh, that's where that came from) and still showing no 
infectivity. This means that prime beef is OK since this is mostly under 
30 months and in any case the incidence in beef herds is very low and 
(although I haven't seen any figures) almost certainly largely confined 
to bought in suckler hereford x friesians from the dairy herd. 

As a consequence I support (and always have) the disposal of the head 
and spinal cord from ALL animals that enter the food chain. SEAC are not 
stupid people, they recognised this problem and ensured that potentially 
dangerous offals should not be eaten until more work was done. Well, now 
the work HAS been done and we know that most of the offals are safe, 
however it really isn't politically sensible to alter the ban at this 
time, is it?

So even if some pre-clinical cases get through, no potentially infective 
material enters the food chain.

Sounds very sensible to me.

>Very difficult to prove I know, but some must get through the net, and I would 
>suggest that the some is in fact more than ever got reported as official BSE 
>cases. If the contaminated feed issue (Re:Scrapie) is true (and it seems to me 
>that more people are going against this theory), than this number will be 
>massively reduced today.

Sorry, I cannot understand what you are saying here.

>You probably regard this as scare mongering, but clearly the prion is in the 
>cow a long time before BSE can be seem, so how could we possibly prevent such 
>animals getting into the beef supply?

That's just what SEAC thought too, so they did something about it. They
knew their stuff.

>>>and checks comfirm that in addition a massive proportion of 
>>>slaughter-houses fail to abide by the goverments (limited) measures.
>
>>Evidence please. 
>>As I understand it a small number of tiny abbatoirs got a bit careless.
>>The inspectors found them, the govt. published the information. One (at
>>least) is being prosecuted. How transparent do you want it? You get the
>>truth, you blow it up, you complain of lies and deception. Do YOU
>>habitually lie and misrepresent? Oh. Well actually most people don't.
>
>On a BBC special (wot, no real papers..) the BBC stated that some high 
>percentage of abbatoirs (I think it was as high as 30%) failed to apply fully 
>the goverment methods of control. This was put to the Ag minister and a 
>scientist speaking on behalf of the goverment (who's name I have forgotten...) 
>neither of them denied it. It was apparently the goverments own figures.

You ever had an inspection from a govt. inspector? They can always find
*something* wrong, hey it's their job. "Fully applied" could just mean
that they don't have red, blue and yellow washbasins and towels for the
appropriate use (I believe that this has become a requirement, for
example). What is important is whether *important* controls are not
being applied, if not they should be fined. I agree. One (at least) has
been, and that's GOOD.

>>>>>Placental transmission has been identified as
>>>>>a likely route in sheep. 
>>
>>>But the potential for it an cattle has been largely ignored. 
>
>>AARRGGH! It was the main worry in 1988. So far evidence has shown it to
>>be nil, or insignificant. We are now many years down the road, if it
>>were to be a problem it would have surfaced by now. At worst it will
>>result in a very, very low level of disease indeed for another
>>generation of cows.
>
>The research started in 1988 has not been published yet (not that I know of 
>anyway). More recent studies initiated by MAFF and BBSRC are also unfinshed.

Eh? Take cow as wot died of BSE. Remove placenta. Perform usual 
extraction procedure. Inject into suitable mice. Wait three years. 
Publish results. I'm sure it's been done. Of course it's been done, hang 
on a tick. Yes, SEAC report after H. Fraser 1994. EC commission 
proceedings.

>Indirect evidance, such as epidemiological studies and models by people such 
>as Dealler

Dealler, ha, ha, laugh.

> suggest BSE did not fit with the epidemiology that was expected for 
>a disease that was passed purely through feed, indeed vertical transmission 
>would fit much better (see http://www.airtime.co.uk/bse/intm.htm).
>
>Again, I do not claim that this is the case, only that supposed rock solid 
>evidance is being questioned.

Shoof. Just look at the epidemiological data. Lacey and Dealler had a
good run for their money, probably got a grant or two, but as far as I
am concerned they discredited themselves, even if they got some self-
publicity.

>>>I am. Why hasn't the research been carried out...
>
>>AARRGGHH! Over 300 papers published, most if not all of the things you
>>have worried about have been investigated. Please go to your univeritly
>>library and look them up! You are in the privilaged position of being
>>able to do so, take advantage of it.
>
>I have actually done so, not on a massive scale, and I have not read the 300 
>or so papers available, but I have read enough to realise that research in 
>other countries does not always supprt what has gone on here in the UK. 
>
>In addition, many of these 300 papers do not actually shed any 
>light on the disease generally and its possible spread as such. 
>
>Could it be that via library searches, veronica, gopher, webcrawlers and all 
>the other nice aids we have at our command we actually know more than you 
>think about the problem. 

Careful, careful. Anybody at all can say whatever they like in
unreferenced material on the net. I really don't believe that you, as a
scientist, would fall for that one.


>>>>>      to prohibit the feeding of material containing animal protein
>>>>>derived from ruminants to cattle and other ruminants;
>>
>>>>Note that this occurred in July 1988. Even allowing a year for odd local
>>>>stocks to be used we should be pretty certain that animals born after
>>>>1st Jan 1990 never ate any infective material.
>
>>>So why are they still going down with BSE? 
>
>>You DO understand the epidemiology? You DO know how long a cow lives in
>>a dairy herd? So why ask this stupid question. Yet again.
>
>Because you aint answered it.
>
>The question has been raised at the National Food Alliance in April 1995 and 
>by others. 
>
>Somehow it would appear that the "official" facts do not tie up. 

There have been cases of pig food fed in error as cow food. I do not
personally believe that feed mills are anything like careful enough to
ensure that potentially infected M&B meal CANNOT get into any cattle
feeds. Dust, mixers, grinders, elevators, bins, you name it - all must
be kept spotlessly clean between poultry & pig, and cattle feed. I doubt
that this is done. It would only take dust from a lorry tipping M&B meal
for pig rations to blow over feed for cattle and you have a risk. It
scares me to death 'cos I cannot get my herdsman to use our own straight
feeds for weaning the calves. Even then I worry if the lorry that brings
my straight vegetable feeds has been carrying M&B meal on the previous
load and I'm damned sure that the driver would never wash out the lorry
between loads. You don't have to be a genius to see how infection can
still take place in the real world. After nearly three years clean I
need another case like a hole in the head.


>Some researchers claim that cattle showing signs of BSE have apparently not 
>received any infected food at all, and that the epidemiology is simply not 
>acceptable as presented, again suggesting horizontal or verticle transmission.

Impossible to prove either way, I'm afraid. Does (did) organic duck or 
chicken feed contain M&B meal? I've no idea. Does 'organic' fertiliser 
contain M&B meal, well it certainly used to. Would an organic farmer get 
struck off if he had been found to be using 'non-organic' feeds, 
certainly. Might suppliers of 'organic' feeds have been a bit naughty, 
was there any contamination elsewhere? Who knows. I certainly don't feel 
like arguing in a situation where the evidence has been gone eight 
years. Despite my efforts to the contrary, I cannot but have a suspicion 
that someone, somewhere (and it may well not be the farmer) did, or 
supplied something they shouldn't have. Or nobody has spotted the 
contamination route.


------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"


From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.environment,uk.environment,sci.agriculture
Subject: Re: : Mad Cow disease, BSE; Justice is served.
Date: Fri, 19 Apr 1996 06:58:42 +0100

In article <4l6r3m$pd2@luggage.rednet.co.uk>, Nick Hunter
<hunter@online.rednet.co.uk> writes

>Only last week in the news, a farmer was in court for breaching BSE beef
>sales rules, 

Yes. Correct. Most notably as being as far as I am aware the ONLY one,
despite rules having been in operation for some years. The vast majority
of farmers are straight and honest, dissapointingly boring though that
is.

>yet I heard today that someone took a blow-up rubber cow in
>a truck all the way from Britain to Hamburg and no-one in customs stopped
>them or even batted an eyelid. The trade in spongyBrit beef is gonna be
>BIG folks ....

I doubt it. Losing a lorry load of beef and collecting a big fine is
enough to bankrupt you, in any case why bother? There's no big fortune
to be made this way.

>I would like to ask people like the Gidleigh Park Hotel: "By what
>standards are organic beef products recognised, and how far back in
>documented herd lineage are all herd members similarly validated as being
>'organic'?" Because I for one, don't believe a word of it.

Well I am NOT an organic farmer. I actually think that much of what they
say is wrong and misguided. However I DO think the vast, overwhelming,
majority of UK organic farmers stick by the draconian rules, which I
rather doubt for other countries. The soil association is evangelical in
it's checking up. So *I* DO believe them.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: BSE contradictions
Date: Fri, 19 Apr 1996 23:13:40 +0100

In article <4l6que$p@cc-server9.massey.ac.nz>, Arnold Chamove
<A.S.Chamove@massey.ac.nz> writes
>       I am a bit confused.
>
>1--First they say BSE came from scrapie sheep meat rendered.
>Then they say it isn't in other countries that render sheep and have scrapie

This was considered a reasonable possibility at the time (1988). Of
course the media somewhat misrepresented it, along with various pressure
groups and publicity seeking scientists. It is looking increasingly
unlikely that BSE derives from scrapie, it's most likely a natural TE of
cattle. Given the ease with which it would normally self-eradicate
itself in cattle it would have been a very low level disease indeed
before M&B meal allowed it to spread.

>2--First they say it started with a change in the rendering process.
>Then they say it was present in a small number of herds before that change.

A new one on me. Have you any references?

>3--First they say it is not contageous.
>Then they say they will kill all of the herds that are high risk, even though 
>the infectious agent is supposedly kaput.

"To increase confidence". There is no point in this at all other than to 
allow the media and others to get their pound of flesh. So to speak.

>4--First they say it is not maternally transmitted or contageous.
>Then they say it was in the UK before the rendering change and presumably kept 
>there, albeit at low levels, by some mysterious process that was not 
>contagion.

Did you know that 15% of the cases of Haemophilia do not come from the 
parents but are a natural (and relatively common) mutation? There are 
quite a number of diseases like this. One would expect that BSE would be 
similar, certainly genetic susceptibility can be very important in the 
transmissibility of TE's. The sheep scrapie eradication scheme is 
largely based on breeding in resistant genes, for example.

>       If the source was defective infected meat processing and that has been 
>stopped (no longer use low temperatures and the absence of chemicals)...
>
>a--then why can't the meat of infected animals be rendered and used by the 
>now-safe old process (and maybe only used for dogfood)?

A very good question. I would suggest pigs and/or poultry myself.

>b--then why do any animals who were not fed before 1990 (or whatever) have to 
>be killed?

Good question.

>c--then why are there such things as 'high-risk' herds?

Well I don't know, but I could guess. For example a herd in a farm
surrounded by pig or poultry housing could well be such an example due
to the ease by which feed using (until recently) M&B meal for the
pigs/poultry could contaminate cattle feed. Dust, human error, escapes
......

>d--then why was there BSE before the change in rendering and how was it kept 
>from going extinct?

See above for a reasonable possibility.

>e--then why isn't there BSE in the USA who feed (14% I recall) beef render to 
>beef and elsewhere?

Good question.

Actually it's not just the US. Continental Europe is in much the same
position. An explanation would be most helpful. Nobody knows why.

I recently went to a BSE conference and saw posted up a map showing the 
cases by county. This was rather interesting. Even allowing for the 
cattle densities in the various counties in the UK it still showed an 
odd distribution. The number of cases pretty much indicated an original 
source in the West Country, with numbers decreasing steadily as you went 
away from a point around Southampton. Scotland, for example, is 
relatively free of the disease. Now Southampton is a major port for the 
import of feedingstuffs into the UK. I have seen quoted that a 
significant quantity of M&B meal was imported into the UK from Africa. 
Africa arguably has the greatest diversity of bovines and related 
species in the world, and I do rather wonder if BSE might possibly 
originate from there, in a closely related host where there is 
significant animal to animal infection as you get in scrapie. This would 
explain the really rapid onset of cases which the more you look at it 
doesn't have the feel of a small number of cases building up to a large 
number by infection. It looks more like a rather large initial infection 
that was then propagated by the animals ending up in M&B meal via the 
knacker. The variable incubation period makes this less obvious, but you 
would really expect a much slower onset than we seem to have had if it 
started from one or two animals. This would mean that the infection was 
in fact identified rather early and although the UK did indeed export a 
large amount of M&B meal to the continent much of it may at that time 
have been uninfected, or only contained trace amounts. In this case the 
very low level of BSE there is not quite so unexpected, although (with
the exception of Switzerland) 'surprisingly low'.

I must point out strongly that the above paragraph is highly 
speculative.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: BSE contradictions
Date: Sat, 20 Apr 1996 08:42:42 +0100

In article <4l6que$p@cc-server9.massey.ac.nz>, Arnold Chamove
<A.S.Chamove@massey.ac.nz> writes

Ooops. I misanswered a question.

>2--First they say it started with a change in the rendering process.
>Then they say it was present in a small number of herds before that change.

These are not exclusive. One or the other might not have caused the 
spread of the disease. Both together, of course, would. So these are not 
contradictions.



------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: jralphb@easynet.co.uk (J Ralph Blanchfield)
Newsgroups: sci.bio.food-science
Subject: Re: BSE panic ends.
Date: Sun, 21 Apr 1996 13:49:36 GMT

On 16 Apr 1996 19:23:25 GMT, proberts@lynx.informix.com (Paul Roberts)
wrote:

>In article <bnDpLBAVPjcxEwN2@upthorpe.demon.co.uk>,
>Oz  <Oz@upthorpe.demon.co.uk> wrote:
>>The European Agriculture Commissioner, Frank Fischler stated to Reuters 
>>yesterday that there was no health risk in eating British beef
>
>I suspect that it will take more than confident statements from Frank 
>Fischler and the pseudonymous "Oz" to set minds at rest on this one.

