From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: How much Hype over this?
Date: Tue, 2 Apr 1996 10:45:36 +0100

In article <637@cornwick.win-uk.net>, Bryan <bryan@cornwick.win-uk.net>
writes

>What you should realise is that warble fly treatment was being
>carried out *after* the banning of sbo in cattle feed.

Wrong. I have been forced to find the actual dates. Here you are:

1)
Warble fly (England and Wales) order 1978. In force 1/Sep/78
Made it compulsory to treat all cattle against warble.

2)
Warble fly (England and Wales) order 1982. In force 15/Mar/82
Revoked the 1978 order, but gave the ministry power to enforce the
treatment of a herd if warbles were found in cattle. (Note that this
would apply if they were found in cattle at a market or at slaughter).

Note that this pre-dates any surmised problem of BSE.
In most herds the cattle that developed BSE were never treated with
warble dressing, as it had already been eradicated several years
earlier.

Many herds (such as ours) had eradicated warble in the early 70's and no
animals with BSE-like symptoms were ever seen. The idea that warble
treatment caused BSE is entirely laughable when the actual evidence is
considered.

>My husband farms organically.  He has an organic suckler herd.  We
>NEVER buy in any feed stuff for our animals - we grow all their
>feed - maize and grass silage.

>We have had three cases of BSE.  Where did they come from?

Did you buy in these cattle as single suckler cows?
Did they ever escape and eat someone elses feed?
Were they ever looked after by someone else whilst you were on
holiday/away who might have fed them without your knowledge?
Did you ever feed them with bought-in organic feed, that might not have
been as 'organic' as you thought?
Did you ever fertilise with that very organic fertiliser meat & bone
meal? Or even bone meal? You may not even have realised the source of
the fertiliser you were applying.

If I spent a few more minutes I could probably think up a few more
possibilities.

*******
Note for those who don't know what warbles are:

Warbles are a particularly nasty parasite of cattle similar to american
screw-fly. They lay their eggs on the legs of cattle and the grubs eat
their way into the legs, munch their way all the way up inside the body
and eventually pupate just under the skin over the backbone. The maggots
by then are (from memory) about 1 1/2" long (35mm) and very fat. These
drop out, pupate on the ground and hatch into a large fly that only has
a range of half a mile or so. They were effectively eradicated by a
pour-on OP, undoubtedly to the considerable relief of the cattle
population.

'Organic' methods of treatment were ineffective.

-------------------------------
'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-another statement
Date: Thu, 11 Apr 1996 07:20:01 +0100

In article <956@purr.demon.co.uk>, Jack Campin <jack@purr.demon.co.uk>
writes

>easterly@zetnet.co.uk (Malcolm Goodall) writes:
>> From: Consultant in Communicable Disease Control, and member of the
>>       Spongiform Encephalopathy Advisory Committee (SEAC)
>
>> 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.
>
>Ralph isn't the only one who can lecture folks on the scientific method;
>what Mark Purdey (who this alludes to) has got most certainly *is* evidence.
>It isn't *probative* evidence, but the scientific method has always
>recognized partial support, suggestive hints, facts that suggest further
>investigation might be in order... only lawyers pretend that human knowledge
>doesn't develop like this.
>
>Finding that all cases of the "new" CJD have been exposed at some time to
>organophosphates (which is what he claims) may not in itself prove anything
>(small group, where's the control?...) definitively.  But evidence it is.

Are we talking CJD or BSE here?

Most children end up at school. Most schools have outbreaks of nits.
Malathion (I believe 1% in alcohol) rubbed into the hair is one of the
commonest treatments. I have no idea how long this has been the case,
but I would think many decades.

They have also all been exposed to lettuces.

In my opinion the OP connection with BSE is completely wrong. Since 1982
was the end of compulsory treatment against warble and in the vast
majority of herds no OP was used after that date. Consequently almost
all of the cattle who have caught BSE were NEVER treated with an OP. On
top of that older cattle who were treated didn't get it.

So to my mind the evidence that OP's do NOT cause BSE is rather
convincing. Very convincing indeed, in fact.

-------------------------------
'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: Mon, 15 Apr 1996 17:15:51 +0100

In article <4ktmtl$qcb@news.uni-c.dk>, Torsten Brinch <iaotb@inet.uni-
c.dk> writes
>Oz wrote:
>: In article <AD96F20F96686FA6F@legolab.demon.co.uk>, Robert Blackburn
>: <rob@legolab.demon.co.uk> writes
>: >Is it organophoshates that unravel those particular prions?
>
>: I blew this argument out of the water about a week ago. Do I have to do
>: it again? Remember that UK cattle were not treated from 1982 onwards,
>: the products are used elsewhere in much higher amounts and Ireland
>: eradicated warble in exactly the same way some five years earlier and
>: didn't have a problem with BSE. It's total rubbish with no foundation.
>
>The 'no warblefly treatment since 1981' is in strong
>contradiction to tabulated data (source stated:MAFF Annual Animal Health
>Reports) by Mark Purdey (Vet.Rec. 1993,132,12). These data
>taken face value, it seems that compulsory warble fly eradication zones
>were  declared as late as 1990 in Devon, Dorset, Cornwall, Gwynedd,
>Anglesey, Gloucester, and Oxfordshire, and that in 1987 compulsory
>eradication zones were declared in more than 30 counties.

Shoof! Have we actually GOT more than 30 counties in England? They have
managed to keep it pretty quiet, I never noticed anything in the farming
press. Even more interesting is that I farm in Oxfordshire and have
never heard of any compulsory eradication zones after 1982.

There could of course be a good reason for this. Given that the warble
fly can only fly a very short distance, I forget what but under one km,
I suspect the zones were probably very small, like one or two farms. So
the reason could well be those naughty people who didn't eradicate
properly. Serve them right. Anyway whatever happened it was in tiny
areas and hardly anything like wholesale use so your statement, whilst
possibly true, is misleading. The animals treated would have been a
minuscule percentage countrywide.

The fact of the matter is that in my herd of 180 cows NONE of the cows
treated with Tiguvon caught BSE, NONE of the cows that caught BSE were
ever treated with tiguvon. Since the order was removed in 1982 I am
pretty confident that this is very typical of UK herds. Also Ireland
eradicated warble several years before the UK using the same technique
and materials and they don't have a problem with BSE. In short the idea
that OP's have anything to do with BSE is laughable.

>Could you please be more specific on *which* products are used
>else*where* in *which* amounts as a warble (or comparable) treatment?

We used Tiguvon at reccommended rates. On this farm treatment started
well before 1975, when we came here. Doubtless you can look up the
rates, we don't have any leaflets left after 14 years.

>The information that Ireland eradicated warble fly (1977?) with
>exactly the same treatments as those applied in UK is new to me.
>I would like to read more about it. Could you lead me
>to a source describing the Irish campaign?

I was discussing this OP dream with a vet who has been interested in BSE
from the very beginning. He was one of the first to find a case of BSE.
He pointed out that the UK eradication scheme was copied straight from
the earlier successful eradication scheme done by the Irish. I can
vaguely remember something about it in the farming press because N.
Ireland joined in voluntarily. Wouldn't have worked else.


-------------------------------
'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, 18 Apr 1996 08:02:47 +0100

In article <4l0bkd$q23@news.uni-c.dk>, Torsten Brinch <iaotb@inet.uni-
c.dk> writes

>Even during the peak of the BSE, no more than 35,000 cases
>were reported annually. That is also only  a miniscule percentage
>(0.3%) of the cattle population countrywide. But you do have a point:
>Appr. 50 % of dairy herds, 85 % of beef suckler herds and 65 % of
>adult breeding herds never had a single case of BSE.
>If herds with purchased cases only are left out, the percentages
>of herds with no cases must be even larger. So if a very high percentage
>of herds were *never* treated with warblecides, the hypothesized
>warblecide/BSE link is off to cloud-cuckoo land.

