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"Mad Cow" Disease : 85 questions
English version
In relashionship with the exhibit "When cows go mad"
Updated: July 12, 2001
This document looks at the main aspects of the Mad Cow disease and its
consequences on public health. It is organized around 85 questions, organized in ten
themes.
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Mad Cow" Disease : 85 questions
1. BSE, "Mad Cow" Disease
2. BSE throughout the world
3. Prions
4. Transmission channels
5. Meat and bone meal
6. The new variant of the Creutzfeldt-Jakob Disease
7. Public health protective measures
8. BSE screening tests
Testing launched in France in 2000
Tests carried out in Europe in 2001
Other questions on the screening test
9. Sheep and other animal species
10. What we have (temporarily) learned from the crisis
Scientific advisor: Dominique Dormont.
Texts: Philippe Dorison.
Translation: Timothy Fox.
Senior editor: Alain Labouze.
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1. BSE, "MAD COW" DISEASE
How to recognise BSE?
The clinical diagnosis established by veterinarians takes into account numerous
possible symptoms, including a certain anxiety or aggressiveness by the animal and
often an exaggerated sensitivity to light and sound stimulation. Motor disturbances can
also appear, such as hypermetria where the animal has a tendency to take very large
strides like a horse. In certain cases the symptoms can regress or even disappear in
the disease's final phases. Generally speaking, clinical diagnosis of BSE is difficult, for
the symptoms and in particular their sequence can vary widely from one animal to the
next. It is only a hypothesis, but to explain this variability we surmise that the order in
which the regions of the brain are afflicted is not always the same.
The formal diagnosis is established only after the animal's death by studying samples
taken from the brain. The disease appears on average five years after infection, and
death occurs within a few weeks.
Where does BSE come from?
No one knows for certain. One theory has it that scrapie in sheep jumped the species
barrier and was passed on to cattle. It was the most widely held theory at the end of the
80s, but it has not yet been proven. Another theory has it that BSE has always existed
in a sporadic and very rare manner and that it degenerated into an epizooty (an
epidemic among animals) through the recycling of infected corpses (or even a single
carcass!) via meat and bone meal. Indeed, one-off cases of diseases similar to BSE
have already been observed in the past, in particular a case in south-western France
that gave rise to an article in a veterinary journal in 1883.
How has it become an epizooty?
Through the use of meat and bone meal. In this sense it makes no difference if the
disease originated among sheep or cattle. The changes in the production method of
this meal in Great Britain in 1980 most certainly played a part in the process. Designed
to lower production costs and improve the quality of protein, the new process went with
a lowering of the processing temperature that probably made it possible for the
infecting agent to develop more widely. But the conclusions of the Phillips report in
1999 implied that even without this change in production methods, the disease might
have spread.
Another important cause of the explosion of this disease comes from the very principle
of the industrial production of the bone meal. It introduces blending on a large scale,
also known as ìpoolingî. Thus a small quantity of infected matter manages to spread in
large volumes.
These ìpoolingî techniques had already been questioned in the French affairs of
contaminated blood and growth hormones.
How did the disease spread in France?
It happened in two phases. The first French animals infected were probably
contaminated by British meal, which corresponds to the very first cases to appear
between '91 and '95. This contamination should have stopped with the animals born at
the end of '89 when the import of British bone meal was prohibited. But we can only
suppose that illegal importing continued and that it prolonged this first wave.
After that, it is very likely that the carcasses of French animals afflicted with BSE were
recycled in the production of French bone meal, thereby provoking the second wave of
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the disease in France. The risk was probably increased by the fact that, at that time,
the specified matter at risk was not withdrawn from the bone meal production circuit.
In the first part of the 90s, BSE seemed a uniquely British problem that affected France
in a purely anecdotal way. Despite the founding in ë90 of a network of passive
monitoring by veterinary health officials, the disease was generally little known and
perhaps wasnít taken seriously enough.
Diseased animals might have gone unnoticed and thereby contributed to the spread of
the epizooty.
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2. BSE THROUGHOUT THE WORLD
How extensive is it in France?
Charts show that it is still expanding and that it has not yet reached its maximum
spread. As of May 2001, 315 cases have been counted. 74 of these were detected by
tests done before any symptoms appeared, and 19 by systematic testing of cows over
30 months old.
Yet it is possible that some cases slipped through unseen, especially in the first half of
the 90s.
How extensive is it in Europe?
The United Kingdom is obviously the hardest hit with more than 180,000 cases since
ë85. This accounts for more than 99% of the cases in Europe. Most other European
countries have been affected, in particular France, Ireland, Switzerland and Portugal.
Up to the end of 2000 the only two countries to have started active detection
campaigns with rapid tests were Switzerland and France, which tends to increase the
number of reported cases.
But by the beginning of 2001, tests are being run throughout Europe, and cases have
appeared in Austria, Belgium, Germany, Italy and Spain. Some time will therefore be
required before knowing the real incidence of the disease in all of Europe.
Only northern Europe (i.e. Sweden and Norway) seems spared so far, but even there
nothing can be confirmed before many studies are carried out.
How widespread is it in the world?
The disease is apparently limited to Europe, but it would be foolhardy to claim this with
any certainty. Indeed, English, German and French cattle and feed have been
exported to numerous countries, and as yet no countries outside of Europe seem to
have equipped themselves with comparable monitoring means.
Have any countries been spared BSE?
In Europe, probably not. In the rest of the world perhaps certain countries like New
Zealand, but we have to be very careful in claiming this. In the United States for
example, encephalopathies would now appear to be found in wild animals in fairly
large numbers. The American health authorities have done a few tests to prove that
there is no BSE in America. But the methods they have used would probably not have
found even the cases that were discovered in England in the mid 80s!
The risk of seeing BSE appear in North America is not negligible. Indeed scrapie exists
in the United States, and the changes in the production procedures of the British feed
incriminated for the part it played in the explosion of the epizooty came from an
American patent.
Why would some countries try to hide BSE?
It is only too clear that the presence of BSE in a country is very bad news for business,
especially for exporters of meat and cattle by-products. Amongst these by-products,
fetal bovine serum is particularly important. It is heavily used in the pharmaceutical
industry, namely for vaccines and biotechnologies. It hasnít been proven that a sick
cow transmits the infection to this product, but, as a precaution, only countries believed
to be BSE-free are allowed to sell it. This is namely New Zealand, Australia, Canada,
and the USA.