Hello All,

Unfortunately, Paul is absolutely right. It has all gone way beyond
scientific considerations, and is embroiled in politics and
economics, inflamed by media hype and by continuing attempts by a few
long-term prophets of doom to justify their past prophesies (as the
well-known saying goes "Well, they would, wouldn't they?").  

I am sure they will be as glad as the rest of us if their prophesies
should in time prove false, but they ought to be careful to avoid
making statements that the media and others might quote or misquote
giving the impression that they would be disappointed to be proved
wrong..

Because their prophecies make the best sensational headlines or TV
programmes, they have always been the ones to be interviewed and
quoted by the media, which has obscured from the public the fact that
the vast majority of scientists who are familiar with the present
state of scientific evidence on the subject do not agree with them. I
can certainly speak for food scientists.

Scientists always have to keep open minds. They have to act on
existing knowledge while recognising that further research will bring
new information and knowledge, which may in turn lead to revised
conclusions. The existing body of scientific knowledge (far greater
today than when BSE first came to light, because of the extensive
research carried out since then) does not provide grounds for
assertion of doomsday scenarios. 

>From The Manchester Guardian Weekly, week ending November 26, 1995 (page 10):

>Renewed fears that "mad cow disease" - bovine spongiform encephalopathy 
>(BSE) - could lead to an epidemic of the Creutzfeldt-Jacob Disease (CJD)
>in humans were raised by a medical microbiologist, who questioned the
>government's assertion that the public were not at risk.

>Dr Stephen Dealler, writing in the British Food Journal, claimed that
>most adult British meat-eaters will, by 2001, have injested a potentially    !!
>fatal dose of meat infected with BSE. 

Not in the quotation from the press report, nor in the British Food
Journal article to which it refers, nor in the printed handout that
Stephen Dealler provided to those attending the meeting referred to in
the next paragraph, was it mentioned that his oft-repeated
calculations would only be of any relevance _if_  it had been
demonstrated that BSE is transmissible to humans, which it has not.
Otherwise the calculations are like medieval speculations about how
many angels can dance on the head of a pin. 

At a meeting of the Parliamentary Food and Health Forum at the House
of Commons on 20 February 1996, he was one of two speakers on BSE (the
other was Dr Robert Will, Director of the CJD Surveillance Unit, and
Vice-Chairman of SEAC). After talking about transmissions among
animals Dr Dealler prefaced his account of his calculations by saying,
in an almost throw-away line "So there is a 70% chance that BSE is
transmissible to man". In the discussion that followed the two
presentations, he was challenged (by me) to produce a  reference to
scientific research that could substantiate such a statement. He was
unable to do so, and was reduced to saying "Well, it can be
transmitted to other animals;  and man is an animal, isn't he?"

The recent events and concerns were precipitated on 20 March, when
SEAC conjectured "On current data and in the absence of any credible
alternative the most likely explanation at present is that these cases
are linked to exposure to BSE before the introduction of the SBO ban
in 1989". This was repeated by the UK Government and led to
far-reaching adverse consequences.

It has now become apparent that SEAC's conjecture, and the official
statements based on it,  had little if any substance behind them . 

It was 17 days later  (and 13 days after the issuing of the IFST
Position Statement Update of 27 March 1996) that the research report
of the CJD Surveillance Unit, on which SEAC's and the UK Government
statements were based,  was published (Will et al, The Lancet (1996),
347, 6 April 1996, 921-925).

 Looking at the shared factor possibilities actually examined in the
paper, apart from eliminating exposure to iatrogenic CJD through well
known routes, the only other possibilities mentioned were working as
butchers, on farms or in abattoirs, or eating beef or beef products --
all, it will be noted, containing the built-in assumption that the
variant CJD is BSE-derived. Eliminating the first three, it was
conjectured that the last was the "most likely" explanation. No
possibilities that did not contain the built-in assumption of
BSE-induced cause were considered.  A result obtained by a  process of
elimination from only a limited number of possibilities all based on
the built-in preconception of that very  answer, and unsupported by
scientific evidence, is not of much (if any) value.

The CJD Unit's research paper did add  (p 924-925) "That it (V-CJD) is
due to exposure to the BSE agent is perhaps the most plausible
interpretation of our findings. However, we emphasise that we do not
have direct evidence of such a link and other explanations are
possible."  SEAC paraphrased and interpreted the first sentence but
failed to mention the second.

The SEAC speculation has been further undermined by subsequent reports
of an apparent case of V-CJD in France and two in Germany (one of whom
was said to be a lifelong vegetarian). Likewise, a few days later, Dr
Gareth Roberts, after having examined the Corsellis Collection of 8000
brains at Runwell Hospital, Essex, was reported as saying that he had
found cases the appeared to be Variant-CJD,  that predated BSE, and
that this cast serious doubt on the SEAC speculation. Dr Roberts's
research has not yet been published, as far as I know, but it will
make interesting reading.

The following three letters in the British Medical Journal of 20 April
1996 are of direct relevance to the above.

Regards to all

Ralph

>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>

Creutzfeldt-Jakob disease and bovine spongiform encephalopathy

Scientists who inflame public anxieties must share responsibility for
resulting panic 

EDITOR - Recent editorials on the danger of bovine spongiform
encephalopathy causing Creutzfeldt-Jakob disease in humans confirm
that academic scientists are as much in the grip of the irrationality
of the mad cow panic as is the public.[i,ii] a Paul Brown recalls his
judgment of last November that the available evidence suggested "a
negligible risk to humans,"[iii] only to confess that it now appears
that I was wrong."[i] However, he adduces no new evidence to justify
this about turn, simply repeating the now familiar refrain that "no
better explanation is presently forthcoming." 

Being unable to advance a better explanation than that offered by a
hypothesis for which there is only the weakest circumstantial backing
is a dubious basis for endorsing that hypothesis. Yet, within a few
sentences, Brown is raising the spectre of "a potential medical
catastrophe." If an eminent scientist can swing in four months from
characterising bovine spongiform encephalopathy as a negligible risk
to warning of potential catastrophe is it any wonder that the public
is confused and frightened? 

With rhetorical flourish, Sheila M Gore demands, "let us have done
with misleading the profession, the public, and the press" and insists
that "all evidence must be quantified."[ii] As there is no evidence
for a link between bovine spongiform encephalopathy and
Creutzfeldt-Jakob disease it cannot be quantified; what is misleading
is to imply that the link is something more than the weakest of
hypotheses. Yet this is exactly the effect of the statement that there
is "no better explanation" or that this is "the most likely cause.
Echoed in parliament and the press, such statements have fuelled the
mad cow panic. Gore's powerful metaphors about British beef consumers
continuing "to play Russian roulette" can only contribute to the
hysteria. 

Gore emphasises the need to learn the lessons of the AIDS crisis. Back
in 1987 I argued that there was no evidence to justify the promotion
of fears of an imminent explosion of HIV infection among heterosexuals
in Britain.[iv] Now, nearly a decade later, we have a health scare not
about a disease but about the possibility of a disease, Scientists who
inflame public anxieties about uncommon or rare or possibly
non-existent diseases (like bovine Creutzfeldt-Jakob disease) must
take their share of the responsibility for the resulting panic and its
consequences. 

MICHAEL FITZPATRICK
General practitioner

Barton House Health Centre
London N16 9JT

References

     i. Brown P. Bovine spongiform encephalopathy and
Creutzfeldt-Jakob disease. BMJ 1996 312,790-1 (30 March.) 

     ii. Gore S. Bovine Creutzfeldt-Jakob disease? BMJ 1996 312,790-1
(30 March.) 

     iii. Almond JW, Brown P, Gore SM, Hofman A, Wientjens DPWM,
Ridley RM, et al. Creutzfeldt-Jakob disease and
     bovine spongiform encephalopathy: any connection? BMJ
1995;311:1415-21(25 November.) 

     iv. Fitzpatrick M. The truth about the AIDS panic. London.
Junius, 1987. 

>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>

Doctors and scientists must be able to communicate degree of risk... 

EDITOR - The handling of the issue of bovine spongiform
encephalopathy[i] is an example of the consequences of poor
communication about risk. Risk management and the communication of
risk are not new, and it is disappointing that the principles of the
communication of risk have not been applied. The Environmental
Protection Agency in the United States has published a set of rules
and guidelines, most of which seem to have been ignored in the past
few weeks[ii].' accept the public as a legitimate partner; listen to
your audience; be honest, frank, and open; meet the needs of the
media; speak clearly and with compassion; coordinate and collaborate
with other credible sources; and plan carefully and evaluate
performance. 

Analysis of the problems encountered in terms of the sources of
information on bovine spongiform encephalopathy and Creutzfeldt-Jakob
disease, the means of communication, the messages that have been
given, and the people receiving the information is revealing. There is
a general lack of trust in the responsible authorities; there has been
disagreement among scientific experts; the reporting of the issues in
the media has dramatised events and emphasised the conflicts; and it
has been difficult to explain the scientific uncertainties to a lay
public that has inaccurate perceptions of risk and demands scientific
certainty. 

While the finger of blame will be pointed at the government, none of
us can afford to be complacent. As doctors or scientists we are asked
to give opinions about a range of issues, not all of which lie within
our area of expertise. We will probably also be asked about issues
that are at the boundaries of medical and scientific knowledge and
about which considerable uncertainty exists. It is incumbent onus to
be aware of all the arguments and to be able to communicate the levels
of uncertainty associated with them in an understandable fashion. We
need to work with the media so that we remain in control of the
debates, and, above all, we must preserve our professional
credibility' at a time when those around us are losing theirs. 

JOHN HARRISON
Senior lecturer in occupational medicine

Department of Environmental and Occupational Medicine
Medical School
University of Newcastle Newcastle upon Tyne NE1 4HH


References

     i. Dillner L. BSE linked to new variant or CJD in humans. BMJ
1996;312:795 (30 March.) 

     ii. Cohrssen JJ, Covello VT. Risk analysis: a guide to principles
and methods for analysing health and
     environmental risks Washington: National Technical Information
Service, US Department of Commerce, 1989, 

>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>

Advisory committee's conclusion was based on "absence of any credible
alternative" 

EDITOR - On 20 March the Spongiform Encephalopathy Advisory Committee
in Britain issued a statement regarding 10 cases of Creutzfeldt-Jakob
disease that showed a previously unrecognised and consistent pattern
of disease.[i] The committee concluded: "in the absence of any
credible alternative the most likely explanation at present is that
these cases are linked to exposure to BSE (Bovine spongiform
encephalopathy) before the introduction of the SBO [specified bovine
offal) ban in1989."  How can a committee of scientists come to a
conclusion on the basis of no credible alternative? Why exposure to
bovine spongiform encephalopathy and not to microwave ovens, high
voltage power lines, or organophosphorus sheep dips? 

These few words have caused an epidemic of hysteria across Europe and
paralysed the British beef industry at home and abroad. Pharmaceutical
companies are being besieged by patients concerned about the possible
risks of medicines of bovine origin. For example, diabetic patients
are asking whether they should continue to take beef insulin (in the
case of the pharmaceutical company to which I am a medical adviser the
insulins are made from pancreases from cattle outside the British
Isles). 

Another concern is that the suicide rate in British farmer - which is
currently among the highest by occupation in Britain - will increase
and that the increase will exceed the number of deaths from
Creutzfeldt-Jakob disease over the coming months. All this when, in
the committee's own words, "there is no direct evidence of a link." 

ANNE WICKHAM
Consultant pharmaceutical physician
PO Box 246
Canterbury CT4 5YY

>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>



******************************************************************
J Ralph Blanchfield
Food Science, Food Technology & Food Law Consultant
Chair, IFST Member Relations & Services Committee
Web Editor, Institute of Food Science & Technology
IFST Web address: http://www.easynet.co.uk/ifst/ 
******************************************************************



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science
Subject: Re: BSE panic ends.
Date: Sun, 21 Apr 1996 18:10:47 +0100

In article <317a3bf3.30642273@news.easynet.co.uk>, J Ralph Blanchfield
<jralphb@easynet.co.uk> writes

>>Dr Stephen Dealler, writing in the British Food Journal, claimed that
>>most adult British meat-eaters will, by 2001, have injested a potentially !!
>>fatal dose of meat infected with BSE. 
>
>Not in the quotation from the press report, nor in the British Food
>Journal article to which it refers, nor in the printed handout that
>Stephen Dealler provided to those attending the meeting referred to in
>the next paragraph, was it mentioned that his oft-repeated
>calculations would only be of any relevance _if_  it had been
>demonstrated that BSE is transmissible to humans, which it has not.
>Otherwise the calculations are like medieval speculations about how
>many angels can dance on the head of a pin. 

Given the difficulty of infecting animals by mouth even when neat brain 
extract is used I would quite like to see how he makes this calculation 
anyway. He must either be assuming that significant quantities of brain 
is being eaten by humans, which is patently untrue, or that meat is 
infective which has been shown not to be true (even when injected 
directly into the brain). So what is his argument?

>At a meeting
>g of the Parliamentary Food and Health Forum at the House
>of Commons on 20 February 1996, he was one of two speakers on BSE (the
>other was Dr Robert Will, Director of the CJD Surveillance Unit, and
>Vice-Chairman of SEAC). After talking about transmissions among
>animals Dr Dealler prefaced his account of his calculations by saying,
>in an almost throw-away line "So there is a 70% chance that BSE is
>transmissible to man". In the discussion that followed the two
>presentations, he was challenged (by me) to produce a  reference to
>scientific research that could substantiate such a statement. He was
>unable to do so, and was reduced to saying "Well, it can be
>transmitted to other animals;  and man is an animal, isn't he?"