This information is a bit off, probably I didn't express myself very
well. You can to all intents and purposes take it that the *whole* adult
UK cattle herd was treated with OP warble treatment in 1979, 1980 and
1981. I don't know about the "Treatment orders" after then but I would
guess they apply pretty much to single farms or at most one neighbour
all round. I don't know the figures, but I would bet that involved a
truly tiny % of the UK herd.

Many (particularly dairy) farmers had already embarked on eradication
before 1975 and were treating the whole herd annually from that time.

However OP warble treatments are used all over the world against insect
pests. Hey, I even use it on my cats and dogs for fleas.

>>The fact of the matter is that in my herd of 180 cows NONE of the cows
>>treated with Tiguvon caught BSE, NONE of the cows that caught BSE were
>>ever treated with tiguvon. Since the order was removed in 1982 I am
>>pretty confident that this is very typical of UK herds. Also Ireland
>>eradicated warble several years before the UK using the same technique
>>and materials and they don't have a problem with BSE. In short the idea
>>that OP's have anything to do with BSE is laughable.
>
>With the evidence you present, this conclusion is premature.

Well, it's quite impressive against the original proposition that OP's
were a DIRECT cause of BSE. There is plenty of other evidence against
this so can we consider OP treatment directly causing BSE in the cow
that was treated (not offspring) as effectively proven to be wrong?

>Firstly: Tiguvon (=fenthion) is one of many OP's. If it is possible
>to rule out Tiguvon, fine. This does not rule out other OP's.

I don't know what % was treated with Tiguvon. Locally it was pretty much
100%. I can find out though (if I remember and given time).

>Secondly: Some OP's have been demonstrated to be able to
>cause brain damage to *offspring* of treated animals, if the treatment
>is made in a critical period during pregnancy. If this does
>not apply to the cases that you have experienced, I would say
>that it is evidence that Tiguvon probably can be ruled out.

There were rules about timing, I have forgotten what they were however I
would hope there would be (and I vaguely remember there was) label
requirements, if so we followed them to the letter.

>Thirdly: Warble fly treatments is not the only way for cows to be
>exposed to OP's. The obvious (but not only) other route for exposure is
>through feed or forage.

I think you can forget forage in the UK. At that time insecticides were
never applied to forage (almost 100% grass in those days). I would be
surprised if insecticides were applied (you presumably mean anti-
infestation treatments) to the feeds we used. They were all processed by
products, US maize distillers, maize gluten, sugar beet pulp, rapemeal
as examples. I would be truly surprised to find any OP's got through any
of the processing even if it were there in the firstplace, which is
doubtful. I think this is a bit of a red hering, frankly. Any rates
would be so low as to be insignificant and would apply world wide anyway
and not just in the UK.

>Fourthly: If we want to find out if OP's could have had any role in
>the emergence of BSE, it is no use to talk about OP's in general.
>The exposure to OP's is worldwide, and BSE is not.
>It is necessary to look for a specific OP, a specific contaminant
>in specific OP-products, or a specific way to use specific OP's,
>which have been largely unique to UK.

Good luck. I think you will find the contrary true. This is of course a
very key issue you have brought up.

>Don't get me wrong. I'm not clinging to straws nor am I married to Mark
>Purdey. I just want to know why and how OP's have been ruled out.

Well, as you look at his claims you find that each one can be rather
easily refuted *once you know the true facts*. As a result he changes
his theory to fit and it gets more and more remote and more and more
implausible. A sure sign of a failed theory.

>>We used Tiguvon at reccommended rates. On this farm treatment started
>>well before 1975, when we came here. Doubtless you can look up the
>>rates, we don't have any leaflets left after 14 years.
>
>That is a no-answer. You stated that *elsewhere* ( i.e.not in the UK)
>the same products was used in *much higher amounts*. Where?
>Which amounts?

Oh dear. I am being forced to get the info, am I not?  :-)

>The products used in UK was not only Tiguvon (=fenthion)
>-- at least Mark Purdey points to phosmet and famphur as warblecides
>used in the UK. He seems to be particularly keen on the phosmet treatments.

You will, I guarantee it, find very many herds with BSE who ONLY used
Tiguvon. Mine amongst them. I take it we are now aiming for an OP's
caused the prion to misfold in some calf somewhere, somewhen that dies
and went to the knacker and then got turned into M&B meal and then
caused the entire epidemic? But just in the UK?

Er, we aren't setting up an unprovable theory are we by any chance?

Clearly the key is other countries that do, and don't use OP's on their
cattle AND have a really efficient veterinary service.

>>>The information that Ireland eradicated warble fly (1977?) with
>>>exactly the same treatments as those applied in UK is new to me.
>>>I would like to read more about it. Could you lead me
>>>to a source describing the Irish campaign?
>
>>I was discussing this OP dream with a vet who has been interested in BSE
>>from the very beginning. He was one of the first to find a case of BSE.
>>He pointed out that the UK eradication scheme was copied straight from
>>the earlier successful eradication scheme done by the Irish. I can
>>vaguely remember something about it in the farming press because N.
>>Ireland joined in voluntarily. Wouldn't have worked else.
>
>I see -- Mark Purdey wrote that the scheme was *not* copied straight
>from the Irish:
>
>a) largely other products were used in Ireland than in UK (cruformate,
>lindane and coumaphos), and

Nasty stuff those, ugh!

>b) only one annual treatment were used in Ireland as opposed to twice
>annually in UK.

I am pretty sure he is wrong here, virtually certain in fact. Check the
label. There were two treatment dates, autumn and spring as I remember.
You did a cow ONCE at either one or the other. Spring was most effective
but some cows could not be treated then (because of the calf??) and so
you had to use the other, less effective, timing. Certainly we only
treated each cow once a year, and we followed the regulations.

>So I guess here is another contradiction to sort out. Your vet friend
>and Mark Purdey cannot both be right.

Well, Purdey has already shifted his ground a huge amount since he
started, he won't mind doing it again, I'm sure.

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

From: iaotb@inet.uni-c.dk (Torsten Brinch)
Newsgroups: sci.agriculture
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: 20 Apr 1996 10:55:35 GMT

Oz wrote:
> In article <4l0bkd$q23@news.uni-c.dk>,
>Torsten Brinch <iaotb@inet.uni-c.dk> writes
>>.. if a very high percentage
>>of herds were *never* treated with warblecides, the hypothesized
>>warblecide/BSE link is off to cloud-cuckoo land.

>You can to all intents and purposes take it that the *whole* adult
>UK cattle herd was treated with OP warble treatment in 1979, 1980 and
>1981. I don't know about the "Treatment orders" after then but I would
>guess they apply pretty much to single farms or at most one neighbour
>all round. I don't know the figures, but I would bet that involved a
>truly tiny % of the UK herd.
>Many (particularly dairy) farmers had already embarked on eradication
>before 1975 and were treating the whole herd annually from that time.
>However OP warble treatments are used all over the world against insect
>pests. Hey, I even use it on my cats and dogs for fleas.

I take your word that the whole adult UK cattle herd was treated
anually until 1982. Guesses & bets are kindly dismissed though, and
what you do to your cats and dogs is irrelevant. Please Take Care.
Impregnating animals with highly toxic compounds to the degree, that their
blood becomes insecticidal is not a thing to be taken lightly.