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3. PRIONS
What is a prion?
It is a protein that lives on the surface of cells and whose role - probably linked to
cell communication - is not very well known. In a healthy organism, this protein is easily
eliminated. But in sick people it becomes very resistant and is no longer destroyed by
the enzymes which normally ìrecycleî it. It aggregates into clusters of 10,000 to
100,000 units which then kill the neurones. The word ìprionî (pronounced ìpree-onî) is
derived from the abbreviation of ìproteinaceous infectious particlesî.
The size of prions makes direct observation practically impossible. To date, only the
crystal structure of a yeast prion (very different from the mammal prions that cause the
TSSEs) has been observed in a cyclotron (a particle accelerator).
Are prions a cause or a consequence of the disease?
There are several theories, but the one of the American Stanley Prusiner, who won the
1997 Nobel Prize for his work, is the most widely accepted today. It sees the
pathological prion as the infectious agent: this protein alone would be the cause of the
disease with no need of a virus or any another micro-organism. This approach is very
radical, for it goes against everything that has been known till now in biology.
This model is globally accepted, but there is no definitive proof to support it. Some
research teams continue to think that there is another infectious agent not yet
discovered, and that the prion is merely a tracer of the disease.
The majority of the scientific community does not share this hypothesis, since todayís
biological techniques are considered to be very effective in detecting viruses whenever
they are present.
How does a prion become pathological?
We donít really know. The difference between a normal prion and a pathological one
most probably has something to do with their 3D shape, i.e. the way in which the amino
acids that make them up (and which are exactly the same for the two prions) are folded
in space. It would appear that a badly shaped prion may be able to transmit this defect
to other, healthy prions, making them change shape. But details of the reaction,
transconformation, remain obscure. It is supposed that other elements take part in this
mechanism, though itís not known which ones.
How do pathological prions get to the central nervous system?
The path taken by the infectious agents for reaching the brain has not been completely
worked out, and describing it is still partly in the realm of hypothesis.
At first the infectious particles enter the digestive tube. As the pathological proteins
become resistant and aggregate into clusters, they cannot be destroyed during
digestion as healthy proteins would be. It is believed that these proteins ìreplicateî in
the lymph tissue linked to the digestive tube, i.e. they spread the infection there and
transform healthy proteins into pathological prions. These mutated proteins then follow
the nerves up to the central nervous system where the infection continues to spread,
causing the death of the neurones.
Is the 3D structure of the human prion known?
The normal prion protein structure has been known since 1996 and is composed of
three helixes. But the shape of the pathological prion is not known for sure. It is
assumed that at least one of the helixes is replaced by a folded layer. It is also
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assumed that there may be several different shapes of pathological protein, which
would explain the presence of several ìstrainsî of the Creutzfeldt-Jakob disease.
Why bother trying to discover the 3D structure of the pathological prion?
It would be a major stride forward for research. By highlighting the abnormal structure,
we would have a better idea of the molecular mechanism involved in the shape
change. By knowing on what level of the molecule this defective folding takes place,
we might even find a way to correct or impede the transconformation.
Why are there so few real results in prion research?
The pathological shape of the protein is very hard to purify and therefore to study. The
size of the infectious agent (at a molecular scale) makes direct observation practically
impossible. Studies on animal models are long because of the incubation time. They
are made more complex by the fact that many animals have to be infected in order to
have only a few develop the disease. Another problem lies in the fact that the
infectiousness of the prion requires a lot of experimental precaution.
Is there enough money for prion research?
The French government has announced plans to triple funds, increasing them from
10.7 to 32 million euros (from 7 to 21 million £) per year as of 2001 - while 76 million
euros (50 million £) were collected in the 2000 myopathy-drive. Moreover this research
is relatively recent, for prior to 1996, it was not a part of the priority programmes. It is
therefore starting up with somewhat of a handicap.
In Great Britain the tradition of research on this subject is greater, because sheep
scrapie has been around for a very long time. It is also certainly very active in the
United States, but with a sizeable part of its funding coming from the private sector, it is
hard to assess the amounts allocated to it.
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4. TRANSMISSION CHANNELS
Are we sure of knowing all channels of transmission?
No, nothing is certain in this field. Although bone meal has clearly been identified as
the main vector of contamination, responsible for spreading the disease on an
industrial scaleî and of the explosion of the epizooty, nothing proves that it is the only
thing able to spread the disease. Itís even probable that there are other channels:
transmission from mother to calf, infection from the zero-milk replacers or transmission
through the blood (something still unconfirmed by epidemiological data).
There may well be other channels still completely unknown. They may be related to
dissemination of infectious agents in the environment. They are generally referred to
as third channel
In any case, each time an animal Born After the Ban (BAB) is contaminated, the
controversy spurs up: was it due to a fraud, or to a non-identified cause?
Does the cow infect her calf?
There are cases that would imply that cattle had been contaminated at birth or before.
But the small number of cases involved and the present state of research do not make
it possible to draw formal conclusions. Moreover, a British study has shown that in the
mother final year of incubation, there was a 5% risk of transmission from mother to calf.
This transmission does not seem to happen in utero.
This question is perhaps more important than it appears: transmission during gestation
would imply a risk for the fetal bovine serum, widely used in the pharmaceutical
industry. As a precautionary measure, only a few countries, reputed as being totally
BSE-free, are authorised to supply this serum.
Is blood a contamination vector?
Experiments with sheep have shown that BSE can sometimes be transmitted through
a complete blood transfusion (one out of nineteen experimentally transfused sheep).
These findings open up research avenues more than provide certainties, for todayís
techniques arenít able to detect pathological prions in blood, though it can be present
in quantities too weak to be measured yet sufficient to transmit the disease.
This risk of blood contamination may seem anecdotal for cattle or sheep, since
exchanging blood between animals is not likely to occur without human intervention.
However, there is still a possibility of transmission of the new variant of the
Creutzfeldt-Jakob disease by blood transfusion between humans. This risk, often
discussed, is taken very seriously.
Can the zero-milk replacers contaminate?