But we don't eat beef brains. What is the man talking about? He must 
have some logic (mustn't he?) what is his argument? Why do we never hear 
it? Does Ralph know what it is?


------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.environment,uk.environment,alt.sustainable.agriculture,
	sci.agriculture,scot.environment,misc.consumers,alt.politics.greens,
	alt.org.earth-first,alt.save.the.earth
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: Mon, 22 Apr 1996 06:39:50 +0100

In article <UW6vhBAl7rexEweO@denby.demon.co.uk>, Paul Clarke
<paul@denby.demon.co.uk> writes

>The trouble with this correspondence is that everybody seems to have a
>view on BSE but few if any of the contributors are sufficiently
>knowledgeable to have a fully informed opinion. 

You must have come in late. There have been plenty of references quoted,
and I don't mean 'The Observer', but refereed scientific ones.

Since 'hay mites' is a completely new one to me, perhaps you would like
to tell us the paper it referred to, I mean the scientific refereed one?

>The latest theory
>(supported by experimental evidence - see The Observer 21/4/96) is that
>the disease is harboured and spread by hay mites - so that whatever you
>do as regards killing off infected or suspect animals, the hay mites
>will spread the disease to any replacement stock!! Rather a worrying
>scenario - what do we do if it's true!?   

The mediafest scare story seems to be dredging the barrel. You were
aware that almost all dairy farms don't feed hay, but silage? 

I think you have been had!

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.environment,uk.environment,sci.agriculture
Subject: Re: : Mad Cow disease, BSE; Justice is served.
Date: Tue, 23 Apr 1996 09:19:47 +0100

In article <jscanlon-2204961634010001@sp78.linex.com>, Jim Scanlon
<jscanlon@linex.com> writes

>Keeping in mind that the present furor in the UK(population 56 million) is
>over 10 cases of Creutzfeldt Jacob Disease, 

Well, this is over two years, and since several of the ten were still
alive, they really belong in statistics for another year. So let's say
three per year (possibly less) out of an average number of UK CJD cases
of around 60 per year or 5% of the CJD cases with an incidence of one in
twenty million population per annum. I for one wouldn't be confident
that cases in the past happened but were not identified due to the
atypical clinical presentation. Ie they were considered too young to be
CJD. I would not be at all surprised to find that cases like these now
turn up all over the world simply because people are aware of it and are
looking out for it.

>I include below an excerpt
>from The Arizona (population 4 million) Daily Star(Tucson, population
>400,00) 19 March 1987 By James Erickson and Cynthia Hubert about how CJ
>Disease confirmation take place in the U.S.
>
>"The Creutzfeldt-Jakob malady was initially believed to have killed about
>20 Tucsonans in the last 10 years. Based on national statistics, that
>would have been an extraordinarily high rate. However, Crom said those
>initial estimates apparently were inflated.
>
>A thorough search of medical records has confirmed that five people have
>died of symptoms associated with Creutzfeldt-Jakob disease in Tucson over
>the past seven years, Crom said.
>
>Based on strict criteria for defining the disorder, two of those cases are
>"definite," two are .'probable" and one is "possible," he said. Two more
>cases among people who lived outside of the city limits are also
>considered definite, he added.
>
>"In my opinion, the data indicate that the rate is not excessively high,
>or high at all," said Crom.
>
>Even if all five of the Tucson cases were classified as definite, Crom
>said, the incidence of the disease locally would be less than 3 cases per
>million people per year.
>
>"If you just  consider the two definite cases, that would work out to
>about 0.8 per million per year," he said. "So this is right in the ball
>park with other studies in other areas of the country. It does not appear
>to be excessive in any way."
>
>Crom said previous studies have put the average incidence at between 0.25
>and 3 cases per million people per year.
>
>Only people whose symptoms surfaced while they were Tucson residents were
>considered in the local study, Crom said. For cases to be definite, a
>diagnosis of the disease had to have been confirmed by "a certain amount
>of clinical data" or by an autopsy or biopsy of the victim's brain tissue,
>he said."

With an incidence of 1:1,000,000 random clusters of cases are
statistically certain to appear from time to time. It's very hard to
explain this to people who do not understand statistics. You know, the
people who think that when you have thrown four sixes in a row, the
chance of the next one being a six is less than one in six.

Of course if Tucson has a higher than average group over 50 years old,
due to it being a popular retirement area for example, one would expect
a higher than average incidence of CJD anyway.


------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: alt.agriculture.misc,rec.food.cooking,alt.sustainable.agriculture,
	sci.environment,uk.environment,sci.bio.food-science
Subject: Re: BSE panic ends.
Date: Tue, 23 Apr 1996 09:20:41 +0100

In article <andy.116.002F32A4@windmill.dungeon.com>, Andy
<andy@windmill.dungeon.com> writes
>In article <HINwQCAlrOdxEwUb@upthorpe.demon.co.uk> Oz <Oz@upthorpe.demon.co.uk> 
>writes:
>
>>Well, see, there's this thing about it taking five to ten years after
>>infection before clinical symptoms appear, and it is generally accepted
>>that some feed in store etc was used up to 1990. I could go on, but many
>>readers in several of the groups posted have heard it all before.
>>Needless to say the decline is exactly what the Govt epidemiologists
>>prediced in 1988, so surprise surprise.
>
>I've heard that view before but I'm struggling to think what feed manufactured 
>before the ban 7/88 might still be usable in or upto 1990.

There were some transitionary arrangements, but I forget the details.
Certainly left over calf food would typically be used the following
year, particularly if calving was seasonal. As I remember at the time it
took (doesn't it always) quite a time for the regulations to be properly
implemented (and probably published) and for stocks in the feed mills to
be used up. I think that MAFF themselves consider 1989 as being suspect
as they went round plugging holes and finding bits of old feed here and
there. As a result it is generally considered that 1990 (ie Jan) as the
point when the ban was really effective (but see below).

>The expiry date on compound cattle feed is generally 3 months from 
>manufacture, the only things I can think of with even a one year shelf life 
>are some mineral supplements (no animal protein) or some calf milk replacers. 
>I know of no calf milk containing meat & bone meal (as defined by SEAC) - 
>surely people aren't suggesting the milk powder and/or tallow in calf milk 
>replacers carry BSE?

The expiry date is typically on the vitamins. Most farms will use old
feed if sweet and clean, maybe blending it with new at say 1 bag of old
to two of new.

>Many other people seem to have assumed that simply because it was permitted to 
>use ruminant meat etc in ruminant feeds that everyone manufacturing cattle 
>feed did do so. Clearly there are going to be exceptions where for a variety 
>of reasons cattle feed was manufactured without meat & bone meal even during 
>the '81-88 period when the "infection" was supposed to have been propagating.

Least cost formulations tend to throw up the same recipe wherever they
are done. So the differences may be less than one might imagine.

I have been discussing the possible contamination of cattle feeds with 
M&B meal used for pig and poultry diets in the feed mills with people in 
the know. I am horrified. The press and various pressure groups have 
been concentrating on the poor old farmer who is doing all he can, 
indeed can do no more. Unfortunately the feed compounders have never 
been examined in depth, yet they are pretty much the only users of M&B 
meal, and they also produce (in many cases) cattle feed. I find it only 
to easy to believe that the (admittedly very small number) of animals 
born after the ban was effective, have in fact been inadvertently 
exposed to contaminated feed by this route. This would produce a 'tail'
of infected animals at very low level for some years to come and is bad
news for the cattle population even if the effect for humans is zero.



------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.environment,uk.environment,sci.agriculture,sci.bio.microbiology
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: Wed, 24 Apr 1996 20:44:31 +0100

In article <317E4B2B.5AE8@brunel.ac.uk>, Stuart D Neilson
<hssrsdn@brunel.ac.uk> writes

>I can't recall a study showing infectivity of blood in scrapie affected 
>sheep, but would appreciate a reference if you have one. 

I cannot offer you one. I have searched my (rather meagre) references 
and the only reference I can locate is one that says that scrapie cannot 
be cultured from sheep muscle, udder and milk. I am pretty sure that 
there has been reference to organs being infective, they are almost 
certainly the same as the SBO's which were derived from the rather 
extensive scrapie work. BSE has turned up in nothing but CNS in cattle 
(see various SEAC reports, these quote references should you wish to go 
further).

I have a nasty feeling that I may have picked this up from someone who 
posts on another newsgroup who quoted this. Now some people make 
statements and give references that are bogus, and since I am not an 
academic I often tend to accept them unless it looks odd since getting 
the papers is not easy. In this case since blood has been tested and 
found to be free of BSE infectivity, I wouldn't have bothered to search 
further.

>Wisniewski et 
>al's piece doesn't mention a mode of transmission between mite and sheep, 
>but blood is not mentioned. I guessed (and no more than that) that mites 
>ingest the agent in the process of consuming hay and not from ingesting 
>sheep blood directly, so faeces, placenta, saliva and other excretions 
>are all potential sources of the mites' infectivity. 

I cannot give you references (I would have come across them if I had 
them) but it seems to be generally believed that amniotic fluid is 
infectious in scrapie. This is not the case with BSE see MAFF BSE a 
progress report Nov '95, table 6. References are given. Actually a 
useful list worth getting. It seems to be considered one of the main 
causes of transmission in sheep.

>I haven't looked up 
>the geographical distribution of the six mite species named, but I will 
>do so - it is most unlikely that none of the species present in Iceland 
>do not also inhabit Britain.

I would consider it unlikely too. However I have never heard of it.

>The text also says that mite suspensions were immunostained with a 
>Western blot test for PrPsc, and immunoreactive bands were present for 
>one of the samples. Is there a test for bovine PrP which could be applied 
>to mites collected from UK farms heavily affected by BSE? If so, is it 
>possible to determine whether this study has any relevance to BSE in the 
>UK?

I am not too sure that this test is regarded as 100%. I did come across 
some references to it, but I'm not searching the 300 again! From memory 
it's used rather widely on brain extracts (ie with a LOT of PrP 
present), and is used quite widely since the much more sensitive and 
accurate in vivo mouse tests are slow and very expensive.

Just out of interest in my search (keyword scrapie) I noticed that 
scrapie has been communicated to just about every animal you can think 
of, in many cases orally. Well, I exaggerate slightly of course, I mean 
they didn't try elephants for example, but marmoset monkeys are in the 
list. Yet we KNOW that scrapie is not transferred to humans under normal 
circumstances, even to knaker workers, indeed there doesn't seem to be a 
single case. Looking at the work on scrapie you would think that the 
risk of catching a scrapie TE would be very high indeed, yet we know 
it's never been known. A thought worth keeping in mind.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: jralphb@easynet.co.uk (J Ralph Blanchfield)
Newsgroups: sci.environment,uk.environment,sci.agriculture
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: Sat, 27 Apr 1996 15:35:02 GMT

On Fri, 26 Apr 1996 23:21:59 +0100, m lomas
<paxml@unix.ccc.nottingham.ac.uk> wrote:

>On Fri, 26 Apr 1996, Oz wrote:
>> <paxml@unix.ccc.nottingham.ac.uk> writes
>[...]
>> >Heads should roll in the powers-that-be for:
>> >Not keeping a tighter check on abbatoir and feed manufacturer practices;
>> 
>> The processes have been in operation for years. Outside the UK they are 
>> (would you believe it) STILL in operation. ...
>
>Just as a Fire Inspector checks over buildings to assess any dangers in 
>how the buildings are currently being used, giving criticism so as to 
>avert fires, present industrial practices in general should be reviewed 
>by a multidisciplinary panel to assess any possible risks in the light of 
>changed circumstances or improved knowledge. Especially so where there 
>are implications for the general public, directly or indirectly.
>
>For the BSE example, the changed practice of reduced cooking temperature 
>and non-use of solvents for carcass-to-feed rendering should have been 
>investigated. Also, the closed feed loop should never have been permitted 
>in the first place for the obvious dangers.
>

What crystal balls would your investigators have used, and what
exactly would they have looked for, apart from a cooking temperature
(70 deg C) high enough to kill salmonella?

The trend to eliminate solvent extraction began in the late 1960s,
long before either BSE or prions were known. Your suggestion is rather
like appointing fire inspectors before mankind discovered fire :-)

Anyway, it really is time to clear up the vast amount of confusion
that  abounds regarding "cooking temperature" and solvent extraction,
often accompanied by references to "deregulation".to remove a heat
treatment of the product..There was in fact no applicable regulation
to deregulate,  and no such change in regulations affecting animal
feedstuffs.. I understand that in the 1960s meat and bonemeal for feed
compounding was sold to the compounders on a commercial specification
of minimum 50% protein, which could only be reached by removing all
the residual fat by a chlorinated hydrocarbon solvent extraction.
Also, in the small-scale batch processing plant of that time, milling
of a product still retaining the residual fat was impracticable.,After
extraction the residual solvent then was removed from the product by
"stripping" it with steam at 120 deg C plus.  The fat-in-solvent
solution was then evaporated to leave the byproduct, tallow. 

Tallow was increasingly being added during  compounding as an energy
supplement,. Realisation gradually dawned that it was ridiculous to go
to all the trouble, expense, hazard and environmental pollution
involved in  taking tallow out,  only for it to be added back in
compounding. This coincided with a worldwide trend to move from
small-scale batch processing to fewer large-scale continuous
processing plants of modern design, which, moreover, were more capable
of milling product with residual fat. This led to a 45% protein meal
with 8-10% fat, which could be made without solvent extraction.

So solvent extraction became eliminated.. And, of course, where there
was no solvent extraction, there was also no need for a
post-extraction steam-stripping  to remove the solvent residues.