>>>The fact of the matter is that in my herd of 180 cows NONE of the cows
>>>treated with Tiguvon caught BSE, NONE of the cows that caught BSE were
>>>ever treated with tiguvon. Since the order was removed in 1982 I am
>>>pretty confident that this is very typical of UK herds. Also Ireland
>>>eradicated warble several years before the UK using the same technique
>>>and materials and they don't have a problem with BSE. In short the idea
>>>that OP's have anything to do with BSE is laughable.
>>
>>With the evidence you present, this conclusion is premature.

>Well, it's quite impressive against the original proposition that OP's
>were a DIRECT cause of BSE. There is plenty of other evidence against
>this so can we consider OP treatment directly causing BSE in the cow
>that was treated (not offspring) as effectively proven to be wrong?

That is not fair Oz. I never made that kind of proposition.
For the record: Have you been doing some evidence-polishing?
In a previous post you stated that *almost* none of you BSE-cases
had been treated with OP. I can't see why you would have to do
the polishing, though. If just one of your cases was never treated,
it would be enough to prove your point.

I noticed that another poster wrote, that he had had cases with
cows that were never fed M&B meal.
I *did* notice all your handwaving  to dismiss *his* point.

>>Firstly: Tiguvon (=fenthion) is one of many OP's. If it is possible
>>to rule out Tiguvon, fine. This does not rule out other OP's.

>I don't know what % was treated with Tiguvon. Locally it was pretty much
>100%. I can find out though (if I remember and given time).

I believe you are right.
AFAIK, Tiguvon was very popular *until* 1985, when there was a
change to other OP's.

>>Secondly: Some OP's have been demonstrated to be able to
>>cause brain damage to *offspring* of treated animals, if the treatment
>>is made in a critical period during pregnancy.<..>

>There were rules about timing, I have forgotten what they were however I
>would hope there would be (and I vaguely remember there was) label
>requirements, if so we followed them to the letter.

Of course you did. But what does that prove? The farmer who killed
100's of birds with a snailicide in Southern Denmark followed the label
instruction. The farmers who damaged the brains of piglets
by treatment of pregnant sows with Neguvon did too.

>>Thirdly: Warble fly treatments is not the only way for cows to be
>>exposed to OP's. The obvious (but not only) other route for exposure is
>>through feed or forage.

>I think you can forget forage in the UK. At that time insecticides were
>never applied to forage (almost 100% grass in those days). I would be
>surprised if insecticides were applied (you presumably mean anti-
>infestation treatments) to the feeds we used. They were all processed by
>products, US maize distillers, maize gluten, sugar beet pulp, rapemeal
>as examples. I would be truly surprised to find any OP's got through any
>of the processing even if it were there in the firstplace, which is
>doubtful. I think this is a bit of a red hering, frankly. Any rates
>would be so low as to be insignificant and would apply world wide anyway
>and not just in the UK.

I didn't mean to set up a red herring. I can follow you a long way
in your arguments. Just one aside: I don't believe that processing
significantly reduces whatever OP-contamination there may be
in feedstuffs. Dilution by mixing with less contaminated feedstuff
may occur.

>>Fourthly: If we want to find out if OP's could have had any role in
>>the emergence of BSE, it is no use to talk about OP's in general.
>>The exposure to OP's is worldwide, and BSE is not.
>>It is necessary to look for a specific OP, a specific contaminant
>>in specific OP-products, or a specific way to use specific OP's,
>>which have been largely unique to UK.

>Good luck. I think you will find the contrary true. This is of course a
>very key issue you have brought up.

Good. My point came through.

>>>We used Tiguvon at reccommended rates. On this farm treatment started
>>>well before 1975, when we came here. Doubtless you can look up the
>>>rates, we don't have any leaflets left after 14 years.
>
>>That is a no-answer. You stated that *elsewhere* ( i.e.not in the UK)
>>the same products was used in *much higher amounts*. Where?
>>Which amounts?

>Oh dear. I am being forced to get the info, am I not?  :-)

If you are truly interested, yes, but I won't force you further.
You've admitted that your argument was based on preconception,
not knowledge.

>>The products used in UK was not only Tiguvon (=fenthion)
>>-- at least Mark Purdey points to phosmet and famphur as warblecides
>>used in the UK. He seems to be particularly keen on the phosmet treatments.

>You will, I guarantee it, find very many herds with BSE who ONLY used
>Tiguvon. Mine amongst them. I take it we are now aiming for an OP's
>caused the prion to misfold in some calf somewhere, somewhen that dies
>and went to the knacker and then got turned into M&B meal and then
>caused the entire epidemic? But just in the UK?

If you can convince me of such a convoluted theory, go ahead.
Until then, to me, the cause of BSE is, as I've stated before: unknown.

>Er, we aren't setting up an unprovable theory are we by any chance?

Dunno. Maybe you are.

>Clearly the key is other countries that do, and don't use OP's on their
>cattle AND have a really efficient veterinary service.

Please explain. This one escapes me.

<..>
>>a) largely other products were used in Ireland than in UK (cruformate,
>>lindane and coumaphos), and

>Nasty stuff those, ugh!

As much as I agree (if you are serious) that does not address the point:
You stated that the products used in Ireland were the *same* as
those used in the UK.

>>b) only one annual treatment were used in Ireland as opposed to twice
>>annually in UK.

>I am pretty sure he is wrong here, virtually certain in fact. Check the
>label. There were two treatment dates, autumn and spring as I remember.
>You did a cow ONCE at either one or the other. Spring was most effective
>but some cows could not be treated then (because of the calf??) and so
>you had to use the other, less effective, timing. Certainly we only
>treated each cow once a year, and we followed the regulations.

I believe that Mark Purdey is referring to some *compulsory*
twice annual treatment in eradication zones and under treatment orders.
There may have been different rules in the period you are referring to
(1979-1981) and the one Mark Purdey is referring to (1985-1990)?
And indeed it may have been difficult to follow the rules in real
life.

To which period is calving timed in the UK?  To which extent have
cows been treated in the first trimester of pregnancy?

--
As the plow follows words, so God rewards prayers.

                                 (Proverbs of Hell: William Blake)

From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: Sun, 21 Apr 1996 08:57:00 +0100

In article <4lafr7$47f@news.uni-c.dk>, Torsten Brinch <iaotb@inet.uni-
c.dk> writes
>Oz wrote:
>
>I take your word that the whole adult UK cattle herd was treated
>anually until 1982. Guesses & bets are kindly dismissed though, and
>what you do to your cats and dogs is irrelevant. Please Take Care.
>Impregnating animals with highly toxic compounds to the degree, that their
>blood becomes insecticidal is not a thing to be taken lightly.

Hey, I expect you are perfectly happy with antibiotics that have NEVER
in most cases been tested for toxicity, and certainly not remotely to
the extent that OP's have that makes your blood become seriously
antibacterial.

>>Well, it's quite impressive against the original proposition that OP's
>>were a DIRECT cause of BSE. There is plenty of other evidence against
>>this so can we consider OP treatment directly causing BSE in the cow
>>that was treated (not offspring) as effectively proven to be wrong?
>
>That is not fair Oz. I never made that kind of proposition.
>For the record: Have you been doing some evidence-polishing?
>In a previous post you stated that *almost* none of you BSE-cases
>had been treated with OP. I can't see why you would have to do
>the polishing, though. If just one of your cases was never treated,
>it would be enough to prove your point.

