Ragwort
– a killer in disguise
Derek
Knottenbelt

Over the last 10 years
Ragwort has infested large parts of the British countryside.
Indeed the plant can regularly be found growing in railway line
ballast, car parks, domestic lawns and school playing fields etc.
Hitherto the plant was restricted and controlled and was only found in a
few isolated habitats. Farmers
and councils were aware of its significance and “rooted it out”.
Through these years of strict control the Cinnabar moth (Tyria
jacobaeae) was plentiful. The caterpillar is recognizable by it's
Cornish Rugby Team Jersey coloration and thrives on a mixture of Ragwort
and groundsell (Senecio vulgaris).
Many lay people driving along comment on how pretty the flowers
are in high summer and how the fluffy seeds can be seen to blow away in
the wind – giving the impression of a dandelion clock!
The yellow peril is lurking and expanding its grip on the UK –
it presents a serious hazard for horses and other grazing animals.
The potential danger of
ragwort has been known for many years and every owner of land was
required to control ragwort either by direct spraying or by lifting and
burning it. Recent
legislation (The Ragwort Control Act, 2004) provides support for the
strict control of the plant on all land in England and Wales (and
hopefully soon there will be a similar Act in Scotland).
Why is control important?

Ragwort is extremely
toxic to horses and somewhat less so to cattle and sheep.
It is quite wrong to assume that cattle and sheep are
‘immune’ to it and that the ingestion of a small amount is of no
consequence in any animal species.
The plant poisons are accumulative and the effects are persistent
(i.e. the liver cannot regenerate damaged cells) and the signs of the
poisoning may be delayed for months or years.
The effects of ragwort toxin are quite different to many of the
other causes of liver damage in that they are irreversible and
persistent. Therefore they
are accumulative i.e. when a horse eats some more there is a dose
related additional damage. The
liver has fortunately a large functional reserve (of over 70%!) and
therefore the signs of damage are not shown at all until over 70 – 75%
of the liver is irreversibly damaged.
At this stage the outcome is inevitably fatal.
In summary the horse (and to a lesser extent cows and sheep) can
eat ragwort for several years showing no clinical effects at all until
there is a dramatic and catastrophic development of evidence of
end-stage liver failure. The end is inevitable. The
additional complication is that a badly damaged liver may be subjected
to other insults such as infections with bacteria or viruses or to the
toxins and this may push the horse over the functional limit and
clinical signs may occur. In
some of these cases aggressive treatment CAN restore the liver to
adequate function because In contrast to the effects of Ragwort most of
these conditions do not cause irreversible damage.
Do horses actually eat Ragwort?
We
have assumed for years that horses will not eat green growing
ragwort plants! This is
based on the casual observation that when horses are grazing in a field
in mid summer the ragwort appears to be untouched.
This is certainly NOT true – they don’t like it and they
would prefer not to eat it but they do occasionally eat some and a few
cases eat more than “a bit”.
The biggest difficulty lies in the palatability of the plant.
In its green growing state it is probably fairly unpalatable but
the wilted or cut and dried plant is not detected at all.
Thus hay that has been cut from a field with ragwort will be
potentially lethal. The
repeated ingestion of a small amount is probably the worst possible
scenario!
As the plant is most
palatable in dried or preserved forage the greatest risk appears to come
from the winter feeding! How
many of us know if the hay or haylage we use is certainly ragwort free?
It is unlikely that any meadow hay is totally free of ragwort in
the UK. This means that
damage can be occurring in the horse over the winter without any sign!
It is a time bomb quietly ticking away!
This probably explains why we see cases of ragwort poisoning in
the late spring and early summer.
In summary:
If horses don’t eat it, how come they are poisoned by it!
There are plenty of cases of ragwort poisoning that have lived
all their lives at pasture and never get any hay or haylage.. where
exactly did these animals get it from?
What
does it do to the horse?
The liver cannot be
directly examined in horses due to its anatomical location.
It is an inherently simple organ comprising of similar cells
arranged in palisades through which blood from the gut
trickles. As the
blood passes through the liver, it is purified and cleaned – toxins
are removed to protect the rest of the body.
In the case of ragwort, the toxins cause irreversible damage to
the cells in proportion to the amount eaten.
Repeated and sustained ingestion of ragwort (or the [unlikely]
ingestion of a large amount in one go) causes progressive fibrosis and
shrinking of the liver. The
organ has numerous vital functions, and failure of any one of these can
easily be life threatening. Any of the functions that the liver performs
can result in clinical symptoms. For
example the liver makes useable proteins from food derived protein
building blocks and if the liver is damaged weight loss and fluid
accumulation under the skin can develop.