These products are used as feed supplements for young cattle when being weaned
from their mothers. They have become necessary because of the use of protein
supplements in cowsí diets. To meet market demand, animal or plant proteins are
given to dairy cows to enable them to produce greater quantities of milk that is richer in
protein. But such enriched milk is indigestible for young calves and heifers who get sick
if they drink it. As zero-milk replacers are subsidised, it is costlier for a farmer to let a
calf suckle its mother, rather than sell her milk and feed the calf with the milk-replacer.
This weaning feed is enriched with animal fat. If bovine fat is used, it is not impossible
that it be one of the BSE transmission channels.
What is meant by a ìthird channelî?
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It refers to all the contamination channels as yet unknown. For instance, the infectious
agent can be disseminated in the environment, and spread via earth, grass, or even
water. At this stage, anything seems possible.
On this topic we can refer to the work of Carleton Gajdusek, Nobel Prize-winner in
medicine for his work on Kuru. He demonstrated that matter infected by the
pathological prion and buried in the soil was still contaminating three years on.
All these possible third channels cause people to worry about the storing and
destroying of bone meal, and more generally over the processing of waste from the
cattle connection.
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5. MEAT AND BONE MEAL
What is meat and bone meal made of?
Meat and Bone Meal (MBM) is derived from slaughterhouse and butchering waste, i.e.
animal carcasses (cattle, sheep and others) from which the meat has been taken, offal
and secondary products not sold for human consumption.
More than half of the animalís weight is often eliminated this way.
The waste is crushed and cooked. Most of the water is eliminated, reducing the volume
and weight considerably. The powder that is produced is very rich in proteins.
Up to the 80s, the process used in Great Britain required a solvent for eliminating fats.
To get rid of the solvent, the mixture then had to be heated to a very high temperature.
A patent imported from the United States made it possible to by-pass this phase with a
result of savings on the solvent, on energy and obtaining better quality protein.
But with a subsidiary result of the advent of the BSE epizooty a few years later, very
probably amplified by this lower cooking temperature.
Under pressure from public authorities, the vast majority of the manufacturers now
seem to have come round to the cooking standards decreed by the German industry,
i.e. 133∞C under 3 bars of pressure for 20 minutes.
Why was animal meal given to cattle?
This meal was never the basic feed for cattle. It has only been used in small quantities
and blended in with other components called ìnitrogenous correctorsî, to improve
cattle-raising profitability. The idea is to increase milk production and to bolster its
protein rate.
Intensive farming requires cows to produce about twice as much milk as they would
naturally. To reach these standards, they would have to eat more grass or forage than
their stomachs can handle. At the beginning of the 20th century, a solution was found:
cows were given an animal or plant protein supplement. This had the added interest of
eliminating cumbersome waste.
Originally, this was done to produce enough milk to feed the population. Today, the
real problem is over-production, and quotas have been imposed. Protein supplements
are now mainly used to increase cattle-raising profitability: an equal amount of milk is
being produced with fewer animals.
The question is: should we keep this up?
Have all cattle eaten meat and bone meal?
No, a large part of French herds have probably never eaten MBM. Itís goal being to
enhance milk production, the meal was given to milk-producing cows rather than to
animals raised for their meat. This is probably why most BSE cases hit dairy cows
hardest (93.3%, as opposed to 6.7% of suckling cows). But other factors might also
explain the small number of BSE cases in suckling herds, in particular the earlier
slaughtering of animals raised for meat.
Yet suckling herds are not entirely immune to BSE. Some cattle raisers have seen a
case appear in their herd although they were convinced they had never used MBM.
This leads to suspicions of accidental blending of feed, frauds, not to mention all the
other possibilities of contamination, known or unknown.
Since when has meat and bone meal been stigmatised?
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Bone meal was prohibited in Great Britain as feed for ruminants in 1988. Amazingly,
this highly suspicious bone meal continued to be imported into France for another full
year, until the end of 1989. And it was not before 1994 that all animal bone meal, even
French, was prohibited for other French ruminants. This bone meal then continued to
be produced for other animals (mainly pigs and fowl). It was in 1996 that the risky offal
were excluded from this feed. From there on, the two production chains for bone meal
have been separate without the possibility of their mixing together. On the one hand,
the bone meal for non-ruminant animal feed could not contain specified risk matter,
which meant that it was composed only of matter authorised even for human
consumption. On the other hand, bone meal produced from butchery waste, including
all risk matter, is earmarked to be destroyed. It is only transformed into meal as an
intermediary step in its destruction, for this makes it less cumbersome to handle and
easier to incinerate.
These two production processes must be completely separate and not even exist in
the same factory.
Moreover, standards have been established for preparing this bone meal, i.e. 133∞C
under 3 bars of pressure for 20 minutes. A process that seems sufficient for sterilising
matter with mid-level degree of infection.
Once all these precautions have been taken, the meal supplied to pigs and fowl is
meant to be perfectly safe. It should not even present a danger for cattle if they should
ingest small quantities by mistake.
Why was a total ban of meat and bone meal imposed at the end of 2000?
If all previous measures concerning meat and bone meal had been perfectly applied,
this ban would not really be justified.
This measure might therefore be taken as a confession of impotence in rendering the
use of meat and bone meal safe. A total ban is probably easier to apply and especially
to monitor.
Another advantage of this measure, supposing it be scrupulously obeyed, is that it
would make it possible to check after a few years time if there are not other causes of
contamination to be looked for, or if this ban puts an end to the disease’s development.
Looking at the vicious circle involved in spreading the disease, one can note that all
possible measures to eradicate it had already been implemented. This total ban
therefore seemed to be the only possible measure taking the fight against the disease
a step further.
However, it is very likely that if this measure had been taken some twelve years earlier,
it would have gone a long way in preventing the spread of BSE. But it would have cost
a lot of money. Would public opinion have accepted that? In any case, it was not
accepted by European political leaders.
Why was this decision so long in coming?
First of all, we might have been faced with the complicated and costly problem of
eliminating all meat-processing waste. The sums involved are put at thousands of
millions of euros. If these measures have been accepted by governments and public
opinion, it is because they appear as an indispensable health precaution.