I checked in the mean time. One has to be careful to be accurate with
all the nitpickers in this group.  :-)

Also remember that there are others who have argued earlier in the BSE
thread, so I am also answering them too.

Can we take this point as 'proven' for now?

>I noticed that another poster wrote, that he had had cases with
>cows that were never fed M&B meal.
>I *did* notice all your handwaving  to dismiss *his* point.

Yup. With the evidence so far in the past, and with so many possible
sources of error and contamination and with such a small number of cases
he has a problem proving anything either way. This is very sad indeed
for him because it may well result in him going bankrupt. Proving a
negative is real hard without a big trial, and even then you are only
talking probabilities. Basically this mediafest superscare has shafted
the organic producer through no fault of his own. I offer (and I really
mean this) my sorrow at his plight. Anyway I might be next, who knows
when science and logic are thrown out of the window?

>>>Firstly: Tiguvon (=fenthion) is one of many OP's. If it is possible
>>>to rule out Tiguvon, fine. This does not rule out other OP's.
>
>>I don't know what % was treated with Tiguvon. Locally it was pretty much
>>100%. I can find out though (if I remember and given time).
>
>I believe you are right.
>AFAIK, Tiguvon was very popular *until* 1985, when there was a
>change to other OP's.

That's what I thought too. However my source says not. About 30% of the
market apparently. I suspect many beef producers in more extensive areas
(and dairy herds there) might well have preferred something that took
out ticks as well.

>>>Secondly: Some OP's have been demonstrated to be able to
>>>cause brain damage to *offspring* of treated animals, if the treatment
>>>is made in a critical period during pregnancy.<..>
>
>>There were rules about timing, I have forgotten what they were however I
>>would hope there would be (and I vaguely remember there was) label
>>requirements, if so we followed them to the letter.
>
>Of course you did. But what does that prove? The farmer who killed
>100's of birds with a snailicide in Southern Denmark followed the label
>instruction. The farmers who damaged the brains of piglets
>by treatment of pregnant sows with Neguvon did too.

Of course I don't know anything about these cases, dates, what changes
to the label etc etc. You have just got too see how long it takes to get
things through the UK approval system (typically two to three years
LONGER than the rest of Europe)  to see how cautious they are. They
drive the manufactures to suicide.

>>>Thirdly: Warble fly treatments is not the only way for cows to be
>>>exposed to OP's. The obvious (but not only) other route for exposure is
>>>through feed or forage.
>
>>I think you can forget forage in the UK. At that time insecticides were
>>never applied to forage (almost 100% grass in those days). I would be
>>surprised if insecticides were applied (you presumably mean anti-
>>infestation treatments) to the feeds we used. They were all processed by
>>products, US maize distillers, maize gluten, sugar beet pulp, rapemeal
>>as examples. I would be truly surprised to find any OP's got through any
>>of the processing even if it were there in the firstplace, which is
>>doubtful. I think this is a bit of a red hering, frankly. Any rates
>>would be so low as to be insignificant and would apply world wide anyway
>>and not just in the UK.
>
>I didn't mean to set up a red herring. I can follow you a long way
>in your arguments. Just one aside: I don't believe that processing
>significantly reduces whatever OP-contamination there may be
>in feedstuffs. Dilution by mixing with less contaminated feedstuff
>may occur.

Eh?? Maize distillers has been fermented with a LOT of water for a few
weeks, distilled, filtered, dried to 88% DM, put on a boat and shipped
to the UK. You don't think this would have an effect on the OP levels
(if any) in the original maize?? I am astonished. Maize gluten has been
wet milled, the starch separated off then filtered and dried. All this
washing must surely significantly reduce the OP level even if there were
any to start with.

>>>Fourthly: If we want to find out if OP's could have had any role in
>>>the emergence of BSE, it is no use to talk about OP's in general.
>>>The exposure to OP's is worldwide, and BSE is not.
>>>It is necessary to look for a specific OP, a specific contaminant
>>>in specific OP-products, or a specific way to use specific OP's,
>>>which have been largely unique to UK.
>
>>Good luck. I think you will find the contrary true. This is of course a
>>very key issue you have brought up.
>
>Good. My point came through.

Never fear. The point occured to me as soon as I heard Purdey's
ramblings many years ago.

>>>>We used Tiguvon at reccommended rates. On this farm treatment started
>>>>well before 1975, when we came here. Doubtless you can look up the
>>>>rates, we don't have any leaflets left after 14 years.
>>
>>>That is a no-answer. You stated that *elsewhere* ( i.e.not in the UK)
>>>the same products was used in *much higher amounts*. Where?
>>>Which amounts?
>
>>Oh dear. I am being forced to get the info, am I not?  :-)
>
>If you are truly interested, yes, but I won't force you further.
>You've admitted that your argument was based on preconception,
>not knowledge.

How do you work that out? I have accumulated a great deal of knowledge
over the years from all sorts of sources. However not being an academic
and not being an expert witness I do not carefully cut them out and file
them. Me farmer, not academic, not legal person. However, as you and
others have noted, I am very often right when I am forced to get
references. (I would put it more strongly, but I am modest). :-)

>>>The products used in UK was not only Tiguvon (=fenthion)
>>>-- at least Mark Purdey points to phosmet and famphur as warblecides
>>>used in the UK. He seems to be particularly keen on the phosmet treatments.
>
>>You will, I guarantee it, find very many herds with BSE who ONLY used
>>Tiguvon. Mine amongst them. I take it we are now aiming for an OP's
>>caused the prion to misfold in some calf somewhere, somewhen that dies
>>and went to the knacker and then got turned into M&B meal and then
>>caused the entire epidemic? But just in the UK?
>
>If you can convince me of such a convoluted theory, go ahead.
>Until then, to me, the cause of BSE is, as I've stated before: unknown.
>
>>Er, we aren't setting up an unprovable theory are we by any chance?
>
>Dunno. Maybe you are.

What is your theory then? Come on, out with it!

>
>>>a) largely other products were used in Ireland than in UK (cruformate,
>>>lindane and coumaphos), and
>
>>Nasty stuff those, ugh!
>
>As much as I agree (if you are serious) that does not address the point:
>You stated that the products used in Ireland were the *same* as
>those used in the UK.

Well, they were if you do it the other way round. The products used in
the UK were all used in Ireland too. I don't approve of splashing
Lindane about where a much more biodegradable alternative exists. I
don't have an abject fear of anything that is an OP whatever it's
toxicity and dose rate, however. I actually have confidence in the trial
work done and assess it rationally.

>I believe that Mark Purdey is referring to some *compulsory*
>twice annual treatment in eradication zones and under treatment orders.
>There may have been different rules in the period you are referring to
>(1979-1981) and the one Mark Purdey is referring to (1985-1990)?
>And indeed it may have been difficult to follow the rules in real
>life.

Only for the incompetent. I mean, how much skill does it take to look at
the calendar and pour the correct amount along a cow's back. I think
anyone who has trouble with this might well struggle to look after the
well-being of his cattle and should be dealt with accordingly.

>To which period is calving timed in the UK?  To which extent have
>cows been treated in the first trimester of pregnancy?

Calving period varies from herd to herd. I will have to see if my
herdsmanager remembers when we did it. It's over 15 years ago remember.

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

From: iaotb@inet.uni-c.dk (Torsten Brinch)
Newsgroups: sci.agriculture
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: 23 Apr 1996 06:47:45 GMT

Oz wrote:
>In article <4lafr7$47f@news.uni-c.dk>, Torsten Brinch <iaotb@inet.uni-
c.dk> writes
>>Oz wrote:

>Hey, I expect you are perfectly happy with antibiotics that have NEVER
>in most cases been tested for toxicity, and certainly not remotely to
>the extent that OP's have that makes your blood become seriously
>antibacterial.