>A recent snippet re BSE:
>
>New Scientist (27 April 1996 p21) quotes an article in Nature (vol380, 
>p675) saying that the bovine gene coding for prion precursor protien is 
>only two amino acids different from the protien coding for Man and apes.
>
>"... one worrying possibility is that the similarity between human and 
>bovine PrP makes it relatively easy for BSE to jump the species barrier 
>and affect humans."
>
>So what is the proportion of the population that may have two appropriate 
>mutations to make the match? (Beyond my genetics knowledge!)


I'll bet this snippet becomes quoted and re-quoted on the Internet and
elsewhere. Thus are myths originated. :-)

The actual paper (by Krakauer, Pagel and Southwood) in Nature says
nothing of the sort, and nothing that could remotely be paraphrased in
that way.

What they do say is very different. They say that, in looking at the
genes coding for prion proteins, out of 1,450 possible different pairs
of substitution sites, they have found 2 pairs of derived
substitutions in common between the respective genes of cattle and
hominoids.

When they look at the possible biological significance of this they
say:-

"One possibility is that the substitutions confer resistance of the
cellular prion protein to modification to the pathogenic form of the
prion protein.
Alternatively, they may improve the efficiency of this protein in the
healthy tissue of these species. As an incidental consequence of the
latter these changes might also have predisposed humans towards a
strain of prion disease occurring in B. taurus."

Regards

Ralph
******************************************************************
J Ralph Blanchfield
Food Science, Food Technology & Food Law Consultant
Chair, IFST Member Relations & Services Committee
Web Editor, Institute of Food Science & Technology
IFST Web address: http://www.easynet.co.uk/ifst/ 
******************************************************************



From: iaotb@inet.uni-c.dk (Torsten Brinch)
Newsgroups: sci.environment,uk.environment,sci.agriculture
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: 28 Apr 1996 21:17:34 GMT

To give an impression of  Prion likeness and differences:
Some examples of prion amino acid sequences lined up for comparison:

1.Line: Sheep (Suffolk)
2.Line: Cow
3.Line: Human


MVKSHIGSWILVLFVAMWSDVGLCKKRPKPGGGWNTGGSRYPGQGSPGGNRYPPQGGGGWGQPHGGGWGQPHGGG
MVKSHIGSWILVLFVAMWSDVGLCKKRPKPGGGWNTGGSRYPGQGSPGGNRYPPQGGGGWGQPHGGGWGQPHGGG
  MANLGCWMLVLFVATWSDLGLCKKRPKP GGWNTGGSRYPGQGSPGGNRYPPQGGGGWGQPHGGGWGQPHGGG
**
                                                                    
WGQPHGGGWGQPHGGGGWG        QGGSHSQWNKPSKPKTNMKHVAGAAAAGAVVGGLGGYMLGSAMSRPLI
WGQPHGGGWGQPHGGGWGQPHGGGGWGQGGTHGQWNKPSKPKTNMKHVAGAAAAGAVVGGLGGYMLGSAMSRPLI
WGQPHGGGWGQPHGGGWGQ        GGGTHSQWNKPSKPKTNMKHMAGAAAAGAVVGGLGGYMLGSAMSRPII
**
                                                                        
HFGNDYEDRYYRENMYRYPNQVYYRPVDRYSNQNNFVHDCVNITVKQHTVTTTTKGENFTETDIKIMERVVEQMC
HFGSDYEDRYYRENMHRYPNQVYYRPVDQYSNQNNFVHDCVNITVKEHTVTTTTKGENFTETDIKMMERVVEQMC
HFGSDYEDRYYRENMHRYPNQVYYRPMDEYSNQNNFVHDCVNITIKQHTVTTTTKGENFTETDVKMMERVVEQMC
**

ITQYQRESQAYYQRGASVILFSSPPVILLISFLIFLIVG"
ITQYQRESQAYYQRGASVILFSSPPVILLISFLIFLIVG"
ITQYERESQAYYQRGSSMVLFSSPPVILLISFLIFLIVG"
**

Kind regards,

Torsten Brinch



J Ralph Blanchfield wrote:

: What they do say is very different. They say that, in looking at the
: genes coding for prion proteins, out of 1,450 possible different pairs
: of substitution sites, they have found 2 pairs of derived
: substitutions in common between the respective genes of cattle and
: hominoids.

: When they look at the possible biological significance of this they
: say:-

: "One possibility is that the substitutions confer resistance of the
: cellular prion protein to modification to the pathogenic form of the
: prion protein.
: Alternatively, they may improve the efficiency of this protein in the
: healthy tissue of these species. As an incidental consequence of the
: latter these changes might also have predisposed humans towards a
: strain of prion disease occurring in B. taurus."

: Regards

: Ralph
: ******************************************************************
: J Ralph Blanchfield
: Food Science, Food Technology & Food Law Consultant
: Chair, IFST Member Relations & Services Committee
: Web Editor, Institute of Food Science & Technology
: IFST Web address: http://www.easynet.co.uk/ifst/ 
: ******************************************************************

--
In seed time learn, in harvest teach, in winter enjoy.

                                                  (Williiam Blake)



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.environment,uk.environment,sci.agriculture
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: Tue, 30 Apr 1996 19:53:19 +0100
 <31823d31.37585452@news.easynet.co.uk> <4m0n9e$ph1@news.uni-c.dk>

Great, good news. So since we know scrapie doesn't transfer to humans in
the normal course of events, we should stop worrying.

Yes?

Also note that ONE switch is enough to make a sheep resistant to
scrapie. It wants to be the right one, of course.

In article <4m0n9e$ph1@news.uni-c.dk>, Torsten Brinch <iaotb@inet.uni-
c.dk> writes
>To give an impression of  Prion likeness and differences:
>Some examples of prion amino acid sequences lined up for comparison:
>
>1.Line: Sheep (Suffolk)
>2.Line: Cow
>3.Line: Human
>
>
>MVKSHIGSWILVLFVAMWSDVGLCKKRPKPGGGWNTGGSRYPGQGSPGGNRYPPQGGGGWGQPHGGGWGQPHGGG
>MVKSHIGSWILVLFVAMWSDVGLCKKRPKPGGGWNTGGSRYPGQGSPGGNRYPPQGGGGWGQPHGGGWGQPHGGG
>  MANLGCWMLVLFVATWSDLGLCKKRPKP GGWNTGGSRYPGQGSPGGNRYPPQGGGGWGQPHGGGWGQPHGGG
>**
>                                                                    
>WGQPHGGGWGQPHGGGGWG        QGGSHSQWNKPSKPKTNMKHVAGAAAAGAVVGGLGGYMLGSAMSRPLI
>WGQPHGGGWGQPHGGGWGQPHGGGGWGQGGTHGQWNKPSKPKTNMKHVAGAAAAGAVVGGLGGYMLGSAMSRPLI
>WGQPHGGGWGQPHGGGWGQ        GGGTHSQWNKPSKPKTNMKHMAGAAAAGAVVGGLGGYMLGSAMSRPII
>**
>                                                                        
>HFGNDYEDRYYRENMYRYPNQVYYRPVDRYSNQNNFVHDCVNITVKQHTVTTTTKGENFTETDIKIMERVVEQMC
>HFGSDYEDRYYRENMHRYPNQVYYRPVDQYSNQNNFVHDCVNITVKEHTVTTTTKGENFTETDIKMMERVVEQMC
>HFGSDYEDRYYRENMHRYPNQVYYRPMDEYSNQNNFVHDCVNITIKQHTVTTTTKGENFTETDVKMMERVVEQMC
>**
>
>ITQYQRESQAYYQRGASVILFSSPPVILLISFLIFLIVG"
>ITQYQRESQAYYQRGASVILFSSPPVILLISFLIFLIVG"
>ITQYERESQAYYQRGSSMVLFSSPPVILLISFLIFLIVG"
>**

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"


From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: uk.environment,sci.agriculture,scot.environment
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: Wed, 1 May 1996 18:15:00 +0100

In article <DqqAt5.IwM@liverpool.ac.uk>, "Dr J.D. Annan"
<annan@liverpool.ac.uk> writes
>Oz (Oz@upthorpe.demon.co.uk) wrote:
>
>: Expect about 50 +-25 cases annually of CJD in the UK or around 1 per
>: million per annum worldwide (ie about 250 cases in US annually).
>
>How many of these would you expect to be under 40? What if I'd asked
>you the same question last year?

I don't know the quantities. I understand was rather high a few years
ago when quite a number of young people who had been treated with CJD
infected growth hormone succumbed to the disease. I believe there was
also some problem with facor eight (? anyway the haemophilia fix). So I
would gues the answer is variable. I believe there was a group of young
people in Tucson some years ago too.

>: Vegetarians get CJD as often as you would expect given their numbers
>: with respect to the general population.
>
>How many of the recent 14 cases is a vegetarian? (answer: 1 AFAIK, and he
>was a meat eater previously when the risk was thought to be highest).

It was reported that a German case was a 'lifelong vegetarian'. This was
from a press report so ought to be subject to caution. Another case was
reported as having lived in Australia for the previous 12 years. I look
forward to a definitive paper on the cases worldwide. Personally I
wouldn't be surprised to find it's rather less unusual than was
originally thought. 

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: misc.education.science,sci.environment,misc.consumers,
	sci.med.nutrition,sci.agriculture,talk.politics.animals,rec.food.restaurants,
	alt.food.mcdonalds,alt.mcdonalds,rec.food.veg
Subject: Re: Mad Cows and English Beef
Date: Mon, 6 May 1996 06:35:37 +0100

In article <318D02F9.2781@phy.ucsf.edu>, Dave Blake
<dblake@phy.ucsf.edu> writes

>He did fault the authors on one major point. He feels that writing a 
>paper that could cause as large a national outcry as this one did would
>have to be warranted by much stronger evidence. He feels it is possible
>that eating BSE cows would cause CJD, but far from demonstrated. I mean,
>ten people more than statistics would predict have died from CJD

I think you are misinformed here. The 10 cases are in fact effectively
spread over at least three years and the natural variation in the
disease is rather high. For example I believe that the UK had (1994?) 55
cases and the following year 29. One must be very careful of
'harvesting' cases from different years. As I understand it this 'middle
aged' CJD has now been found in other countries and some of the UK cases
are clearly 'harvested'. For example one wouldn't normally include
someone who lived the last 12 years in Australia as a UK case. For some
reason the histories of the cases hasn't been published, so it's hard to
work out exactly what is going on.


>in the UK, and the timing is linked to the BSE outbreak. For this we
>are going to kill thousands and thousands of cows ?

At least one case of the same pathology has been fround in preserved
specimens from, I believe, 1953. To say that the timing is linked to the
BSE outbreak is trite, so is the destruction of the ozone layer. The
real point is that more than adequate precautions are taken for human
consumption of beef. The disease is rapidly declining in cattle, it's
not infectious (something that Europeans have a problem getting their
heads round) and only a truly tiny number of cattle are infected. The
proposed slaughter is equivalent to exterminating a whole town if one
case of AIDS is found there. Stupid.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: BSE sense at last!
Date: Mon, 20 May 1996 18:39:22 +0100

In article <Pine.SOL.3.91.960517121125.19869A-
100000@suma3.reading.ac.uk>, "Ralph J. P. Blaney"
<aerblney@reading.ac.uk> writes
>
>On 15 May 1996, S p webber wrote:
>...I was under the impression that there was no definite age at which BSE 
>'develops', only an age at which clinical symptoms are displayed.  

The slowly culled herd of 100% infected (a massive dose was given in
their youth) indicates that this is not true. I believe that the animals
at 30 months showed no infectivity, even from their brain tissue, when
injected into suceptible mice. I think this is where the 30 month limit
originated from.

>Whether parts of the animal will contain the BSE prion will depend upon 
>how much contact it has with the agent, surely ? And recent reports 
>suggest that there could still be contaminated feed reaching cows.

It is now clear that there has been a small, but significant, cross
infection between cattle feed and pig feed containing M&B meal in feed
mills and trucks. I said that this was a likely problem some many months
ago. The thing that is really important to keep in mind is that M&B meal
is rather dusty and you could almost guarantee that workers in the
rendering plants, and feed mills will have inhaled significant
quantities of dust. This contamination would also have occurred when the
M&B was highly contaminated with BSE in the mid-late 80's. Were BSE to
be a significant human disease these workers should have already shown a
very high incidence of CJD and they are not. Remember in Kuru it was not
the men that ate the human brains who primarily went down with the
disease, but the women and children who prepared the bodies. This is one
of the many reasons why I, and my family, continue to happily eat
British beef.

>
>> 2]     All parts, that have proved capable of transmitting the disease,
>> are removed and destroyed from all of the animals at slaughter.
>
>...In theory.

Speak to you local council and ensure that they are doing their job of 
checking abattoirs and prosecuting offenders. It's their job to inspect, 
not the governments.

>> No other country does this.
>
>...This is because they don't have a problem with BSE !

Few countries in Europe have not admitted to at least a few cases. Since 
the result is whole herd slaughter, and most of the farmers employ no 
staff, you can perhaps appreciate why beef consumption has plummetted on 
the continent. It is interesting that Switzerland, a tiny country most 
of whose animals are effectively organically farmed, but who are the 
epitome of law abiding upstanding honest citizens, have an inordinately 
large number of cases compared to their neighbours.

>>  It is now time for the EU, and other
>> supermarkets and burger chains who by their actions turned a scare into a
>> crisis to follow this lead.
>
>...I don't think you can really blame the supermarkets for this problem! 
>As you stated earlier in your post sales of beef at UK supermarkets has 
>returned to roughly the level before the announcement of the possible 
>BSE/CJD link.  The problem has been that the government reacted too 
>slowly to the problem of BSE initially, and thus the confidence of 
>overseas buyers was lost.