Furthermore, animal meal is a cheap source of protein, which is especially important in
low-margin industries such as pig-raising. Eliminating it will necessarily mean a rise in
the production costs of certain meats. The free circulation of merchandise in Europe
made decision-making more difficult: a country that might have applied such decisions
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unilaterally would have prevented its cattle-raisers to compete on equal footing with
competitors in other countries. And most of the European countries that thought they
were left unscathed by the BSE, in particular Germany, weighed in with all their clout to
prevent such measures being taken.
Were the many precautionary measures fully implemented?
This is the crux of the problem, and we can suppose that their application is often
imperfect for several reasons: technical difficulties, fraud, lack of zeal, profitability It is
also hard to implement frequent and systematic monitoring to enforce the rules.
There are strong suspicions that illegal importation of British bone meal continued after
it was prohibited. A judicial inquiry has been opened, but the case seems complex.
Likewise, withdrawing risk matter is often easier said than done. For example, it is very
hard in abattoirs to completely eliminate the spinal cord, at least as long as the
backbone is sectioned down the middle.
Also, it has not been proven that the separation of the bone meal production lines was
implemented within the set deadlines.
Finally, if these regulations were not respected and have led to contamination, it is
nearly impossible to establish the fact in hindsight. Tracking the elements contained in
animal feed is practically impossible, especially when this means going back four to six
years to find out what might have made the cow sick.
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6. THE NEW VARIANT OF THE CREUTZFELDT-JAKOB DISEASE
What is the Creutzfeldt-Jakob Disease?
This disease, first identified in the early 20s, attacks the central nervous system. It is
always fatal and can be classified as a TSSE. Just over 1 person out of a million is
afflicted with it every year. It exists in three forms.
The form known as sporadic is the most frequent: it represents 85 to 90% of all cases.
There is no direct cause explaining its appearance, and it generally attacks people
over 60.
The genetic form is much rarer (10 to 15% of cases) and is explained by a mutation in
the gene coding for the normal prion protein.
The iatrogenic form is due to contamination through a surgical or medical act. The best
known example, especially in France, is the contamination by the so-called extractive
growth hormone in which 76 people developed the disease. For a while, this hormone
was obtained from the brains of dead people, certain of whom, it turned out, were
carriers of the agent of the Creutzfeldt-Jakob disease. Since then, itís become possible
to produce this hormone through genetic engineering.
What is the new variant of the Creutzfeldt-Jakob disease?
This disease bears close resemblance to the Creutzfeldt-Jakob disease, but it differs
enough on a certain number of points to classify it as a new disease. First of all, it is
likely to affect much younger people, sometimes even teenagers, and it lasts longer.
The infection spreads to more parts of the body (tonsils, appendixÖ) than with the
Creutzfeldt-Jakob disease, where it remains confined to the brain. But most of all, an
examination of the brain reveals a very specific signature in the form of ìfloride platesî,
particular aggregations of pathological prion proteins that cause the neurones to die.
As in Alzheimerís disease, they form amyloide plates, but made up of a different
protein. This examination is the only one today that allows a positive diagnosis.
Unfortunately, it can only be done after the personís death.
Symptoms can vary from case to case. The first signs are sometimes confused with
psychological problems that could indicate a depressive condition. As it develops, the
disease attacks the brain functions and prevents victims from communicating, moving
or eating. Death occurs in fourteen months on average, but can sometimes last up to
two years.
Are there other neighbouring human diseases?
The best known is Kuru, which killed about 2,000 people of the ForÈ tribe in Papua
New Guinea in the 50s. It was studied by Carleton Gajdusek, who in 1976 received the
Nobel Prize for his efforts. He proved that this disease was linked to funeral rites that
included cannibalism in which the brain was eaten. No ForÈ born after 1959, when the
rite was outlawed, has contracted the disease.
Can we be sure that BSE is indeed the cause of the new variant of the
Creutzfeldt-Jakob disease?
The only absolute certainty would be obtained by willingly infecting humans. But this
strong assumption relies on a sheaf of proofs that nobody seems to doubt. For
example, mice infected by an injection of tissues of patients having developed the
nvCJD and an injection of tissues from cattle with BSE develop exactly the same
disease. The same experiment with primates yielded the same results, but lasted
much longer.
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Is the disease contagious?
It is not contagious but is communicable, which is not the same thing. You can live for
years in close contact with an infected person without incurring any risk of being
contaminated. Beside the cannibal practices of the Kuru epidemic, transmission can
occur through contact between the nervous system and infected elements. This can
occur, for example, during surgery if an instrument touches an infected zone and is
then used on another person.
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Does blood transfusion present risks?
No studies carried out in cases of the classic Creutzfeldt-Jakob disease concluded that
there was a risk in transfusions. However, experiments aimed at detecting the
infectious agent in the blood of persons afflicted with the new variant Creutzfeldt-Jakob
disease are now underway, making it too early to conclude on the dangers of
transfusion.
As a precautionary measure, certain countries have decided to ban from the list of
blood donors anyone having made an extended stay in countries with a high incidence
of BSE, in particular the United Kingdom or France.
This risk linked to transfusion is hard to assess, for people who might be incubating the
disease are impossible to recognise. On the other hand, excluding too many blood
donors through excessive application of the precautionary principle might lead to
another health danger, i.e. the lack of blood in hospitals.
How many people have been diagnosed with nvCJD?
As of May 28, 2001, there are 100 cases in Great Britain. There has been one
confirmed nvCJD-related death in Ireland, and 3 in France.
How many people will die of nvCJD?
Impossible to predict, especially in France where the number of declared cases is too
few to serve as a basis for an epidemiological study. British projections are hardly
more precise. The uncertainty of the diseaseís incubation time has led to exploring 5
million different scenarios. In the end, the bracket is very wide: from a maximum of
136,000 cases over the next century for incubation times that come close to human life
expectancy, down to 6,000 cases over the next fifty years for an incubation time
averaging thirty years.
What risk has the French consumer been exposed to?
This, too, is hard to evaluate precisely, but the main risk probably comes from British
offal imported between 1988 and 1994. Up until 1987 these imports were less than 400
tons per year. In 1988 they increased tenfold and continued to increased regularly until
they reached 8,000 tons per year in 1993 and 1994. These years correspond to the
greatest number of BSE cases in the United Kingdom. The offal imported were those
with a high risk of infection, the consumption of which was forbidden in Great Britain.
The way in which this offal was consumed in France cannot be known precisely, but it
may have been included in meat-based preparations such as mince, certain sauces,
raviolisÖ
How long does the illness incubate?