This is *definitely* a red straw-herring.
Rare catch. Rare species. I think I'll let him go. :-)

<..>

>>I noticed that another poster wrote, that he had had cases with
>>cows that were never fed M&B meal.
>>I *did* notice all your handwaving  to dismiss *his* point.

>Yup. With the evidence so far in the past, and with so many possible
>sources of error and contamination and with such a small number of cases
>he has a problem proving anything either way. This is very sad indeed
>for him because it may well result in him going bankrupt. Proving a
>negative is real hard without a big trial, and even then you are only
>talking probabilities. Basically this mediafest superscare has shafted
>the organic producer through no fault of his own. I offer (and I really
>mean this) my sorrow at his plight. Anyway I might be next, who knows
>when science and logic are thrown out of the window?

The other poster told us that they had 3 cows  exposed to a contamination
from a neighbourhood spray  AND  a compulsory treatment with warblecide
in the period after the SBO ban (1989 onwards). The cows
had still-born calves and the following year the 3 cows were
confirmed as BSE-cases.
The 3 cows had never been exposed to meat and bone (MB) meal.
The observation is consistent with the hypothesis, that warblecide
treatment was involved in the causation of BSE --
and inconsistent with the hypothesis, that MB meal was involved.

None of *your* cows have been treated with warblecide since 1981.
They have been exposed to M&B meal. You had x BSE-cases.
First you thought, that almost none of these x cases had been treated
with warblecide (i.e. although x is unknown, x>3).
After checking your notes from 1981 you found that *none*
of your BSE-cases had actually ever been exposed to warblecides.
This observation is inconsistent with the warblecide hypothesis
and consistent with the MB meal hypothesis.

Alakazam! Both hypothesises disproved?

>>AFAIK, Tiguvon was very popular *until* 1985, when there was a
>>change to other OP's.

>That's what I thought too. However my source says not. About 30% of the
>market apparently. I suspect many beef producers in more extensive areas
>(and dairy herds there) might well have preferred something that took
>out ticks as well.

I see, Tiguvon (=Fenthion) had a major part of the market,
but it did not dominate it.

Mark Purdey wrote, that in 1985, the milk withdrawal period for
Fenthion was extended from 6 hours to 5 days, and that this led
to a swift change to the remaining two useable compounds present
on the market, Famphur (1 product) and Phosmet (4 products).

Quotes from a phosmet fact-sheet:

"    No birth defects were noted in studies with pregnant rabbits
fed 10 to 60 mg/kg for three weeks during pregnancy or in monkeys
given 8 to 12 mg/kg on days 22 to 32 of gestation (3).  Rats fed
10 to 30 mg/kg on days 6 through 15 of gestation suffered some
maternal toxicity at the higher doses but no abnormalities
appeared in the pups.  In another study however, single moderate
doses of 30 mg/kg administered to rats between day nine and
thirteen of gestation, produced an increase in brain damage
(hydrocephaly) in 33 of the 55 embryos examined.  Embryo toxicity
was dose-dependent (1).  The results of these studies, viewed
together, are somewhat ambiguous and make it difficult to draw
firm conclusions about possible teratogenic effects in humans."

"    The tests on the mutagenicity of phosmet have produced mixed
results. Several tests with bacteria did not cause any mutations
though there was one positive test with one strain of bacteria
(S. typhimurium) (4).  There have been no tests conducted
directly on animal or human cells (8).  However, among workers
producing the compound Safidon, some changes in their
chromosomes were noted (12)."

>>>Secondly: Some OP's have been demonstrated to be able to
>>>cause brain damage to *offspring* of treated animals, if the treatment
>>>is made in a critical period during pregnancy.<..>

I believe you requested references for this piece in another posting.

Mehl et al. (1994) Neurochemical Research, 19, 5,
"The effect of trichlorfon and other Organophosphates on Prenatal
Brain Development in the Guinea Pig":
.. were administered to guinea pigs between day 42 and 46 of gestation ..
a severe reduction in brain weight in the case of
trichlorfon and dichlorvos.. it is suggested that alkylation of DNA may be
involved in the development of the lesion .. The teratogenic potency
of trichlorfon was first discovered in pigs when the piglet offspring of
sows treated late in gestation showed severe locomotional disturbances
including ataxia (Ref.1-7)..

<..>

>>>>You stated that *elsewhere* ( i.e.not in the UK)
>>>>the same products was used in *much higher amounts*. Where?
>>>>Which amounts?

>>>Oh dear. I am being forced to get the info, am I not?  :-)

>>You've admitted that your argument was based on preconception,
>>not knowledge.

>>How do you work that out? <..>

Apologies. My statement is not true. I don't know what your argument
was based on.

<..>

>What is your theory then? Come on, out with it!

A reasonable theory should fit the observations.

The incidence of BSE has a peculiar geographic pattern
with highest incidence in the south of UK
yet it did not spread as a contagious disease
from animal to animal -- it seemingly came from nowhere
with low incidence in herds over large areas in the UK --
and within herd incidence remained low,
while the number of cases rocketed.

Feed and Pharmaceuticals/Pesticide-products are the obviously
possible vectors.

Whatever the causative agent is, it does not seem to have been
present at low incidence among cows before the early 80ties --
that is: it did not occur before it was introduced into the
population, and it was admirably quickly acknowledged as
a new phenomenon by your veterinarians.

To state the self-evident: The causative agent is chemical or biological.
More exoticly, it could be a yet unknown interaction between
a chemical and a biological agent.

If it is biological, it is not very contagious (if at all).
Mind you, it does seem to be about as contagious as a chemical :-)

Bacteria and vira have not been found. We do have the prion-theory
and all the experiments with brain homogenate injections in a
multitude of species. Multiple strains of prions have emerged,
whole gangs of rogue proteins, who enlist new members from
molecules of an old highly conserved protein that has recided in animal
nervous systems for millions of years.

Strange creatures to pop up suddenly in the British dairy herds.
Exiting and obviously frigthening if it's true.

The culprit might 'just' be this prion thing -- although some
elusive virus has not been ruled out -- and (excuse me)
it might, by chance, be some chemical.

It is easy for me to place my preferences among these options.
But the probabilities? No way.


Kind regards,

Torsten Brinch

--

What is now proved was once, only imagin'd.

                         (Proverbs of Hell: William Blake)

From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: Wed, 24 Apr 1996 13:52:59 +0100

In article <4lhueh$cef@news.uni-c.dk>, Torsten Brinch <iaotb@inet.uni-
c.dk> writes

>The other poster told us that they had 3 cows  exposed to a contamination
>from a neighbourhood spray  AND  a compulsory treatment with warblecide
>in the period after the SBO ban (1989 onwards). The cows
>had still-born calves and the following year the 3 cows were
>confirmed as BSE-cases.
>The 3 cows had never been exposed to meat and bone (MB) meal.
>The observation is consistent with the hypothesis, that warblecide
>treatment was involved in the causation of BSE --
>and inconsistent with the hypothesis, that MB meal was involved.

Not to their knowledge. OK, now prove it didn't happen?
There are a lot of potential routes, I gave some earlier. Do the have
ducks, chickens, pigs? Can anyone be sure that their supplier of feeds
didn't contaminate what was supplied. Can you be sure they, or a
neighbour, didn't use M&B meal as a fertiliser? Can you be sure the
calcified seaweed was not delivered in a lorry that had previously
carried M&B meal? You don't know, they don't know. You cannot prove a
negative this way round. And what's more you know it. Naughty Torsten.