They said they would publish all the information as they received it. 
The problem with that is that it doesn't give anyone a chance to soberly 
consider the information. Particularly when an organisation needs some 
more funding.

>> Steve Webber
>> 
>> ********* Stuff the EU - Eat British Beef. ************
>
>...It is also worth noting that some countries imposed a ban on the 
>importation of UK beef long before the EU ban came into force, e.g: USA 
>and New Zealand. Thus, a lifting of the EU ban will not restore all of 
>the markets. Many importation bans came into force just before the EU 
>ban, how likely are these to be lifted ? So, how about bashing the 'stupid' 
>yanks..etc? or, like many others in this country (esp. the Tory Right), is 
>the beef ban just an excuse for you to put the boot into the EU and our 
>fellow europeans on the continent ?

The Americans and N.Zealanders, who import no british beef worth 
considering but who are restricted from exporting into the EU by various 
devious means, jumped at the opportunity to get a little revenge on the 
EU.

One expects better from our 'colleagues' in the EU. I have been a
lifelong european, but I now view the blatant nationalistic advantage
taking of the various governments as quite unethical. Do I want to be
too closely connected with countries who behave this way? I mean Italy
still hasn't set up her milk quota system and gets away with it. If
britain had done this we would be up before the european court and fined
a few billion ECU's, and that's just one example of very many.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.med.nutrition,sci.agriculture,talk.politics.animals,
	rec.food.restaurants,alt.food.mcdonalds,alt.mcdonalds
Subject: Re: Oprah and Mad Cow Disease
Date: Tue, 21 May 1996 13:52:27 +0100

In article <4ns89p$li0@news2.tds.net>, Dale Anderson
<danders3@waun.tdsnet.com> writes
>Oz <Oz@upthorpe.demon.co.uk> wrote:
>
>>>> It has been suspected that humans can get sick from
>>>>eating diseased beef.
>>>
>>> This is the closest we ever get to _any_ kind of scientific evidence
>>>that proves that CJD comes from BSE. More research is always in order
>>>when we have questions like this. There is no real reason for panic.
>
>>Actually no. There is a lot more evidence than this. 
>
> Feel free to present some, then. So far all we've seen is maybes and
>possiblies...
>
>>And you certainly shouldn't panic. The best informed (and that's not
>>saying much) population in the world is the UK public. In the UK beef
>>consumption quickly returned to near normal after the recent scare.
>
> I never did "panic." I could see from the beginning it was only a
>"maybe."
>
>>BSE probably came into Britain in the early 1980's although it was not 
>>identified as a potential problem and controls imposed until 1988.
>
> See? Another "probably" comes into an already unstable equation. :-)

You want perfect, absolute, knowledge then you will have to wait until
you go to heaven. However it is true. Nobody knows exactly when the
outbreak first started.

> Doesn't the above timeframe also coincide with when the British gvt
>lessened the requirements imposed on the British rendering industry?
>Seems to me BSE is far more related to cannibalism issues than
>anything.

It did, to the same system used in the US and the rest of europe. MAFF
trials have since shown that NEITHER treatment deactivates prions.
Further work has shown that BSE is most unlikely to have come from sheep
scrapie as they seem to be different TE's. This leaves, as far as I can
see, two possibilities. Either it is a natural low level disease that
occurs naturally that eventually managed to get (by chance) to high
enough levels in M&B meal to trigger an explosive disease outbreak, or
it is a natural disease of some other bovine. I find it interesting that
the incidence is related to distance from Southampton, or another
western port since I remember reading that M&B meal has been imported
from Africa into the UK, and these would be the natural ports of
discharge. I need hardly remind you that Africa contains the widest
diversity of deer and bovines in the world. 

>>There is no doubt that the infection was spread via meat and bone meal. 
>>This product is a dusty meal. If BSE was easily, or even with 
>>considerable difficulty, transferable to humans then those handling 
>>this product would be at extremely high risk. They would be inhaling and 
>>handling highly infective material that before the various bans was 
>>certainly heavily contaminated. This is quite a big group which includes 
>>those working at the renderers, feed mills and truck drivers. They show 
>>absolutely no increase in CJD whatsoever. At worst this shows that BSE 
>>has absurdly low infectivity to humans, and at best none at all.
>
> I honestly don't think there is a link across species, to begin with.
>I am still open to looking at real scientific evidence that proves
>otherwise, though.

I agree. To my mind the evidence, although circumstancial (which is
inevitable in this case), is overwhelming that BSE is highly
UNinfectious to humans if at all. It can be transferred to suceptible
animals from other species with difficulty under extreme conditions,
like direct injection of extracted prion into the brain. So it is
possible. Oh, by the way I omitted abattoir workers, probably by far the
highest risk group, no increase in CJD has been observed in this group
either.

If you did that with e.coli you could be sure of a rapid 100% death
rate.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"


From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: BSE Cohort Cull.
Date: Thu, 23 May 1996 18:22:56 +0100

In article <4o045i$i21@news.uni-c.dk>, Torsten Brinch <iaotb@inet.uni-
c.dk> writes
>Oz wrote:
><..>
>: 2) If any animal in a herd born goes down with BSE (say born Dec 1991) 
>: then ALL the cattle in that age group born sept-aug <ie sept 1991 to aug 
>: 1992) will be culled.
><..>
>: 4) This is a strange way to go about doing a 'blood money' cull.
><..>
>
>Strange indeed, Oz. It would be interesting to know how and why
>anyone could possibly decide that calves born sept 1991 to aug 1992 belong
>to the same cohort. April 1991 to March 1992 would be a more
>reasonable choice, as most UK calves are born between July and 
>December, with calving peaking exactly in August-September.

I would have put the peak on most holdings around October, all the same 
a July -> June group would be preferable and a six monthly one more 
appropriate.

I have been talking to MAFF and the NFU. The MAFF vets were aware of the 
problem that animals leaving a holding before weaning had commenced 
could not have eaten any infected feed. The proposals are now likely to 
have clauses in that allow the MAFF vets the ability to identify this 
situation and prevent culling of these inappropriate cohorts and also to 
identify as cohorts groups infected on a rearers holding.


------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: aquilla@salus.med.uvm.edu (Tracy Aquilla)
Newsgroups: misc.education.science,sci.environment,misc.consumers,
	sci.med.nutrition,sci.agriculture,talk.politics.animals,rec.food.restaurants,
	alt.food.mcdonalds,alt.mcdonalds,rec.food.veg
Subject: Re: Mad Cows and English Beef **STOP THIS THREED**
Date: Fri, 24 May 96 16:12:51 GMT

In Article <azw.12051.15A49000@aber.ac.uk>, azw@aber.ac.uk (Andy Woodward)
wrote:
>There is no evideence it as dangerous, but there are smidgeons of it. And here 
>is equally no evidence it is safe.

Actually, there is plenty of evidence indicating it is safe. Numerous
experiments have demonstrated that it is extremely difficult to transmit the
disease from cattle to other species. So far, the only way this has been
accomplished is by direct injection of infected brain tissue. This indicates
that there is virtually NO RISK from eating meat, even if it comes from
BSE-infected cattle.

>The estimates of huan deaths per year 
>range from a best case of 10 to a worst case of 10^6.

From where did you pull these numbers? There is no evidence to support
numbers like that! Please cite the source of these 'data' you have presented.

>My sympathies are with the European politicians who put the health of their 
>electorate first instead of ours who ppput a few jobs in the beef industry 
>first.

You actually have it completely BACKWARDS! Brit beef was banned from Europe
for political/economic reasons, not for legitimate health reasons.
Tracy



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: misc.education.science,sci.environment,misc.consumers,
	sci.med.nutrition,sci.agriculture,talk.politics.animals,rec.food.restaurants,
	alt.food.mcdonalds,alt.mcdonalds,rec.food.veg
Subject: Re: Mad Cows and English Beef **STOP THIS THREED**
Date: Tue, 28 May 1996 14:28:19 +0100

In article <LsAufJADjsqxEwPj@objectech.co.uk>, Ken Tough
<ken@objectech.co.uk> writes

>Canadian authorities acted very quickly & strongly, in 1989 destroying
>all cattle recently imported from Britain, and imposing an import ban.

Not a bad idea when it is something like, I guess but say 0.01% of your
herds. Of course you then have the problem that there is a big incentive
to cover the odd case up. I suspect this is NOT a problem in N. America
since you don't seem to have BSE.

>British authorities did take action, with the Specified Bovine Offal
>stuff changing feed requirements in 1989.  We're still living with this
>"time-lag" waffling though, about why the rate of new cases hasn't
>rocketed down. (claimed to be because farmers continued to use up old
>feed stocks.)   What kind of crap is this?  If they could blame it on
>inaction of the previous Labour government, I'm sure this government
>would.

Come on, that's unfair. A high percentage of animals in a UK herd are
over six years old, many close to 10 who would have been born before the
ban. In practice it took quite a long time for the ban to be sorted out,
and also quite a long time for infected feed to clear through the system
so 1990 is generally regarded as the effective start. Remember that in
1989 this was primarily a cattle disease with no effect expected on
humans, much the same position as we are now as far as evidence is
concerned.

>If they were concerned enough to make this feed ban, why didn't they
>make a better plan to inforce it properly, and have its action
>immediately effective?  When I see the sensitivity to rabies in this
>country, I don't understand why strict BSE control programmes should
>raise hackles.

This is a valid point. I have commented on it before. Quite wrongly IMHO
the feed mills were allowed to make ruminant non M&B feed in the same
plants, and using the same trucks, as M&B containing feed. The potential
for contamination is clearly very high, and I have already heard it said
that there is a high incidence (relatively) of BSE in cows born after
1990 in areas with high pig populations. One of the reasons for this may
well be the media (and various activists) concentrating on lambasting
farmers and thus directing the effort in that direction so that other
areas got very neglected. It's a pity that self-appointed 'experts' like
Prof Lacey and other 'activists' were not smart enough to spot this sort
of thing, but politics makes people blind. 

>Other things which could have been implemented early:
>- Develop a quality plan for tracking animals from birth to table.
>  This would feed-back into the feed programme, since animals with
>  BSE detected could be traced back to source; related high-risk
>  animals could then be removed.

We know which animals and which herds have had how much BSE already.
OK, you have a herd with 1% cases of BSE. Do you cull it? Do you cull a
herd that did have 10% BSE, but has not has a case for three years? This
is the problem with BSE, it's very very hard to identify a herd with a
high risk of BSE. OK, a tiny minority perhaps, but the rest? Would you,
for example cull a herd with 10 cases of BSE, but none of these cases
was born after 1/1/1988 and there are only five animals of this age left
in the herd? Tricky, yes?

>- Better monitoring of slaughter practices to ensure SBO contamination
>  on human food doesn't happen.

Agreed. Actually I think this was always pretty good, now it's better.

>- Implement selective culling on herds with high instances of BSE.
>- Develop, back in 1989, a quality certification scheme where beef
>  farmers could confirm that they've started "with a clean slate".  
>  They could identify their meat as from cattle raised from imported
>  BSE-free lines, 

BSE is NOT NOT NOT passed from mother to calf.
BSE is NOT NOT NOT spread from animal to animal.

Most of the larger and medium sized herds have had cases of BSE, usually
with the suckler cows since the beef animals never lived long enough to
develop the disease. If you have 5 beef animals you probably (on the
laws of averages) lucked in in most cases, a lot of herds but not much
beef. The cost of importation would have simply bankrupted you before
you even started. Sad, but true.

>fed on certified feeds, 

See my comment above. All ruminant feed from 1989 onwards has met this
criterion. But ......

>and with certified/inspected
>  practices.   

Like?

>The big blathering buzz-word is "consumer confidence".
>  This, simply, is exactly how it could be done.

Except the beef producers couldn't have afforded to import. The sale of
the huge numbers of surplus animals would have bankrupted the rest. The
feed ban had loopholes and the identification of 'high risk' herds is
very problematical.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: misc.education.science,sci.environment,misc.consumers,
	sci.med.nutrition,sci.agriculture,talk.politics.animals,rec.food.restaurants,
	alt.food.mcdonalds,alt.mcdonalds,rec.food.veg
Subject: Re: Mad Cows and English Beef **STOP THIS THREED**
Date: Sat, 1 Jun 1996 08:40:09 +0100

In article <Michael.Warhurst-3005961508030001@mikew.civ.ed.ac.uk>,
Michael Warhurst <Michael.Warhurst@ed.ac.uk> writes
>In article <dam-2905961707070001@kerrera.dcs.gla.ac.uk>,
>dam@kerrera.dcs.gla.ac.uk (The Nit Nurse) wrote:
>
>>In article <4o82tl$7oh@news2.tds.net>, danders3@waun.tdsnet.com (Dale
>>Anderson) wrote:
>>
>>|> Oz <Oz@upthorpe.demon.co.uk> wrote:
>>|> 
>>|> >It's all a matter of understanding how the disease works. Mindless
>>|> >culling for a non-infectious disease that has appeared in most UK herds
>>|> >at an amazingly low level is remarkably stupid.
>>|> 
>>|>  It's akin to destroying whole towns when someone is found in the town
>>|> having aids...
>>|> 
>>
>>Just for the record, in the UK, there were around 120,000 cases of BSE. These
>>are reported cases to MAFF. It is accepted that this is a *low* estimate.
>>Next on the world list of BSE infected herds is Switzerland. They have had
>>205 (yup, 205) cases since 1990.
>
>It's also worth mentioning that 50% of UK herds have had at least 1 case
>of BSE, and 90% of UK cattle are in a herd that has had at least one case
>of BSE (since the larger herds have usually had cases).
>
>One of the hypotheses to explain the transfer of infective tissue from gut
>to brain was for it to go via the immune system (see Nature, about 6 weeks
>ago). I was surprised, therefore, that the government defined Lymph Nodes
>as specified bovine offal only about 6 weeks ago (ie up until then they
>were in the human food chain). 