We donít know. The only way to get an idea will probably be through epidemiological
monitoring, but the findings probably will not give precise answers before some twenty
years at least. In the meantime, the epidemiological projections of British
bio-mathematicians include in their hypotheses an average incubation time extending
beyond sixty years.
What is the infection threshold of the pathological prion for Man?
We donít know. We suppose itís very low. Here again, the only way to measure it
would be to infect humans on purpose! As a comparison, it is known that one gram of
infected brain is enough to contaminate a cow. We can suppose that a larger quantity
would be necessary to contaminate a human, for the disease must leap the species
barrier. But so far that is absolutely unproven.
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Is everybody as likely to catch the disease?
All cases that have appeared up until now concern people who share a common
genetic trait. This trait is fairly widespread, since 40% of the population carry it. But not
having this trait probably doesnít make people immune to the disease: it may simply
prolong the incubation period. This is indeed what was observed in iatrogenic CJD,
due to the injection of contaminated extractive growth hormones.
Eating habits may also be a risk factor: are people afflicted with the disease big
meat-eaters, for example? An epidemiological study along these lines was carried out
in Great Britain, but it didnít lead to conclusive results as no link could be made
between eating habits and the risk of developing the disease.
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7. PUBLIC HEALTH PROTECTIVE MEASURES
Is the embargo on British beef still justified?
Despite the still significant number of diseased cattle in the United Kingdom, it has not
been proven that meat consumed in England is any more ìdangerousî than that
consumed in France. But here again scientific certainty is hard to come by.
In a report from November, 1999, the European Food and Veterinary Office (FVO)
confessed that it couldnít decide between two options:
ï considering that the conditions proposed by the United Kingdom for resuming its
exportation of de-boned meat2 were satisfactory, and that no proof could be offered
that this meat presented a risk for the consumer;
ï or putting off the decision about raising the embargo for from 12 to 24 months in order
to gather supplementary data.
Nearly a year later, in September, 2000, the board concluded that nothing proved that
the consumption of whole British veal carcasses, slaughtered between 6 and 9
months, presented any risk.
New opinions will probably be given after the publication of studies underway in Great
Britain, which aim at clarifying certain points about the present state of the disease
among British livestock.
1. The Fvo is made up of 16 members, each representing himself. It is headed by
GÈrard Pascal, of the French Inra, and also head of Afssaís scientific board.
2. A few of these conditions: cattle whose meat would be eligible for exportation must
be under 30-months old and be born on a farm that has been free of BSE for several
years. Their mother must have lived at least six months after their birth without any
symptoms of BSE. And, of course, specified risk matter must be scrupulously weeded
out.
What is SRM (Specified Risk Matter)?
For animals that belong to species likely to be affected by BSE, SRM are those parts of
their organism in which a prion-infection can be detected at one phase or another of
the disease.
These parts include the brain, the spinal cord, the eyes, the intestines (and above all
their extremities, the ileum) as well as the spleen and the thymus. This list changes
constantly as scientific research progresses. Its items must absolutely be eliminated.
Though bone marrow is not considered infectious, all cattle bones may soon be
prohibited in the fabrication of gelatine. The point of this measure isnít to ban bone
marrow, but the vertebrae, which could be infected by surrounding nerve tissues.
On the other hand there are no plans to change the production of cosmetic products
which use purified cattle fat. These production areas do not seem problematic.
Another part of cattle that raised some doubts was the rib on the bone, which is close
to the spinal cord. It is a problem that can be detoured by changing the butchering
technique at the abattoir.
As for the milk and muscle (red meat), they are supposed to not be dangerous for
consumption. However, doubts about the innocuousness of red meat are frequently
expressed, because muscles contain nerve tissue which might convey the infection.
Furthermore, it isnít known if the non-detection of the prion in meat and milk proves it is
not there or that the tests are simply not sensitive enough. And in cases where the
prion is present in weak doses, we do not know if this quantity could infect humans.
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Scientists are inclined to think not. In any case, attempts to contaminate laboratory
animals by injections of crushed muscle have never made it possible to observe the
diseaseís development.
Are we sure we are isolating sick cattle from human food?
No, and that is why risky offal has been withdrawn. About 750,000 sick cows are
estimated to have been eaten in the United Kingdom. A British researcher estimated
that some 100 incubating cows might have entered the food chain in France in 2000.
Is systematic culling scientifically justified?
More than anything else, it is a measure intended to reassure the consumer, decreed
at a time when the number of BSE cases in France was very small. Little scientific data
exists for justifying or invalidating this principle.
In the United Kingdom, where systematic culling was not practised, it was observed
that there were on average four sick cows per farm, and up to fifty in some cases. Two
thirds of the English herds had more than one case of BSE. This may seem reasonable
insofar as all the cows in the same herd probably ate the same feed. These
observations clearly favour total slaughter, but the epizooty reached such proportions
in Great Britain that comparison with other countries is difficult. In contrast, studies in
Switzerland imply that in a herd where there is a sick cow, the other animals in danger
of being ill too are part of the same birth cohort (same age, more or less one year). This
argues in favour of selective culling. But these studies deal with insufficient numbers to
be able to draw conclusions on a scale of a country like France.
The complete findings of the 48,000-test campaign should yield more precise data,
better adapted to the French situation. Indeed, a few weeks after the start of this study,
it was decided to add to these tests all the animals slaughtered because of the
precautionary principle.
Pressure from cattle-raisers, who wanted to know if their destroyed herds were
afflicted with BSE, lead to this decision. Unfortunately it did not include the first herds
slaughtered.
Why is it so difficult to harmonise decision-making in Europe?
The European Union was not created for health-risk management but to facilitate
trade. Anything that might thwart or unbalance this trade is therefore extremely hard to
tackle by this institution. For instance, several countries, including Germany, were long
opposed to a generalised moratorium on MBM. They were convinced they did not have
BSE, and refused to deprive themselves of this cheap source of protein. Moreover, the
advent of the single market in early 1993 made it much more difficult to monitor imports
and exports. For such measures to be effective, they must therefore be taken on a
European-wide scale. But that is not the role of the European Commission, and we
return to the beginning of the paragraphÖ
Can scientists be of any help in making the right decisions?