>None of *your* cows have been treated with warblecide since 1981.
>They have been exposed to M&B meal. You had x BSE-cases.
>First you thought, that almost none of these x cases had been treated
>with warblecide (i.e. although x is unknown, x>3).
>After checking your notes from 1981 you found that *none*
>of your BSE-cases had actually ever been exposed to warblecides.
>This observation is inconsistent with the warblecide hypothesis
>and consistent with the MB meal hypothesis.
>
>Alakazam! Both hypothesises disproved?

I am afraid not. As you are well aware. I also have epidemiological
evidence. Cows were treated with Tiguvon for VERY many years before BSE
and also you have the problem with OP cattle treatments in other parts
of the world. You have lost this one Torsten. The evidence is
overwhelmingly against you.

>>>AFAIK, Tiguvon was very popular *until* 1985, when there was a
>>>change to other OP's.
>
>>That's what I thought too. However my source says not. About 30% of the
>>market apparently. I suspect many beef producers in more extensive areas
>>(and dairy herds there) might well have preferred something that took
>>out ticks as well.
>
>I see, Tiguvon (=Fenthion) had a major part of the market,
>but it did not dominate it.
>
>Mark Purdey wrote, that in 1985, the milk withdrawal period for
>Fenthion was extended from 6 hours to 5 days, and that this led
>to a swift change to the remaining two useable compounds present
>on the market, Famphur (1 product) and Phosmet (4 products).

I believe the product had such vanishingly small sales once warbles had
been eradicated, it simply wasn't worth while re-registering it in the
UK.

>Quotes from a phosmet fact-sheet:
>
>"    No birth defects were noted in studies with pregnant rabbits
>fed 10 to 60 mg/kg for three weeks during pregnancy or in monkeys
>given 8 to 12 mg/kg on days 22 to 32 of gestation (3).  Rats fed
>10 to 30 mg/kg on days 6 through 15 of gestation suffered some
>maternal toxicity at the higher doses but no abnormalities
>appeared in the pups.  In another study however, single moderate
>doses of 30 mg/kg administered to rats between day nine and
>thirteen of gestation, produced an increase in brain damage
>(hydrocephaly) in 33 of the 55 embryos examined.  Embryo toxicity
>was dose-dependent (1).  The results of these studies, viewed
>together, are somewhat ambiguous and make it difficult to draw
>firm conclusions about possible teratogenic effects in humans."
>
>"    The tests on the mutagenicity of phosmet have produced mixed
>results. Several tests with bacteria did not cause any mutations
>though there was one positive test with one strain of bacteria
>(S. typhimurium) (4).  There have been no tests conducted
>directly on animal or human cells (8).  However, among workers
>producing the compound Safidon, some changes in their
>chromosomes were noted (12)."

I already commented on this. You can, I believe find similar evidence
for water, too. All the licencing authorities would reject a product
that was effectively teratogenic. As you are well aware.

>>>>Secondly: Some OP's have been demonstrated to be able to
>>>>cause brain damage to *offspring* of treated animals, if the treatment
>>>>is made in a critical period during pregnancy.<..>
>
>I believe you requested references for this piece in another posting.
>
>Mehl et al. (1994) Neurochemical Research, 19, 5,
>"The effect of trichlorfon and other Organophosphates on Prenatal
>Brain Development in the Guinea Pig":
>.. were administered to guinea pigs between day 42 and 46 of gestation ..
>a severe reduction in brain weight in the case of
>trichlorfon and dichlorvos.. it is suggested that alkylation of DNA may be
>involved in the development of the lesion .. The teratogenic potency
>of trichlorfon was first discovered in pigs when the piglet offspring of
>sows treated late in gestation showed severe locomotional disturbances
>including ataxia (Ref.1-7)..
>
><..>
>
>>>>>You stated that *elsewhere* ( i.e.not in the UK)
>>>>>the same products was used in *much higher amounts*. Where?
>>>>>Which amounts?
>
>>>>Oh dear. I am being forced to get the info, am I not?  :-)
>
>>>You've admitted that your argument was based on preconception,
>>>not knowledge.
>
>>>How do you work that out? <..>
>
>Apologies. My statement is not true. I don't know what your argument
>was based on.
>
><..>
>
>>What is your theory then? Come on, out with it!
>
>A reasonable theory should fit the observations.

Right.

>The incidence of BSE has a peculiar geographic pattern
>with highest incidence in the south of UK
>yet it did not spread as a contagious disease
>from animal to animal -- it seemingly came from nowhere
>with low incidence in herds over large areas in the UK --
>and within herd incidence remained low,
>while the number of cases rocketed.
>
>Feed and Pharmaceuticals/Pesticide-products are the obviously
>possible vectors.

Amongst many, true.

>Whatever the causative agent is, it does not seem to have been
>present at low incidence among cows before the early 80ties --
>that is: it did not occur before it was introduced into the
>population, and it was admirably quickly acknowledged as
>a new phenomenon by your veterinarians.

Doubtful actually. Many animals that die do not have any proper
diagnosis made. This is also true amongst humans. Only if more than one,
usually within a reasonably short timespan, occur and there are worries
of a possible epidemic of some sort building up within the herd is a
really thorough PM done. Even then it is common to find that no cause
stands out. BSE was picked up because the vet (or farmer, I forget
which) had seen another identical case recently and went to some
considerable lengths to find a cause. I would not expect a disease that
has incidence of say 1:10^6 to be readily spotted, particularly as the
brain is rather hard to reach without serious cutting equipment. It
could easily remain unobserved. It happens quite often in humans too.
hepatitis D, for example has just been identified, yet it has been
killing a significant number of humans annually who previously died of
'liver failure'. Your hypothesis is very shaky here indeed to put it
mildly.

>To state the self-evident: The causative agent is chemical or biological.
>More exoticly, it could be a yet unknown interaction between
>a chemical and a biological agent.
>
>If it is biological, it is not very contagious (if at all).
>Mind you, it does seem to be about as contagious as a chemical :-)

But this is typical of a TE, of course.

>Bacteria and vira have not been found. We do have the prion-theory
>and all the experiments with brain homogenate injections in a
>multitude of species. Multiple strains of prions have emerged,
>whole gangs of rogue proteins, who enlist new members from
>molecules of an old highly conserved protein that has recided in animal
>nervous systems for millions of years.
>
>Strange creatures to pop up suddenly in the British dairy herds.
>Exiting and obviously frigthening if it's true.

Well, it's not as if they are so surprising. We have had scrapie for
over 200 years. I wouldn't be surprised if you found TE's in most
mammals if you looked carefully enough.

>The culprit might 'just' be this prion thing -- although some
>elusive virus has not been ruled out -- and (excuse me)
>it might, by chance, be some chemical.

Yup. A strange chemical that only attacks english cows. Perhaps it's a
left over from WWII's NAZI chemical weapons shops, something that only
kills english things, the master weapon that never got used, gosh
Britain was lucky! Come off it Torsten, you wouldn't fall for that one.
You are having me on. And probably confusing the heck out of everybody
else. A chemical that speaks english indeed, pshaw.

>It is easy for me to place my preferences among these options.
>But the probabilities? No way.

Not really. It fits a TE to the letter. Sporadic natural cases at low
level. Rapidly spread by cannibalism. Absolutely classic case. In short
it fits the evidence perfectly.