Similarly the liver makes blood clotting factors so a failed
liver means that blood clotting may be prevented.
Clearly this is a life threatening event.
The liver also cleans the blood of potentially damaging toxins.
Photosensitisation occurs because the liver fails to remove plant
pigments that then are allowed to circulate. These are deposited in the
white skinned areas and when the sun shines on this skin it causes
massive destruction. The
pigmented skin is not usually affected.
The brain is also a major target for the toxins that escape the
filtration mechanism. This
means that nervous signs including, blindness, fits, lethargy and
depression, coma and bizarre behaviour are all possible.
However, the individual
signs are very variable in poisoned horses – not all show the same
range or severity of signs and the multiple functions of the liver means
that some signs are very subtle and easily missed in the early stages at
least. Pathologists can
easily detect the effects of rawort poisioning but for this it has to be
either a post mortem examination or a liver biopsy (neither an easy nor
a totally hazardless procedure).
Once
significant signs are present the horse is probably beyond treatment but
just occasionally we can save them at least temporarily.
The clinical syndromes of ragwort poisoning is a very distressing
condition for both horse and owner and indeed many horses hurt
themselves and / or hurt the owner.
The horse is suffering and invariably needs to be destroyed.
How
can we diagnose the problem?
While
the mildest signs of liver damage are not usually detectable from the
outside, damage to liver cells can be detected by blood samples.
The acute (fresh) damage to liver cells causes leakage of enzymes
from the cells into the blood stream, which can be measured.
Once the liver is in a funvtional deficit other tests are used to
detect this stage. However,
all these tests are not necessarily specific indicators of ragwort
poisoning. Currently the
only definitive tests are liver biopsy or post mortem examination!
We are trying to develop a new blood test that will detect even
tiny amounts of ragwort in the blood so that the owner can take
preventive action at a stage when removal of ragwort from the feed will
be possible and the horse will then live a normal active life.
It is the repeated ingestion of ragwort that is the most
insidious danger.
If any of the toxin is
detected the horse is eating ragwort and the food can be changed to a
better type! Ragwort toxins
cause permanent and irreversible damage.
The best option is to prevent its sustained ingestion!
Unfortunately the blood test is not yet available.
We expect that when the test is developed a proportion of the
horses in a yard would be blood tested every month or two and if no
toxin was present then the feeding could reasonably be expected to be
safe (with respect to ragwort only of course!)
We need financial support for this project and if you are
interested in helping us to develop the test please contact me.
Can
it be treated?
Liver failure cannot be
treated – it can only be assisted to repair itself.
Terminal cases of liver failure are not treatable at all.
In these circumstances the only hope is to try to control the
central signs by reducing the formation of ammonia and the other organic
acids that are blamed for the development of the signs.
Once seizures, blindness, depression and coma develop it is not a
kindness to keep trying – although there are a few reports of
recoveries and these are usually diagnosed as a reversible disease
superimposed on borderline terminal liver failure due to ragwort.
In the early stages
detected by blood samples taken from horses with vague malaise or
photosensitisation or mild mentation problems intensive care may help
and of course the critical issue is to prevent further ragwort
ingestion. Failure to
address this means certain failure in the end!
Having once removed the source of the problem, the horse should
be fed a healthy diet with easily digestible proteins and a high
carbohydrate availability that does not rely too heavily on hepatic
function (therefore small intestinal digested starches etc are probably
best. Treatment also
involves the avoidance of any further liver insult and the support of
liver function.
SUMMARY:
¨
Ragwort is becoming a potentially serious threat to the health of
our horses.
¨
It is unlikely that there will be a state sponsored control
mechanism that forces the elimination of the weed.
¨
We do not know IF horses eat growing Ragwort although they
certainly do not do so in quantity.
¨
Horses are not able to detect and reject ragwort in preserved
forages but the alkaloid remains poisonous in this type of feed.
¨
The early signs of ragwort poisoning are not obvious (or even
detectable by current means)
¨
The alkaloid itself inhibits reparative mechanisms in the liver
and results in chronic megalocyte formation and progressive perioportal
fibrosis.
¨
Once the signs are advanced the damage is usually severe and
probably beyond repair.
¨
Treatment is palliative at best
Donations towards the
Development of the Blood Test for Ragwort can be sent to:
Dr DC Knottenbelt,
University of Liverpool, Leahurst, Neston, Wirral CH64 7TE
Cheques
should be made payable to University of Liverpool (Ragwort)
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