More or lessÖ Their opinions are only consultative, and the effect of the measures they
recommend depends an awful lot on the quality of their implementation, something
which scientists simply cannot control.
On the other hand, it has now become very difficult for politicians to make decisions in
such fields without expert approval. But scientific data are not the only parameters
taken into account by decision-makers, who must also consider economic and political
realities.
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In the end, risk management and communication with the public are really in the hands
of the political leaders.
Is the public correctly informed about these issues?
No, and farmers arenít either. First, the subject is complex. It affects little known
diseases for which there are many outstanding question marks. Furthermore, scientific
communications are indecipherable for the general public in their original form. Efforts
must be made to ìtranslateî and circulate this information, including towards the press.
Scientists are not trained to do this, and politicians often prefer to ìfilterî information so
as not to create panic. With a boomerang effect that could be gauged in the autumn of
2000 in France when public anxiety was largely fed by the lack of understanding.
Were all the precautions taken in time?
Probably not. There were delays, and most of all a certain laxness in implementing
them. It may also well be that certain decisions were not applicable in practice.
On this topic, the Phillips Report might be referred to, as it did an in-depth study of the
management of the crisis in the United Kingdom. In France a survey, known by the
name MattÈi Report, did a similar job, dealing above all with the suspicions of fraud
and illegal imports. Also to be mentioned is the report of the French Senate, published
in May 2001, which rekindles the controversy on the tardy ban of bone meal. Finally,
there are a number of investigations underway.
Is traceability truly a guarantee?
In certain cases it can provide security, but it cannot resolve all problems. Firstly, it is
not practised in all countries, which is a problem in an open market. Secondly, a certain
number of composite and converted products get through completely. Here again the
blending and distribution techniques used by the industry are at fault. And of course, it
is in these products that the potentially infected tissue may end up, sometimes only by
negligence or lack of professionalism.
What is at stake in the precautions taken regarding the nvCJD?
The cost of these measures might seem disproportionate to the health risk.
Considering that the people who will develop the nvCJD are already infected, the
implementation of the precautionary principle can be questioned.
Is public health the main concern, or is it protecting the politicians, who fear a new
scandal comparable to what France witnessed with HIV-contaminated blood? Is the
economic future of the cattle industry the real stake?
There are obviously no simple answers to these questions.
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8. BSE SCREENING TESTS
Two screening test campaigns are being jointly applied in cattle. They have common
points but also differences.
TESTING LAUNCHED IN FRANCE IN 2000
To what purpose?
This is above all a research procedure to better understand the extent of BSE in
France. It creates an active monitoring network that complements the passive
monitoring network in use since '90. This passive network is intended to report all BSE
cases detected by a clinical diagnosis of the symptoms. It relies on a network of
co-ordinator vets who are named one to a department (96 in Metropolitan France) to
centralise and validate all suspicious cases reported by their colleagues after visits to
cattle-raisers.
What targets?
These tests are applied to cattle over 24 months old and considered as risky. This
covers several scenarios:
ï animals that die in the field or on the farm, whether the cause of death is known or not;
ï animals killed in an emergency because of a wound or disease.
These tests are therefore not done in a random manner but among cattle that are most
likely to catch BSE so as to detect the greatest number possible.
What means?
These tests are aimed at 48,000 cattle in metropolitan France, i.e. 40,000 in the three
major western regions (Brittany, Lower Normandy and the Loire, 12 departments) and
8,000 in all other departments.
The number of tests was determined by a statistical calculation relying on the
supposed prevalence of the disease (from 0.1 to 3 per 1,000), the number of cattle in
France (slightly more than 20 million head) and the precision wished for in the
measurement.
In addition to these 48,000 tests, there were other tests carried out on animals
destroyed as a precaution, i.e. when a test is positive, all the other animals in the same
herd are destroyed. It should be noted that this complementary measure was
implemented a few weeks after the beginning of the testing campaign and that several
hundred cattle were killed and incinerated without their brains being examined.
What results?
The pilot sampling campaign ended on March 16, 2001. The tests were carried out on
44,000 cattle of the regions of western France, and on 8,600 cattle in other regions as
a complementary study. The number of cows tested is therefore slightly higher than
initially planned.
In a report published on May 29, 2001, the French Food Safety Board (AFSSA) gives
its analysis of the test campaign.
The tests found 74 cattle in the incubation stage, which represents an average
prevalence of some 1.6 per 1,000 amongst the at-risk cattle.
This figure cannot be extended to include the entire French cattle population. One
must take into account the different categories of cattle amongst which the sick
animals were spotted. Indeed, destroyed animals were afflicted by BSE three times
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more often (3 per 1,000) than those who died of natural causes (1 per 1,000); nearly
90% of sick cows were born between 1993 and 1995.
As expected, this study cannot give formal conclusions on the spread of the disease
nation-wide. It can only shed some light on what maximum prevalence can be
expected in the worst-case scenario, i.e. amongst at-risk cattle. The study also
validates retrospectively some of the implemented measures, such as taking wounded
animals out of the food chain.
Most of all, this study is a source of data to better understand the disease. It may
provide arguments against the systematic culling of herds where a case is found.
Tests carried out in Europe in 2001
To what purpose?
The tests' main objectives are to increase food safety for consumers, and to regain
their confidence by eliminating the largest possible quantity of cattle in the BSE
incubation phase.
Gradually applied to the entire European Union, these tests should also shed light on
the situation in regions or countries that have officially remained free of BSE in an
almost miraculous manner.
They should therefore help obtain a more realistic picture of the disease on a
continental scale.
What targets?
These tests are for all cattle over 30 months old when slaughtered, even without any
symptoms of BSE.
Animals this age, who are not tested for one reason or another, are therefore removed
from the food chain and destroyed.
What means?
The European Commission funds a part of the test: 15 euros (about £10) per test, or
about 20% of the average cost. Each country has to contribute the complementary
means, including the logistics and the choice of accredited laboratories for processing
the samples.
In France, these tests have been run on more than 700,000 animals during the first five
months of 2001. They are on-going, at a rhythm of 30,000 to 42,000 tests per week.
What results?
As of May 2001, these tests have identified 24 animals in the incubation stages of the
illness. This validates the assessments published at the end of the year 2000 by British
epidemiologist Chrystl Donelly. Indeed, she surmised that about 100 infected, but
symptom-free, animals may have been included in the French food chain during that
year.