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

From: iaotb@inet.uni-c.dk (Torsten Brinch)
Newsgroups: sci.agriculture
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: 25 Apr 1996 08:30:33 GMT

Oz wrote:
> In article <4lhueh$cef@news.uni-c.dk>, Torsten Brinch <iaotb@inet.uni-
> c.dk> writes
>>The other poster <..>
>>The 3 cows had never been exposed to meat and bone (MB) meal.
>><..>
>>inconsistent with the hypothesis, that MB meal was involved.

>Not to their knowledge. OK, now prove it didn't happen?
>There are a lot of potential routes, I gave some earlier. Do the have
>ducks, chickens, pigs? Can anyone be sure that their supplier of feeds
>didn't contaminate what was supplied. Can you be sure they, or a
>neighbour, didn't use M&B meal as a fertiliser? Can you be sure the
>calcified seaweed was not delivered in a lorry that had previously
>carried M&B meal? <..>

You miss the point. The observation *is* inconsistent with the
MB meal hypothesis. You suggest possibilities to explain
the inconsistency.

>>None of *your* cows have been treated with warblecide since 1981.
>><..>
>>This observation is inconsistent with the warblecide hypothesis

>>Alakazam! Both hypothesises disproved?

>I am afraid not. As you are well aware.

Yes. It takes more than a few  Usenet observations
to disprove a hypothesis :-).

But seriously, where do you suggest to look for a possibility
to disprove the MB meal hypothesis, if not in farms that did not
use MB meal? Who looked?

And conversely: To disprove the warblecide hypothesis, cases like
yours should be considered. Who did that?


>I also have epidemiological
>evidence. Cows were treated with Tiguvon for VERY many years before BSE
>and also you have the problem with OP cattle treatments in other parts
>of the world. You have lost this one Torsten. The evidence is
>overwhelmingly against you.

Yawn. Which treatments? Where?

If I understand you correctly, for dairy cows Tiguvon was effectively
deregistered in 1985? What is the critical period for the
hypothesised exposure to OP as a cause for BSE?

>I believe the product had such vanishingly small sales once warbles had
>been eradicated, it simply wasn't worth while re-registering it in the
>UK.

>>Quotes from a phosmet fact-sheet:
>><..>
>>(hydrocephaly) in 33 of the 55 embryos examined.  Embryo toxicity
>>was dose-dependent (1).  The results of these studies, viewed
>>
>>producing the compound Safidon, some changes in their
>>chromosomes were noted (12)."

><..>You can, I believe find similar evidence
>for water, too. All the licencing authorities would reject a product
>that was effectively teratogenic. <..>

ROFWL. Yeah Dude. Go ahead.
Do a literature search on water+teratogenicity+mutagenicity
and see what you come up with.

The licencing authorities would certainly reject a product
KNOWN as effectively teratogenic. You seem to twist this to
mean something like 'a licensed product cannot be teratogenic'?


--
If others had not been foolish, we should be so.

                            (Proverbs of Hell: William Blake)

From: iaotb@inet.uni-c.dk (Torsten Brinch)
Newsgroups: sci.agriculture
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: 25 Apr 1996 08:34:32 GMT

Oz wrote:
> In article <4lhueh$cef@news.uni-c.dk>, Torsten Brinch <iaotb@inet.uni-
> c.dk> writes
>>Whatever the causative agent is, it does not seem to have been
>>present at low incidence among cows before the early 80ties --
>>that is: it did not occur before it was introduced into the
>>population, and it was admirably quickly acknowledged as
>>a new phenomenon by your veterinarians.
<..>
>Doubtful actually. Many animals that die do not have any proper
>diagnosis made.<..> I would not expect a disease that
>has incidence of say 1:10^6 to be readily spotted, particularly as the
>brain is rather hard to reach without serious cutting equipment. It
>could easily remain unobserved.
<..>

Your vets detected BSE when the annual incidence was 1:10^5.
Amazingly and admirably efficient.

You have excellent epidemiologists. They have concluded
(based on the epidemiological evidence) that BSE is a
novel disease in cattle.

Your theory may have a serious weakness here.


>>If it is biological, it is not very contagious (if at all).
>>Mind you, it does seem to be about as contagious as a chemical :-)

>But this is typical of a TE, of course.

Sure. Almost by ... definition?

<..>
>>whole gangs of rogue proteins, who enlist new members from
>>molecules of an old highly conserved protein that has recided in animal
>>nervous systems for millions of years.

>Well, it's not as if they are so surprising. We have had scrapie for
>over 200 years. I wouldn't be surprised if you found TE's in most
>mammals if you looked carefully enough.

Well if this is your good news, don't pass the bad.

I am genuinely surprised. You are paving the road for vegetarianism.
Do you want to scare the world off animal protein?

>>The culprit might 'just' be this prion thing -- although some
>>elusive virus has not been ruled out -- and (excuse me)
>>it might, by chance, be some chemical.
<..>
>>It is easy for me to place my preferences among these options.
>>But the probabilities? No way.

>Not really. It fits a TE to the letter. Sporadic natural cases at low
>level. Rapidly spread by cannibalism. Absolutely classic case. In short
>it fits the evidence perfectly.

Let us say it does.
Why do you think that your hypothesis is the most *probable* hypothesis?


Oh just one more thing:

If you can have pre-1985 BSE-cases for *your* theory,
surely the OP theory can have some too?

Kind regards,

Torsten Brinch
--
Truth can never be told so as to be understood, and not be believ'd.

                                    (Proverbs of Hell: William Blake)

From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.agriculture
Subject: Re: Mad Cow disease, BSE; Justice is served.
Date: Fri, 26 Apr 1996 07:46:29 +0100

In article <4lndeo$jg5@news.uni-c.dk>, Torsten Brinch <iaotb@inet.uni-
c.dk> writes
>Oz wrote:
>> In article <4lhueh$cef@news.uni-c.dk>, Torsten Brinch <iaotb@inet.uni-
>> c.dk> writes
>>>Whatever the causative agent is, it does not seem to have been
>>>present at low incidence among cows before the early 80ties --
>>>that is: it did not occur before it was introduced into the
>>>population, and it was admirably quickly acknowledged as
>>>a new phenomenon by your veterinarians.
><..>
>>Doubtful actually. Many animals that die do not have any proper
>>diagnosis made.<..> I would not expect a disease that
>>has incidence of say 1:10^6 to be readily spotted, particularly as the
>>brain is rather hard to reach without serious cutting equipment. It
>>could easily remain unobserved.
><..>
>
>Your vets detected BSE when the annual incidence was 1:10^5.
>Amazingly and admirably efficient.

Yup. Two cases in quick succession makes alarm bells ring. Particularly
with such obvious and distinctive symptoms. One a decade to one a year
is a BIG difference. Sooner or later you'll get two in one month by
chance and then ......

>You have excellent epidemiologists. They have concluded
>(based on the epidemiological evidence) that BSE is a
>novel disease in cattle.
>
>Your theory may have a serious weakness here.

You never replied to my comment on imported African M&B meal.
Quite a number of vets have said that in their view they have seen odd
cases of with symptoms like BSE over their (the vets) lifetimes. I
already explained why these would never have been taken to a full PM.

>>>If it is biological, it is not very contagious (if at all).
>>>Mind you, it does seem to be about as contagious as a chemical :-)
>
>>But this is typical of a TE, of course.
>
>Sure. Almost by ... definition?

Eh? What are you on about now?

