Pontifications on Poison
Being some ramblings on events associated with poisonous plants.
Sunday 16th October 2011
I’m grateful to Esther Hegt, whose 'Ragwort, myths and facts website is such a useful resource, for drawing my attention to some new research on Equine Grass Sickness (EGS). I hadn’t even heard of this condition until a couple of months ago when Esther explained that it produces far more problems that Jacobaea vulgaris, common ragwort, but does not provoke the same reactions.
‘Grass Sickness is a disease of horses, ponies and donkeys in which there is damage to parts of the nervous system which control involuntary functions, producing the main symptom of gut paralysis’. That quote is lifted straight from the Equine Grass Sickness Fund, a charity trying to raise funds for research into this condition.
EGS, first described in 1907, can be a fatal disease and, it is said, it was such a prevalent condition in the 1920s that the replacement of horses by tractors was accelerated. It is usually said to be a bigger problem for the UK than other countries though there is a lot of interest in it from other places.
The biggest problem with EGS is that no-one knows what causes it. From the descriptions given, for example, ‘Grass sickness occurs in three main forms, acute, subacute and chronic’, it is not even clear, to me, that it is a single condition and not a number of different conditions producing broadly the same symptoms.
Almost everything said about how the disease arises is followed by a ‘but’; a high clover content was thought to be a risk factor ‘but’ the disease does occur on pasture with no clover, grazing is strongly associated with the disease ‘but’ there have been cases in animals with no access to pasture and so on.
For a time, the suspicion has been that the disease is caused by Clostridium botulinum Type C. There seems, however, to be another ‘but’ as the presence of the bacterium does not, always, result in the disease. There seem to be other factors that determine whether the disease is triggered.
The research Esther pointed out to me suggests that, in some way, buttercups, plants in the Ranunculus genus, are involved. The latest study found a higher ranunculin content in the plants in pasture where there had been an outbreak of EGS when compared to pasture with no occurrence of EGS.
Ranunculin occurs in all plants in the family Ranunculaceae. Hydrolysis, which can occur during the crushing associated with ingestion, converts it to protoanemonin and it is this that produces symptoms of poisoning. The taste of buttercups is usually described as ‘acrid’ and voluntary ingestion by grazing animals is rare.
This new work has led some people to start talking about removal of buttercups in the same way they talk about removing ragwort but it is important to understand what the researchers are actually saying.
There seems to be no suggestion that EGS is caused by eating buttercups, though they are toxic. As with ragwort, horses, like cattle, don’t seem to be interested in eating buttercups. What appears to be being suggested is that, whatever the environmental factor is that causes the Clostridium intoxication to produce EGS, it also produces higher levels of ranunculin in the buttercups in that pasture.
I think the researchers are suggesting that work to find what increases ranunculin production in buttercups could lead to finding the environmental factor(s) that produce EGS.