Not really surprising. The dates match nicely.
Please remember that Lymph nodes have been shown NOT to be infectious in
BSE. (Progress report 1995).
So it's surprising that they have been placed as SBO's. I think
governmental paranoia may have something to do with this change.

>If it has been theorised for some years
>that the prion was passing through the immune system, wouldn't it have
>been sensible to stop people eating lymph nodes? Though, with 50% of UK
>slaughterhouses failing to carry through the specified bovine offal
>regulations correctly last year, there are clearly also problems with the
>enforcement of these regulations.

The figures were recently published, I thought I had posted them here.
From memory I believe that in just over 1000 inspections there was only
four cases where one might be a little concerned. I wonder how many
laboratories would pass health and safety checks perfectly, very few I
would think. However I would be surprised that any failings would
directly affect safety and would be on the lines of a dirty towel by the
wash basin. Still, a failure none the less.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Some BSE Stats.
Date: Sat, 1 Jun 1996 10:26:54 +0100

Report of the Working Party BSE, Feb 1989.
**Note this is very early on in the spread of the disease.**

This shows a remarkable distribution of the % of dairy herds infected.

Guernsey and Berks: 17.2 & 17.6 % !!!!!
Hants, Kent, Surrey, W,Sussex, Cambridgeshire: 11-14% 
The rest of S. UK (give or take): 5-9% mostly at ~6%
The north: <2%

Just in passing I seem to remember that Guernsey never had warbles
anyway.

Given some oddities, such as W.Sussex: 13.6% and E.Sussex: 5.6% it has
all the feel of feed distributed by individual feed companies. Where a
company(s) is strong there are a lot of cases, where weak, far fewer. It
ought (for interests sake) to have been possible to identify, at least
to some extent, what shipments went to both Guernsey and Berks to
produce this high infection rate.

===============

BSE & the protection of animal health. MAFF Feb 1996

I have taken this from a graph, so please allow some leeway,
particularly for the smaller figures.

Peak of confirmed cases of BSE with known dates of birth. (Monthly)
Data valid at 2nd Feb 1996. Note that one should expect there to be
increases, possibly significant, in 90 onwards.

1981    100
1982    <100
1983    300
1984    900
1985    2000
1986    4500
1987    8200
1988    3400 (Peak post July 88 feed ban)
1989    2000
1990    450  (Peak pre Sept 90 SBO ban)
1991    200
1992 onwards not readable or nil.

Even allowing for some more cases to me this looks like a most
substantial reduction. It is hard to believe that cases for 1991 will be
much over say 330 which gives a reduction of 25 times from the peak.

This might suggest that perhaps something in the order of a fourfold
reduction in cases due to the '88 feed ban in 89 if you take all these
cases as due to feed cross contamination, or 1:20 if you take the 1990
figures. Personally I would place the reduction between 89 and 90 mostly
on feed that was on farm being consumed since farmers would have
expected this food to be uninfectious due to the '88 ban.

I, for one, find this reduction most encouraging.


-- 
O.F.A.  Hotz de Baar.    UK

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.med.nutrition,sci.agriculture,talk.politics.animals
Subject: Re: Oprah and Mad Cow Disease
Date: Sun, 2 Jun 1996 08:25:32 +0100

In article <4oquq6$svh@niktow.canisius.edu>, Greg Pavlov
<pavlov@niktow.canisius.edu> writes

>Dale Anderson (danders3@waun.tdsnet.com) wrote:
>: 
>:  What I found interesting in the series of articles you recommended is
>: how the supposed connection of scrapie and BSE created a problem by
>: convincing people there was no connection between humans and cows.
>: Shoot, if there was no conection between cows and sheep, wouldn't that
>: disprove the cow/human connection more? ;-)
>
> I probably have this wrong, but here goes anyway :-) .   It's generally 
> believed/accepted that scrapie does not result in CJD.  If nothing else, it's
> been around a good long while, so if it is the cause, the incidence of CJD
> has been low enough that there would be no reason to panic if scrapie is a 
> cause.  SO if BSE is "cow's version" of scrapie, the argument can be made
> that BSE is not dangerous to humans. And that was the primary argument made.   
> If, on the other hand, BSE is it's own disease, then all bets are off.  


Just in passing I came across a note in MAFF BSE and the protection of 
human health Feb 96. Marmosets (primates) challenged with scrapie 
(presumably by injection into the brain) succumbed in 36 months, but 
with BSE took 48 months. Unfortunately no references were given. To me 
personally this is of great importance since the relative infectivity of 
BSE and scrapie to humans is crucial. The only TE of animals that we 
KNOW humans have been exposed to regularly for hundreds of years without 
any effect is scrapie. Scrapie is not a hazard to humans. So evidence of 
the relative infectiveness for primates between these TE's is to me of 
importance. I have come across a reference to scrapie and marmosets, but 
not with BSE and marmosets before.

>BSE
> was first "diagnosed" relatively recently; its incidence has been increasing;
> it may be vertically transmitted; CJD may have a long latency period.  

Yes. This latency period seems to get one year longer every year, I have
noticed. Originally the scaremongers talked about 5-10 years. Now they
talk about 15-25 years. Doubtless in 2001 they will be talking about 20-
30 years. I suppose when they get to 70-100 years we can stop bothering.

> As I said, there are a lot of twists and turns in this and the full gamut of
> articles summarized on that WEB page present an amazing range of 
> possibilities.  I don't think that any intelligent individual could read them
> and say that there is a definitive answer.  But I did reach one ancillary 
> conclusion: BSE/CJD is not simply a political EU issue.  There is definitely
> some serious digging and examining to do.

When reading technical articles it is as well to match up scrapie and 
BSE experiments of the same kind. I recently did a search on scrapie 
abstracts and by the end, having discovered that scrapie has been 
transferred to most animals I could think of, I began to wonder about 
the dangers of scrapie. I had to bang my head on the wall several times 
to get some sense into it. About the one thing we can be sure about is 
that scrapie is not infectious to humans. We have been carrying out a 
natural infection experiment in humans all over the world for 200+ years 
and the results show that scrapie is NOT infectious to humans as lamb.

Keep this in mind or you will get overwhelmed by the technical arguments 
and unproven and probably wrong suppositions.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: misc.education.science,sci.environment,misc.consumers,
	sci.med.nutrition,sci.agriculture,talk.politics.animals
Subject: Re: Mad Cows and English Beef **STOP THIS THREED**
Date: Mon, 3 Jun 1996 06:22:48 +0100

In article <4otdts$muv@niktow.canisius.edu>, Greg Pavlov
<pavlov@niktow.canisius.edu> writes

>Dave Blake (dblake@phy.ucsf.edu) wrote:
>: 
>: That still fails to explain the tens of thousands of cases that occurred in
>: cows BORN AFTER THE FEED BAN WENT INTO PLACE ! The most likely 
>: explanation is that the farmers used up their old feed
>: stock after the ban went into place.
>: 
>
> The response of farmers is that this isn't likely; the stuff simply doesn't
> "age" very well...

Obviously concentrate feed is better made or formulated in the UK than 
the US, although I find this unlikely.  :-)

There are two obvious ways that feed made before the ban can be used 
after.

The first is in weaner pellets. These are very, very, expensive and if 
kept dry will store for a year without problem. There is some reduction 
in vitamin levels, but that's about all. Certainly there is no point 
throwing away several hundred $$ worth for no reason. It is also not 
unlikely that new stock was placed over old on some farms with poor 
first in first out stock handling, in which case the stuff at the bottom 
could be very old. Note that this material is almost entirely sold in 
25kg bags.

The second is in feed bins. Unless a positive decision was made at some 
point to empty the bin completely and refill with new feed, material can 
remain on the bottom sides for a very, very long time indeed. It simply 
remains there because bins empty like sand egg timers, they empty from 
the TOP and since they are filled from the top a bin actually operates 
as a first in first out store. For a dairy herd using purchased feed it 
is technically and often physically very difficult to actually 
completely empty a bin. It is utterly essential that the cows are fed at 
the correct time so feed trucks must arrive at exactly the correct time 
and the bins emptied between feeds. For some feeding systems, like out 
of parlour feeders, it is actually impossible to do this without 
preventing the cows normal access to feed for a period. In practice most 
farmers do not appreciate the mechanism that produces the first in first 
out handling in a bin and merely reorder when the bin gets 'low'. It is 
perfectly possible for a 15T bin to have 3-5T of feed in it that never 
gets used except when deliveries are delayed or ordering gets temporally 
forgotten. In that case the bin empties rather further than normal 
delivering a slug of one (or even two or three) year old feed to the 
cows. This may have unfortunate consequences.

Then we have to consider cross infection between pig/poultry feed and 
cattle feed in feed mills. This is significant. Also cross infection 
from trucks that previously hauled M&BM. It appears that many of the 
farms who have had 'born post 90' cases also have pigs on their farms.

As at 31 January 1996 since the disease started effectively in 1988 the 
total animals with confirmed BSE was 160,000. The number born after the 
feed ban in July 1988 was 25,000.

The PEAK monthly numbers of animals with confirmed BSE born in each year 
is as follows:

1981     <50
1982     200
1983    1000
1984    2000
1985    2800
1986    4500
1987    8200
1988    3400 (Peak post July 88 feed ban)
1989    2000
1990     450 (Peak pre Sept 90 SBO ban)
1991     200 
<Note that there will be some more cases for 90 and 91 over the next 
years.>

You cannot fail to notice the HUGE reduction in cases following the ban. 
Between 87 and 90 the reduction is about twentyfold and will certainly 
be more than 13-fold even allowing for many extra cases.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"


From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science
Subject: Re: BSE statistics posted by OZ
Date: Mon, 3 Jun 1996 12:58:57 +0100

In article <4os51e$o28@neptunus.pi.net>, Jan Verhoeven <javr@pi.net>
writes

>>Report of the Working Party BSE, Feb 1989.
>>This shows a remarkable distribution of the % of dairy herds infected.
>>
>>Guernsey and Berks: 17.2 & 17.6 % !!!!!
>>Hants, Kent, Surrey, W,Sussex, Cambridgeshire: 11-14% 
>>The rest of S. UK (give or take): 5-9% mostly at ~6%
>>The north: <2%
>>
>>Just in passing I seem to remember that Guernsey never had warbles
>>anyway.
>>
>>Given some oddities, such as W.Sussex: 13.6% and E.Sussex: 5.6% it has
>>all the feel of feed distributed by individual feed companies. Where a
>>company(s) is strong there are a lot of cases, where weak, far fewer. It
>>ought (for interests sake) to have been possible to identify, at least
>>to some extent, what shipments went to both Guernsey and Berks to
>>produce this high infection rate.
>>
>Remarkable indeed. But there are many factors influencing figures.
>>
>>===============
>>
>>BSE & the protection of animal health. MAFF Feb 1996
>>
>>I have taken this from a graph, so please allow some leeway,
>>particularly for the smaller figures.
>>
>>Peak of confirmed cases of BSE with known dates of birth. (Monthly)
>>Data valid at 2nd Feb 1996. Note that one should expect there to be
>>increases, possibly significant, in 90 onwards.
>>
>>1981    100
>>1982    <100
>>1983    300
>>1984    900
>>1985    2000
>>1986    4500
>>1987    8200
>>1988    3400 (Peak post July 88 feed ban)
>>1989    2000
>>1990    450  (Peak pre Sept 90 SBO ban)
>>1991    200
>>1992 onwards not readable or nil.
>
>I remember, and looked up your frequency table on confirmed BSE posted
>in april.
>What is the difference? not only per year and per month I think.

If I remember correctly what I posted in April was the number of animals 
per year coming down with clinical disease IN THAT YEAR. Nothing to do 
with when they were born, just when they succumbed to clinical disease.

What the above table shows is a measure of the number of animals who 
have gone down with BSE BY DATE OF BIRTH. The measure I chose (because I 
had to read it off of a graph) was the number in the PEAK month of that 
year. It thus shows the decline without the confusing superposition of 
animals succumbing to the disease at various ages. Also note that these 
are the figures for animals *where a date of birth can be confirmed*, 
typically from Dairy and better managed single suckled beef herds only.

Torsten spotted an error or two, the below includes his corrections.

>1981     <50
>1982     200
>1983    1000
>1984    2000
>1985    2800
>1986    4500
>1987    8200
>1988    3400 (Peak post July 88 feed ban)
>1989    2000
>1990     450 (Peak pre Sept 90 SBO ban)
>1991     200
>1992 onwards not readable or nil.

Torsten said:
This is just for the record. Your conclusion, a significant reduction
observed from the 1988 calving season and onwards, is unchanged.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.environment,sci.med.nutrition,sci.agriculture
Subject: Re: Mad Cows and English Beef **STOP THIS THREED**
Date: Mon, 3 Jun 1996 16:51:48 +0100

In article <STEINN.96Jun3160637@sandy.ast.cam.ac.uk>, Steinn Sigurdsson
<steinn@sandy.ast.cam.ac.uk> writes

>Note truncated followup:
>
>In article <cUw+INAVTssxEw$F@upthorpe.demon.co.uk> Oz <Oz@upthorpe.demon.co.uk> 
>writes:
>
>   In article <4ou8rbINNljq@bhars12c.bnr.co.uk>, pgh@bnr.co.uk writes
>
>   >An investigative TV program 6-12 mths ago had no problem buying animals
>   >at sales that were subsequently shown to have BSE at post mortem. If 
>   >they hadn't been bought by the program they would have gone into the
>   >food chain.
>
>   Reference please. They are very clever since nobody else has managed to
>   be able to identify them before they show clinical disease. On the other
>   hand one could easily make it look as if you had succeeded like getting
>   a pathologist to say "I cannot be certain that this brain here has NOT
>   got pre-clinical BSE".
>
>This sounds like ITVs World in Action special on the BSE issue,
>would have come out mid-march -- mid-april. They bought cattle
>at market, and then had the brain autopsied, found something
>like 1% (+/_ ???) had presymptomatic BSE - although it is true
>that they did not say explicitly if this was a positive diagnosis
>or a double negative one. 