>>>whole gangs of rogue proteins, who enlist new members from
>>>molecules of an old highly conserved protein that has recided in animal
>>>nervous systems for millions of years.
>
>>Well, it's not as if they are so surprising. We have had scrapie for
>>over 200 years. I wouldn't be surprised if you found TE's in most
>>mammals if you looked carefully enough.
>
>Well if this is your good news, don't pass the bad.
>
>I am genuinely surprised. You are paving the road for vegetarianism.
>Do you want to scare the world off animal protein?

Eh? People still eat sheep. Anyway, I don't believe in hiding the truth.
If that's the way it is, then you gotta face up to it *rationally*. You
have to asses risk accurately. Lets face it I could die of a stomach
cancer caused by eating brussel sprouts or cabbages.

>>>The culprit might 'just' be this prion thing -- although some
>>>elusive virus has not been ruled out -- and (excuse me)
>>>it might, by chance, be some chemical.
><..>
>>>It is easy for me to place my preferences among these options.
>>>But the probabilities? No way.
>
>>Not really. It fits a TE to the letter. Sporadic natural cases at low
>>level. Rapidly spread by cannibalism. Absolutely classic case. In short
>>it fits the evidence perfectly.
>
>Let us say it does.
>Why do you think that your hypothesis is the most *probable* hypothesis?

I said so already.

>Oh just one more thing:
>
>If you can have pre-1985 BSE-cases for *your* theory,
>surely the OP theory can have some too?

Yes. Strongly correlated with where it is used, worldwide. Now then you
would have a much better case.

-------------------------------
'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: Wed, 1 May 1996 07:07:22 +0100

Come off it Torsten, you have lost this argument. I have coutered all
your explanations. Mostly several times. It is past being a boring train
of conversation. The OP hypothesis just doesn't stand up, and I can't
believe you do not see why. The evidence is overwhelming.

I really cannot be bothered too keep repeating the same convincing
arguments. Her they are, some at least, for the last time.

In article <4m2ilb$ou8@news.uni-c.dk>, Torsten Brinch <iaotb@inet.uni-
c.dk> writes
>
>BSE incidence in warblecide treated vs. untreated herds:
>
>MB meal hypothesis predicts *no* difference --
>Warblecide hypothesis predicts a difference.

ALL UK herds should have been (and were) treated with OP to control
warble fly. NOT all UK herds have had a case of BSE. Not all UK herds
were fed on M&B meal. The distribution of BSE does not follow OP
treatment, it follows a typical single source spread.

>BSE incidence in MB meal exposed  vs. unexposed herds:
>
>MB meal hypothesis predicts different incidence --
>Warblecide hypothesis predicts *no* difference.
>
>
>The organic farmers have *very valuable* information,
>because MB meal is not used on their farms.

It is used as an organic fertiliser.
They DO buy in stock from non-organic farms, sucker cows I believe, for
example.
There are plenty of possibilities for inadvertant contamination. I gave
a long list already.

>It seems
>that this information has not been collected. Why not?
>It certainly should be collected! If MAFF can't do it
>someone else could. I'd be glad to help :-).

How do you know that no information was collected? Initially a sample of
herds may well have been investigated, confidentially of course.

>You have suggested, that unintended contamination etc.
>could lead to a MB meal exposure even in organic herds.
>It should be added that *theoretically* there is also
>a possibility that *intended* irregular feeding with
>MB meal have occurred in a few organic herds.
>IMO the probability for this is very low.
>That is simply not the way of an organic farmer!

Very good.

>For testing purposes the possibilities for MB meal exposure
>is not really a problem, because the BSE incidence can be
>compared in warbletreated and non treated *organic* herds.
>MB meal contamination (if any) should be equal in the two groups.

It will depend on whether you chose Scotland (OP's used, little BSE) or
Somerset (OP's used much BSE).

>If the incidence of BSE is higher in warblecide treated
>than in non-treated organic herds it seriously weakens
>the MB meal hypothesis, and strengthens the warblecide hypothesis.

Even organic farmers had to treat. Most did so in the 79-81 period
because it was the law. A few did not, breaking the law, and were forced
to since their cattle were seen to have warbles when they were sold. I
do not trust people who break the law.

>With non-organic farms the picture is slightly different, as there
>has been widespread MB meal exposure. This means that within
>non-organic herds, it is difficult to design a test which could
>disprove the MB meal hypothesis. The warblecide hypothesis should
>be testable however.

You can chose your sample from areas with different incidence of BSE.

>The MB meal hypothesis is not consistent with a higher incidence
>of BSE in non-organic treated herds than in non-organic untreated
>herds. It predicts *no* difference.

Eh? Have you said what you mean?

>AFAIK these tests have not been made. Questionnaires
>sent to farmers with BSE-cases do not seem to have
>asked information on warblecidal treatments in the affected
>herds.

Because they ALL would have been treated. It was the law. Or do you
think that someone would admit to breaking the law in a questionnaire?
Get real. It would have been another pointless question.

>The only suggestive evidence we have, is the geographical pattern
>of BSE incidence, which seems to show similarities to the
>geographical pattern of warblecide eradication zones and
>treatment orders 1985-1990. This suggestive evidence is *not*
>in favour of the MB meal hypothesis.

Garbage. I have already pointed out this error several times. What about
the vast majority of people who never treated after 1981 yet got BSE?
Give it up, this is a rubbish argument.

>It is frequently asserted that the UK organic herds have
>a lower BSE incidence than non-organic herds. This observation
>(however interesting it is, if true) is not valuable for
>hypothesis testing. BOTH the warblecide hypothesis AND
>the MB meal hypothesis predict this difference.

Not true. Organic herds should have, and in most cases were, treated
with warblecide 79-81.

This discussion is boring. The OP hypotheses is full of holes, and I am
through repeating it over and over again.

Also note that BSE is transferrable experimentally as an infectious
prion protien without the use of OP. Your argument fails experimental
evidence too. It is a duffer. It is dead, it is no more. It is indeed a
dead parrot that certain people keep waving around and saying 'it's
alive'. See Monty Python scetch of the same name.

-------------------------------
'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, 9 May 1996 07:48:43 +0100

In article <4mkqrq$d5u@news.uni-c.dk>, Torsten Brinch <iaotb@inet.uni-
c.dk> writes

>Consider though, that we may have an observation, that BSE is less
>prevalent in organic herds. This is consistent with
>the MB hypothesis, because organic herds can be assumed to be
>less exposed to MB meal than non-organic herds.
>Unintended or even intended MB meal exposure could explain the
>number of BSE cases which *have* occurred in the organic herds.
>
>What would happen to our explanation if we also had the observation
>of a correlation between BSE and warblecide-treatment in the organic herds?

>Could we propose then, that warblecide treatment in organic herds
>has been correlated to MB exposure?

Only if you could also show that BSE in non-organic herds was correlated
with OP exposure. It isn't (that much at least we agree on).

It's odd that you never seem to hear from any of the very many (vast
majority?) organic farmers who obeyed the laws in 1979 to 1981 and
treated their cattle and eradicated warbles when the rest of the country
did. You only hear from those that were forced to during outbreaks in
the mid 80's, either because they hadn't treated in the first place or
because of local outbreaks (like from imported French cattle).

Could it be that the organic farmers who treated in 1980, being aware
that none of the cattle they treated went down with BSE, wonder what all
the fuss is about? Why don't we hear from farmers in other countries,
who are surely humane enough to treat their cattle against this horrible
pest, pointing out that they haven't had BSE despite treating their
cattle (annually?).

Perhaps it's because the evidence of their own experience suggests the
the OP and BSE link is a joke.


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