Looking at the cases detected by the tests, it appears that the regions of western
France are the hardest hit, though the illness has also been spotted in some
departments of eastern France.
The extent of the campaign has helped boost consumer confidence in bovine meat.
However, it mustn't let people believe that the French food chain is now perfectly free
of infected animals.
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Indeed, though rapid tests can detect the illness many months before the first
symptoms appear, they cannot pinpoint sick animals in the early stages of incubation.
As AFSSA has clearly stated, the systematic testing should not dampen the
scrupulous control over the elimination of SRM. This remains the centrepiece in the
system of public health protection.
Finally, it should be noted that 170,000 cattle over 30-months old were slaughtered
without being tested, between January 1, 2001, and May 20, 2001.
Of course, they were not included in the food chain, but incinerated. This measure was
taken for economic purposes, to support the cattle industry and prevent market
decline. Although these test-less slaughters did not incur any risks for public health, it
is nevertheless a missed occasion to collect scientific data.
Other questions on the screening test
Which rapid tests have been approved in Europe?
The Biorad test has been perfected by the CEA (French Centre for Atomic Energy) and
developed by the American company, Biorad France.
Prionics is a Swiss test from the Prionics AG company, produced and sold in France by
the AES laboratory in Brittany. This is the one selected for the campaign of 48,000
tests begun in mid-2000 in France.
The Irish test, Enfer (Enfer Technology, Ltd.) is the third test approved by the
European Commission.
Five other tests from the following agencies are being studied: Id-Lelystad, Holland;
Imperial College of Science Technology and Medicine, United Kingdom; The Institute
of Neurodegenerative Diseases / University of California, San Francisco(IND/UCSF),
United States; PerkinElmer Life Sciences, United Kingdom; Prionics AG (Elisa),
Switzerland. There is also a complement to the CEA France test that may make it
possible to distinguish BSE from scrapie.
How were they chosen?
The European Commission received ten applications from test producers.
The four most promising on paper were then assessed in the field on a series of 1,400
samples from both healthy and sick animals. 1,064 samples were taken from 1,000
healthy animals, and 336 were done from animals who had been confirmed as BSE
cases.
How reliable are these rapid tests?
Three of the four tests correctly identified all the samples that they were given ìblindî.
The fourth test found 70% of the sick animals and 90% of the healthy ones. It was not
approved.
Generally speaking, the approved tests are more sensitive than those used to detect
diseases such as undulant fever and tuberculosis, even when used in advanced
stages of these diseases.
ìDilutionî trials were also run. These consist of trying to spot the infectious particles
mixed in at ever weaker concentrations with healthy tissue. In this trial the Biorad-CEA
test proved to be the most effective. It was able to detect prions in an infected brain that
was crushed up and diluted to 1%. The Prionics test showed it was limited in this area
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to concentrations about ten times higher, and the Enfer test performances were
somewhere between the two.
What is the principle of the BSE screening tests?
The general principle is the use of a specific antibody capable of binding to the prion
protein. Whether the protein is the cause of the disease or just a tracer is of little
importance at this stage.
This method can undergo changes to make it faster to implement and to ease its mass
application, especially in rapid test cases, but is based on the principles commonly
used in biochemistry to recognise and distinguish proteins.
The problem with prion proteins is in distinguishing the pathological form incriminated
in BSE from the healthy form, which all mammals carry. Indeed, the antibodies used
are not able to distinguish between these two forms.
The solution is to first eliminate the healthy prion proteins from the sample by
attacking them with an enzyme. This reaction is the one that occurs naturally in the
organism. It does not affect the pathological proteins, which resist elimination. If there
are infectious prions present, they will thus be the only ones to resist destruction by the
enzyme and to be recognised by the antibodies.
The fast test is applied to samples taken from the brain stem. Results are obtained
within a few hours.
The specifics of each test lay in the use of different specific antibodies, each then being
observed in its own way.
Are these tests the only way to detect BSE?
No, the above-mentioned tests are ìrapid testsî. They are not considered to be
reference methods and must then be confirmed by immunocyto-chemistry (the
examination of histological crosscuts of the brain) or by ìWestern-blotî.
In a ìWestern-blotî, a protein associated to its specific antibody migrates by
electrophoresis in a gel where it leaves a marking specific to its chemical composition
(mainly of its molecular mass), as a kind of signature.
This technique is very routinely used in biochemistry. For example, it is used for finding
other specific proteins that appear in Alzheimer's disease.
One of the goals of the 48,000-test campaign done in France is to compare the results
of the Prionics rapid test with the more traditional ìWestern-blotî method.
It should be noted that the rapid test does not make it possible to detect the infection
earlier than the other methods. It is simply useable on a mass scale, which is a clear
advantage.
What more can be asked of these tests?
To detect the infection earlier. To detect the incubating animals as early as possible,
during the long five-year period before any symptoms appear.
Measurements in the intestines and above all in its extremity, the ileum, would be
interesting. This is the first organ to be infected, but on a level too low to be detected by
present means. This method has already led to a few results, but only in cases of
experimental infection obtained with large doses of infecting matter.
Ideally, it would be possible to test living animals by non-invasive sampling, e.g. with
blood or urine. No technique to do this was yet been found.
This might first be feasible in sheep prior to death from scrapie, as the infection
spreads more widely than in cattle and is seen outside the central nervous system.
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It is hoped that eventually a test for the massive screening of all living cattle will be
available and that the disease will thus be quickly eradicated.
Another research avenue is perfecting a test to detect the infection among humans.
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9. SHEEP AND OTHER ANIMAL SPECIES
What animal species are affected by the TSSEs (transmissible subacute
spongiform encephalopathies)?
BSE may be the most ìfamousî of the TSSEs, but it is not alone. Sheep scrapie
appeared in Europe in the mid-18th century, and has since been widely exported. It
was suspected of being at the source of the BSE epizooty through sheep carcasses
being recycled into meat and bone meal. But this has not been proven, and the original
infection may well have come from a sporadic case of BSE, unknown to veterinary
medicine. Under scrutiny for more than two centuries, scrapie has clearly never
crossed the species barrier to contaminate mankind.
On the other hand BSE has contaminated cats, probably through feed containing offal.