OK. Pity their pathologist didn't write it up. That is a little odd 
since a freebee paper that would almost certainly have got published is a 
nice thing for any practitioner. On the other hand it does take several 
months to write it up and get it refereed. We aren't talking April 95 
are we??

>In either case, one of the UK governments many failures is they
>apparently are not sampling randomly slaughtered cattle (although
>this would be relatively easy and cheap) 

Actually not that easy and certainly not cheap. However it IS possible.

>to see what fraction, 
>if any, are infected without having clinical symptoms.

On it's own this would be of little help unless some of said animals
were tested for infectiveness.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: steinn@sandy.ast.cam.ac.uk (Steinn Sigurdsson)
Newsgroups: sci.environment,sci.med.nutrition,sci.agriculture
Subject: Re: Mad Cows and English Beef **STOP THIS THREED**
Date: 3 Jun 96 16:06:37

Note truncated followup:

In article <cUw+INAVTssxEw$F@upthorpe.demon.co.uk> Oz <Oz@upthorpe.demon.co.uk> writes:

   In article <4ou8rbINNljq@bhars12c.bnr.co.uk>, pgh@bnr.co.uk writes

   >An investigative TV program 6-12 mths ago had no problem buying animals
   >at sales that were subsequently shown to have BSE at post mortem. If 
   >they hadn't been bought by the program they would have gone into the
   >food chain.

   Reference please. They are very clever since nobody else has managed to
   be able to identify them before they show clinical disease. On the other
   hand one could easily make it look as if you had succeeded like getting
   a pathologist to say "I cannot be certain that this brain here has NOT
   got pre-clinical BSE".

This sounds like ITVs World in Action special on the BSE issue,
would have come out mid-march -- mid-april. They bought cattle
at market, and then had the brain autopsied, found something
like 1% (+/_ ???) had presymptomatic BSE - although it is true
that they did not say explicitly if this was a positive diagnosis
or a double negative one. 

In either case, one of the UK governments many failures is they
apparently are not sampling randomly slaughtered cattle (although
this would be relatively easy and cheap) to see what fraction, 
if any, are infected without having clinical symptoms.




From: steinn@sandy.ast.cam.ac.uk (Steinn Sigurdsson)
Newsgroups: sci.environment,sci.med.nutrition,sci.agriculture
Subject: Re: Mad Cows and English Beef **STOP THIS THREED**
Date: 4 Jun 96 14:07:23

In article <jYAxLdAUowsxEwZ2@upthorpe.demon.co.uk> Oz <Oz@upthorpe.demon.co.uk> writes:

   In article <STEINN.96Jun3160637@sandy.ast.cam.ac.uk>, Steinn Sigurdsson
   <steinn@sandy.ast.cam.ac.uk> writes

   >Note truncated followup:

   >In article <cUw+INAVTssxEw$F@upthorpe.demon.co.uk> Oz <Oz@upthorpe.demon.co.uk> 
   >writes:

   >   In article <4ou8rbINNljq@bhars12c.bnr.co.uk>, pgh@bnr.co.uk writes

   >   >An investigative TV program 6-12 mths ago had no problem buying animals
   >   >at sales that were subsequently shown to have BSE at post mortem. If 
   >   >they hadn't been bought by the program they would have gone into the
   >   >food chain.

   >   Reference please. They are very clever since nobody else has managed to
   >   be able to identify them before they show clinical disease. On the other
   >   hand one could easily make it look as if you had succeeded like getting
   >   a pathologist to say "I cannot be certain that this brain here has NOT
   >   got pre-clinical BSE".

   >This sounds like ITVs World in Action special on the BSE issue,
   >would have come out mid-march -- mid-april. They bought cattle
   >at market, and then had the brain autopsied, found something
   >like 1% (+/_ ???) had presymptomatic BSE - although it is true
   >that they did not say explicitly if this was a positive diagnosis
   >or a double negative one. 

   OK. Pity their pathologist didn't write it up. That is a little odd 
   since a freebee paper that would almost certainly have got published is a 
   nice thing for any practitioner. On the other hand it does take several 
   months to write it up and get it refereed. We aren't talking April 95 
   are we??

Nope, 1996. They ran it close to the time of the ministerial 
announcement. They also claimed some cattle sold at market
had preliminary clinical symptoms (ie they were shaky on their
feet - could be incipient BSE, could be a number of other issues).

   >In either case, one of the UK governments many failures is they
   >apparently are not sampling randomly slaughtered cattle (although
   >this would be relatively easy and cheap) 

   Actually not that easy and certainly not cheap. However it IS possible.

The sampling is easy. Testing is harder, the expense is relative...

   >to see what fraction, 
   >if any, are infected without having clinical symptoms.

   On it's own this would be of little help unless some of said animals
   were tested for infectiveness.

Well, that's the big unknown. On the other hand, if they are infected
but not yet clinically ill, some fraction of them is very plausibly 
infectious. We just don't know enough yet about how BSE is 
transmitted. It is possible that human infection through the
digestive track is hard, and that most infections (cf Kuru)
are through bloodstream contact - but this doesn't work both
ways: infection through bloodstream doesn't preclude (weaker)
infectivity through the digestive system, whereas if it infects
through the digestive system it is almost certain to infect
through direct blood contact also.

BTW, Guardian 03/06/96 reports 5 new clinical cases in humans
(not autopsied or confirmed yet) and 6 new possibles. In 3 months.
All under 40 apparently.

I'll predict that there will be little newspaper of TV reporting
of new human cases in the UK for a while - if the incidence rises,
frontline reporting will be negligible until cases are in the 
thousands at which point there will be a prolonged media panic
 - this prediction is invalid if there is a journalist reading it :-)



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.environment,sci.med.nutrition,sci.agriculture
Subject: Re: Mad Cows and English Beef **STOP THIS THREED**
Date: Tue, 18 Jun 1996 21:58:53 +0100

In article <STEINN.96Jun18190649@sandy.ast.cam.ac.uk>, Steinn Sigurdsson
<steinn@sandy.ast.cam.ac.uk> writes
>
>You mean as opposed to an "expose" on a prime time TV investigative
>programme? ;-)
>
>   they haven't begun to suffer from Alzheimers disease. Without further
>   information I reserve judgement. It would indeed be remarkable, if they
>   had found per-clinical BSE, that it wouldn't have been splashed all over
>   the headlines.

Precisely.


>Nature 13 June 1996, a correspondance on a possible pre-clinical
>test for BSE.
>
>Anyway - even in the absence of a rigourous test, a news programme
>is perfectly capable of buying cattle with a "looks a bit shakey"
>criterion, and then _autopsying_ them to see what fraction
>are in fact in early stages of the disease.

If anyone had identified what the pre-clinical stages looked like.
Perhaps you can give a reference here, since I have never heard of one.


>   >   Anyone who has actually seen one case of BSE, let alone several, would
>   >   not possibly mistake it for anything else. Nobody who thought there was
>   >   the faintest chance of BSE would send a cow to market PARTICULARLY one
>   >   "a bit shaky on its feet" when they could get another 200++UKP by as a
>   >   BSE infected animal. MAFF was smart enough to work that one out. On top
>   >   of that ALL the buyers, RSPCA and farmers round the market would have 
>   >   spotted the signs a mile off.
>   >
>   >Hmm, "Nobody"?  It was my impression that MAFF compensation was
>   >inadequate in general, and that part of the problem was that
>   >(some) farmers tried to sell off cattle for slaughter rather
>   >than have them put down and get less in compensation.
>
>   Here you are simply incorrectly informed.
>
>Hmm, Panorama, BBC1 17 June 1996: (paraphrasing)
>"the [BSE advisory board" recommended full market value
>compensation for culled cattle, the MAFF refused and decided
>to pay 50% of market value. This provided an incentive
>for farmer to dump cattle on markets [for human consumption]
>if they suspected a cattle was in the early stages of BSE"
>
>You can't both be right. Either the media is out and out
>lying about the value of compensation, and you should contact
>the Beeb pronto - or you are mistaken in the level of
>compensation  (I expect Panorama to check such claims
>rather more thoroughly then I'd expect you to).

Well, I have been in the unfortunate position of actually claiming it.
In the very early days, for a brief time, I believe they did operate a
50% rate. This did not last long, from memory under a year since SEAC
knew even then that public confidence was involved. Bearing in mind that
by the time an animal had BSE it was quite unsalable and was worth about
50UKP from the knacker. As a result even 50% looked pretty good (maybe
300UKP). This is from someone at the sharp end. Take note.


>   >If the compensation is adequate, indeed if it is larger than
>   >the market price, than why are farmers complaining?
>
>   I haven't heard farmers complaining about the current compensation for
>   BSE confirmed animals. Indeed I haven't heard them complain for years.
>
>I have. Driving through Suffolk listening to a call in show on
>local radio...

About BSE compensation. I doubt that.
However it is a farmer's unalienable right to complain. If your survival
depended on a fickle weather, and now on a fickle public that is
generally completely uninformed, it's hardly surprising.


>   Since I am a farmer and know quite a few, I think you might take my word
>   on this. In this area MAFF (after some prodding early on) has set it up
>   properly to achieve what was wanted.
>
>   >   These animals were sent to market because they were old and frail and it 
>   >   was time for them to make way for a new young heifer. It's not 
>   >   surprising some were a bit unsteady, they were old!!!
>   >
>   >I think you're exaggerating for effect here.
>
>   Right. Stupid farmers send off young cows with years of life left in
>   them. I mean, being so thick what can you expect. No, of course they
>
>Nope. The scenario is: "farmer sees Mabel is looking a bit shakey,
>worries she'll be diagnosed with BSE and be unsellable, the market
>price is higher than the MAFF comp. better send her off to market
>now - after all the "scientists" assured us BSE doesn't spread to
>humans, so whats the harm?"

The market price is based on tha animal as a commercial healthy milker.
You wouldn't begin get that from your six year old animal past her
prime. You certainly won't get anything like that of she is 'a bit
shakey'. Cull cows aren't worth much you know, bit tough for steaks and
not much meat on them. Makes a good scare story for ignorant non-
agriculturalists to fall for though, and farmers never get a chance to
comment so you are never any the wiser.


>   don't, I am being sarcastic. If you have known the animals mother,
>   grandmother and probably great-great-great-great grandmother. If you
>   have calved a fair few of them, nursed them through illness, trimmed
>   their feet and stroked their faces you don't let them go until their
>   time really has come. Experience tells you that they won't last for too
>   much longer and the time comes that they must go to be replaced by a new
>   heifer, the daughter and grand-daughter of, well I am sure you get the
>   picture. The cycle of life turns another turn as it has done for
>   thousands of years. It's kinda nice to think that in a couple of hundred
>   years some great grandson of the cowman will be milking the great^10
>   daughter of one of the animals his great-grandfather milked for the
>   cycle of life applies to humans too.
>
>I ain't a farmer, but not all farms are like that. And I spent enough
>time on a farm to know not all farmers are like that either.

All the dairy farmers I know are. You can't get up a 4AM every morning
to milk them six days a week unless you do. You can't care enough to
spot when things are amiss and get the animal treated and you won't stay
up past 2AM calving an animal either.


>Well, they got back to it on the 17th, and the allegations
>are now stronger. Better watch CJD incidence in under 40s in
>Kent, and personally I'd like to know when the disease was 
>detected in other counties.


You should read the article by Pearlman, Towfighi, et al in Neurology in
1988. One of his references quotes a statement made in a book, published
in 1977 (pre BSE) in New York (US) saying that about 13% of CJD cases
occur in younger people under 40.


>   >   >   >In either case, one of the UK governments many failures is they
>   >   >   >apparently are not sampling randomly slaughtered cattle (although
>   >   >   >this would be relatively easy and cheap) 
>   >   >
>   >   >   Actually not that easy and certainly not cheap. However it IS 
>possible.
>   >   >
>   >   >The sampling is easy. Testing is harder, the expense is relative...
>   >   >
>   >   >   >to see what fraction, 
>   >   >   >if any, are infected without having clinical symptoms.
>   >   >
>   >   >   On it's own this would be of little help unless some of said animals
>   >   >   were tested for infectiveness.
>   >   >
>   >   >Well, that's the big unknown. On the other hand, if they are infected
>   >   >but not yet clinically ill, some fraction of them is very plausibly 
>   >   >infectious. We just don't know enough yet about how BSE is 
>   >   >transmitted. It is possible that human infection through the
>   >   >digestive track is hard, and that most infections (cf Kuru)
>   >   >are through bloodstream contact - but this doesn't work both
>   >   >ways: infection through bloodstream doesn't preclude (weaker)
>   >   >infectivity through the digestive system, whereas if it infects
>   >   >through the digestive system it is almost certain to infect
>   >   >through direct blood contact also.
>   >
>   >   You haven't been reading your Progress Report 95, have you? Blood is NOT 
>   >   infective. Nothing is infective except brain and spinal chord. So this 
>   >
>   >Other way around. If contact of infectious tissue with (human) blood
>   >transmits infection, (as is eminently plausible, both from Kuru 
>   >histories and, a neurologist tells me, from clinical problems), this
>   >does not preclude the infection also (but more weakly) being 
>   >transmitted through the digestive system. The converse is almost
>   >certain - if infection is transmitted through the digestive tract,
>   >then it is virtually certain also to be transmitted by infectious
>   >tissue-(recipient) blood contact.
>
>   Read the document I quoted. BSE seems to be very uninfectious, even in
>   cattle the only know route is from consuming infected feed and even then
>   it's not very efficient. We have no evidence of horizontal transmission,
>   whilst in scrapie it's normal. TE's are not all the same so whilst it is
>   sensible to speculate by comparison, once the experimental results are
>   in you ought to accept them. All else is scaremongering. Blood from
>   clinically ill cows was NOT infective, actually nor was cerebrospinal
>   fluid so you can see how localised it is.
>
>Hmm, no one claimed it was. The point was the infectious tissue
>contacting the blood of the _recipient_ is most likely
>a transmission path, but this does not preclude (possible weaker)
>infection path from infectious tissue through gut.
>
>A neuro guy I know treats CNS tissue from infected people
>with extreme care. Muscle is apparently safe. That leaves
>some open areas, like lymphatic tissue.