Some eighty cats were thus contaminated in England in the early ë90s with Feline
Spongiform Encephalopathy.
Minks in the United States have suffered from a similar disease known as TME
(Transmissible Mink Encephalopathy). This contamination probably originated from
the sheep and cattle carcasses used to feed minks on mink farms. It spread rapidly
because minks are carnivorous animals that eat the other minks that die around them.
Other ruminants in North America have been affected too: moose, stag and wapiti
deer. Wapiti deer are sometimes raised on farms, but stags and moose are wild
animals, making epidemiological studies difficult. It is nonetheless estimated that the
proportion of afflicted animals in Wyoming varies between 6 and 15%. The origin of
this disease may also be found in the bone meal that is sometimes made available to
these animals in the winter months.
This disease, known as Chronic Wasting Disease or CWD, raises an important
question: is it or is not transmissible to humans? Three hunters under thirty died of the
Creutzfeldt-Jakob disease in Utah in 1998. The possible link between these cases and
CWD is being evaluated.
Are sheep in danger of being contaminated by BSE?
It has been proven in laboratory conditions that the BSE bovine agent is capable of
infecting sheep orally. They develop a disease that is very hard to distinguish from
scrapie but could have much more harmful consequences for humans. To date, this
contamination by the BSE agent has never been observed in a natural setting in herds.
But the similarities between the two diseases call for very intense monitoring to ensure
that sheep do not develop this form of BSE. Indeed, although it has not been a general
rule, that sheep may have consumed animal meal cannot be excluded. Moreover,
because monitoring facilities have been bolstered in France, the number of reported
cases of scrapie in 2000 has increased, which calls for even more vigilance.
What threat would this sheep disease represent?
In contrast to scrapie, it could easily be passed onto humans for it is caused by the
same infectious agent as BSE, which has shown what harm it can do among humans.
Whatís more, although the cattle disease remains limited to the nervous system and
does not seem to infect tissue such as the muscles, it would not necessarily be the
same for sheep BSE. A larger part of the organism would be affected, in particular the
ganglions. Recourse to the total destruction of the animals would be necessary and not
just a withdrawal of Specified Risk Matter.
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The possibility that this variant of BSE might appear is sufficiently serious for AFSSA to
have published a report about it in July, 2000, and a warning in February, 2001. It has
also worried the British Food Safety Board, which has called for a very careful
monitoring of all cases of scrapie.
Is there any relationship between foot and mouth disease and BSE?
On the health and biological levels, they are two different diseases without any points
in common. Foot and mouth disease cannot be passed on to humans.
However, it can be argued that the extent of these diseases point to insufficient
surveillance and preventive measures. Indeed, the fact that both epidemics broke out
in the United Kingdom after the health services had all but been taken apart, may not
be haphazard.
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10. WHAT WE HAVE (TEMPORARILY) LEARNED FROM THE CRISIS
Can fingers be pointed?
It seems extremely hard.Some cattle raisers probably ran the risk of buying cheap
bone meal soon after it was prohibited in the United Kingdom. Others were tardy
perhaps in declaring suspicious cases of sick cattle. Still others may have unknowingly
fed their animals with infected meal after theyíd been mixed in with feed supplements.
But generally they have undergone a production-oriented system that shows them
clearly how to improve their income and supply products that meet market needs.
There were probably also illegal imports and a lack of rigour in the manufacturing of
certain feed. But with the animals showing the first signs of the disease only several
years after being infected, it is generally impossible to establish a direct
cause-and-effect link. As with the ìpoolingî techniques, mistakes and corruption add up
and spread all over the country, even the continent.
True responsibility for the disease and its consequences for mankind must most
certainly be sought in a global social model rather than with identifiable real persons or
legal entities.
By intensifying cattle raising and above all by making cows produce a lot more milk
than they can do by just eating forage, we have made food correctors and protein
supplements a necessity.
Every step in this crisis, which, in hindsight, might appear to be a reprehensible
mistake, was seen at the time as an intelligent way to increase productivity and
profitability.
And then there is the question of political leadership. This has been the object of
several reports, some more controversial than others.
Should the production systems be changed?
This crisis can be seen as that of a food production system. It concerns the entire
cattle-raising and cattle products industry. This is an industry that made enormous
efforts to lower its production costs in a few dozen years, with a highly laudable view to
supplying meat and milk products to the entire population at affordable prices. In many
countries, attaining those goals has compelled the cattle industry to enter an
industrialised period and to become intensive. The agricultural revolution has
succeeded well beyond its initial goals, creating a situation nearing over-production.
But habits die hard, and the rationale of optimal productivity has continued to develop
without retreating.
The ìmad cowî crisis has now cast a new light on the situation, and calls for a return to
reasoned farming are increasing. Numerous players in the cattle industry say they are
ready to go back to square one in their practices and to think about other production
methods. We will have to wait a few more years before seeing if, beyond statements
aimed at reassuring the consumer, lessons have truly been learned from this crisis.
What will cattle eat tomorrow?
The total ban of meat and bone meal raises questions, including what is going to
replace it in cattle feed. Although the most obvious solution consists of using plant
protein, it runs aground on certain shoals. Indeed, the agreements signed within the
framework of the World Trade Organisation (WTO) supervises very closely the aid
each country may allocate to its farmers for producing oil-producing grains. France
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may be compelled to import large quantities of plant protein, a goodly part of which
may be developed from GM (genetically modified) grains.
The long-term consequences of using GM foods are to date totally unknown, and the
implementation of the precautionary principle is caught in a crossfire.
There may however be a solution for getting round these difficulties. It would mean
giving up supplementing cattle feed with proteins and letting cows produce their
ìnaturalî quantity of milk.
Obviously such a solution would reduce productivity.
Will Europe learn to manage health risks?
The draft proposal for creating a European Food Safety Authority is without a doubt a
very interesting initiative. It will have to be given time for implementation and then find
its operational cruising speed before we can judge its effectiveness. There are a lot of
potential questions concerning its independence, its possible powers (not just
consultative) and its ability to go counter to the commercial and industrial interests of
European member countries ñ all the more complex in that they are different from one
country to the next. Yet this project is the only hope at present for Europe, on
agriculture and health issues, to expand its expertise in subjects other than just
arbitrating trade conflicts.
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