BSE is NOT CJD is NOT scrapie. They are different TE's. Different bits
are infectious. Ring MAFF and get a copy of the 1995 report. They tested
about all the body parts you can think of, and quite a few you wouldn't
have thought of. Lymphatic tissue was not infectious.



------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: BSE
Date: Thu, 27 Jun 1996 18:54:55 +0100
 <o7+3GHAV1U0xEw7T@upthorpe.demon.co.uk> <724119401wnr@chatham.demon.co.uk>

In article <724119401wnr@chatham.demon.co.uk>, Oliver Sparrow
<ohgs@chatham.demon.co.uk> writes
><Oz@upthorpe.demon.co.uk> writes:
>
>> Allowing for exposure there is no difference between breeds.
>
>Thank you for your comments. I would be grateful for a source which validates
>this statement. Certainly, the industry believes - perhaps through self-
>delusion - that the confinement of the problem to the Friesian and and 
>F.-outcross population is very sweeping. It would be helpful to see some data.

Try MAFF home page.

http://www.open.gov.uk/maff/bse

This has been confirmed by a MAFF spokesman in BSE-L. They looked quite
hard because it would have simplified any culling scheme. Anyway I know
at least one farmer with only pure beef breeds who has had cases of BSE.
It merely depends on whether or not they were fed M&BM, typically as
young animals.

>I wonder at the stability of PSc in its viable allomer: it seems almost 
>inconceivable that there cannot be spontaneous flips somewhere, sometime; 
>and that this is not open to elimination. Is the work to which you refer in 
>vitro or in 
>vivo? Chaparonins and ubiquitin systems are, of course, complex creatures 
>which are not always switched on and not always transferrable to glass. 

Well, they are not very effective of they exist at all. Certainly it
would be nice to find an enzyme that degrades PSc, but certainly none of
the general purpose very agressive ones work. Indeed I sometimes wonder
if one of the reasons why prions are very much less infective when
ingested is because they can't be broken up by gut enzymes so are too
big to be absorbed by the gut.

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: alt.agriculture.misc,sci.agriculture,sci.bio.food-science
Subject: Abattoir CJD death.
Date: Fri, 28 Jun 1996 19:21:24 +0100

I just heard a report on the decision of a coroner's Court on the case
of an abbatoir worker who succumbed to CJD. UK Radio 4, News @ 19.00.

I did not record it, but here the salient features:

1) NOT a V-CJD case, but a normal CJD case.
2) He worked in an abattoir for 'about a year' in the 80's (?early?).
3) Reported as an enthusiastic eater who ate many things and liked beef.
4) The coroner recorded death by misadventure and said that BSE had
nothing to do with the CJD.

A statistian a few weeks ago pointed out that the number of workers
coming under high infection levels will be very much greater than the
base numbers would suggest due to changes in jobs.

A side effect of this is the difficulty of defining someones job over a
period ove over a decade, which one do you chose?

------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science
Subject: Re: Information wanted about BSE in Sheep.
Date: Thu, 25 Jul 1996 10:36:32 +0100

In article <4t2dji$foo@morse.ukonline.co.uk>,
chris.brooking@ukonline.co.uk writes

>I have heard today that there is a possibility that the BSE agent was also
>passed to sheep, but the symptoms may have been disguised by incidents of
>scrapie. Can anyone give me more info on this ? I am also worried that BSE
>may be present in other food sources, for example turkeys, which are fattened
>and slaughtered so quickly that there is not time for the symptoms to develop.
>Is there any meat that is `safe' in the UK, or should I go vegetarian. I
>am not a food-science expert, just a consumer who is very worried and does
>not believe the UK government propaganda.

Well, nobody else has replied so .....

Well if you believe that all the UK govt says is propoganda that's a
problem for a start. They have funded most of the trial work too.

I suppose one needs to start by deciding what is a reasonable risk in
this situation. This is your choice. Would you fly on an aeroplane or
drive a car or be a pedestrian? Very different levels of risk. However
let us start with some facts.

1) Despite BSE entering the UK herd about 1980 (ie 16 years ago),
peaking in 1987 (nine years ago) and if you assume that V-CJD is caused
by BSE (currently unknown) then the incidence rate for V-CJD at present
in the UK is about 1:10,000,000 population per annum or about 1/10th the
rate of CJD. Did you ever seriously worry about getting CJD? Compare
this risk with other risks that you voluntarily take. Make a decision.

2) BSE infectivity has only ever been found in brain and upper spinal
chord in cattle. This has been out of the human food chain for ALL UK
cattle since Nov 1989.

3) Sheep, as ruminants, have been forbidden to be fed meat & bone meal
since July 1988. Ewes rarely (often never) get any compound
feedingstuffs anyway.

4) Sheep only live around 6 years. The economics of sheep breeding do
not allow the use of much (if any) bought in feed except possibly for
hitting a premium market such as easter lamb. Even then they are often
fed nothing but whole barley or maize gluten or other low cost vegetable
feed. 

5) Note that #(4) does not apply to the same extent in much of Europe.
The much higher price of lamb there and the climatic conditions reduces
the use of grass and increases the use of concentrate feed. They have
also not had a ban on feeding M&BM to ruminants (until recently?).

6) BSE has never been found in sheep so far. I have read (but I can't
find the reference) that the UK expected and looked for an increase of
scrapie in sheep because for a long time BSE was thought to be scrapie
(In cattle). They observed no such increase.

7) In the current food scare climate it is prudent to remove any
unnecessary public concern (we passed the necessary some decades ago)
and butchers on UK TV have said that sheep brain has never been used in
human food (except as a delicacy) anyway. A ban thus has little economic
effect except as an added disposal problem. However IMHO this has been
handled very badly indeed since it's not a matter of reducing risk
(since there really is no evidence whatsoever of there being a risk),
but as a cheap way to improve public confidence. The knowledge that BSE
is not scrapie has been known for a long time. Certainly nobody who has
followed this group's discussion would be remotely surprised that BSE
infects sheep, that scrapie infects cattle has been known for quite a
long time. However there has never been the slightest evidence that
sheep have ever infected cattle over the 200 years that scrapie has been
known, despite cattle and sheep sharing the same fields and often the
same buildings for much of that time.

8) So, personally, I don't worry in the slightest. I shall keep on
eating lamb, it's worth a 1:10,000,000 (probably zero) risk to be able
to see a new crop of lambs gambolling in the fields each year, and sheep
grazing on hillsides as they have for centuries. Incidentally I have no
sheep, none of my friends have sheep, none of my family have sheep and I
would only farm them if I was forced to.   :-)

Postscript: Gadjdusek, Science, 2 Sept 1977, Vol 197 No 4307 943-960.
[I bet Ralph will get this asap!]

P958. "Scrapie has now been found to cause a disease clinically and
neuropathologically indistinguishable from experimental CJD in two
species of Old World Monkeys." 

Note that this is experimentally, and by injection into the brain. Some
indication at least that if scrapie was a problem, it might look like
CJD and thus would figure in higher levels of CJD in the UK, which is
*NOT* observed. Marmosets infected with scrapie succumbed to the disease
more quickly than they did to BSE.


------------------------------- 
'Oz     "When I knew little, all was certain. The more I learnt,
        the less sure I was. Is this the uncertainty principle?"

From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: BSE Concealment.
Date: Tue, 4 Feb 1997 13:47:10 +0000

In article <5d77ij$irf$1@mhade.production.compuserve.com>, DMacK
<106633.2412@CompuServe.COM> writes
>Concerning the rate of false positives in BSE diagnosis in 
>Britain, versus zero diagnoses in Holland: your false positive 
>rate would only apply in areas where vets and farmers were 
>expecting to find BSE, hence include it regularly, and 
>occasionally wrongly, as an option when diagnosing a sick animal. 

Actually, it's a little more definite than this. The farmer (very
occasionally the vet) becomes suspicious that an animal has BSE. He
informs MAFF. MAFF sends out an inspector (all those I have come across
have been qualified vets, probably all are) who specialises in BSE
detection. At this point the animal is NOT as BSE suspect case.

After inspecting the animal typically including spooking it and
carefully observing it's behaviour the inspector decides if it is a
suspect case or not. The inspector is clearly also looking for other
symptoms that would indicate other diseases. If he has any doubt, or if
he is certain, the animal becomes a suspect case and restriction orders
are placed upon it. In recent years the tendency in cases of doubt for
the animal to be held in isolation for a couple of weeks since
differential diagnosis is clearer after a period has elapsed. 

The animal is sent for slaughter and it's brain post mortemed to
confirm, or not confirm, the original diagnosis.

Note carefully that nowhere else in the world have farmers and
inspectors remotely as much experience of identifying BSE as the UK. The
normal result of inexperience is a (usually very) much higher number of
false negatives. If you are being suitably careful and cautious, that
is.

>In areas that consider themselves free of BSE, such as the 
>Netherlands, one would not be predisposed to see cases. On seeing 
>odd neurological symptoms, a vet would be very unlikely to 
>diagnose BSE. Hence the problem in countries hitherto apparently 
>free of BSE is not, how many false diagnoses of BSE are being 
>made, and does this approach the British rate, but how many 
>diagnoses of other diseases with similar intial symptoms are 
>false, because in fact the animal had (undetected) BSE. 

It is rather common to have animals sick and be unable to make a good
diagnosis. So any animal showing 'neurological' symptoms could be taken
to have mineral deficiency (or toxicity), a metabolic deficiency or
parasites. This was of no real importance pre-BSE, but does have so now.
Any animal showing behavioural disturbance and not positively confirmed
(eg by blood test) should be considered a BSE suspect as far as Europe
is concerned if you are going to be serious about monitoring for the
disease. This is MUCH less applicable to the US, which (unlike Europe)
never imported any infected MBM from the UK.

>I'd like 
>to know how many false diagnoses of rabies, espeially in France 
>and Belgium, have turned out not to be rabies-- and in that case, 
>what were they? Are these cases being examined? There is in fact 
>a fairly high false diagnosis rate for rabies in French cattle, 
>at least, and the symptoms of onset of rabies and BSE-- often 
>little more than that the animal is "acting funny", or appears 
>shaky or weak-- are similar. Does anyone know anything more about 
>any of these issues? Especially rates of false diagnosis of 
>neurological diseases of cattle in Europe, especially rabies, and 
>whether any examinations of past post-mortem tissue samples is 
>being undertaken. Such a retrospective study was underway in 
>France, but I never heard the results (surprise). Seriously, 


I am still waiting for someone to positively confirm or deny the lack of
suspect cases in non-UK cattle in Europe that have progressed as far as
a BSE postmortem test.

-- 
'Oz     "Is it better to seem ignorant and learn,
         - or seem wise and stay ignorant?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: BSE Concealment.
Date: Wed, 12 Feb 1997 16:51:33 +0000

In article <10wUoMAe3z9yEwM9@upthorpe.demon.co.uk>, Oz
<Oz@upthorpe.demon.co.uk> writes

>I am still waiting for someone to positively confirm or deny the lack of
>suspect cases in non-UK cattle in Europe that have progressed as far as
>a BSE postmortem test.

In the absence of any denial, either here or any of the other groups
posted to, including BSE-L and PROMED, I have come to the conclusion
that there have been NO suspect cases appear in cattle with no UK link
outside the UK, Ireland and Switzerland.

This goes to show how smart the SEAC committee were in specifying NO
whole herd cull for positive cases found; and pushing for, and
obtaining, slightly generous compensation for suspect cattle.

I wonder how long it would take if someone were to offer a million
pounds for the first such case?

Whilst I doubt that the US has any such cases, continental europe is
playing a most hazardous game in putting politics over science IMHO.

-- 
'Oz     "Is it better to seem ignorant and learn,
         - or seem wise and stay ignorant?"



From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: UK MBM imports and BSE
Date: Fri, 1 Aug 1997 18:53:22 +0100

Following a (UK) Parliamentary question from Lord Lucas, the UK Govt
confirmed yesterday (31st July) that between 1970 and 1980 the UK
imported MBM from various African countries including South Africa,
Botswana and Namibia. The imports stopped shortly after this period.

Source:
An article in The Independent (UK Newspaper) on the 1st August.
NB The Independent is a quality newspaper.

This confirms my previous statement when I was arguing the case that
African ruminants are a plausible source for the genesis of BSE. I hope
that this encourages some further investigation of this theory. Until
the genesis of BSE is known, no country can reasonably claim BSE free
status.


-- 
'Oz     "Is it better to seem ignorant and learn,
         - or seem wise and stay ignorant?"

Index Home About Blog