Bright yellow, daisy-like flowers in fields and on verges may look pretty, but these yellow beauties are a threat to horses as they are poisonous and if eaten can result in irreparable liver damage which can be fatal so it is essential to eliminate these plants from pastures.

These daisy like flowers are Common Ragwort (Senecio jacobaea) which is classed as a hardy biennial, meaning that it flowers in its second year. The young ragwort plants can be seen from the autumn until early June and have a distinctive flat ’rosette’ shape. Generally the leaves on these rosettes divide into terminal ovals and smaller lateral lobes. They are often a glossy looking green, and the stems may be purple-coloured.

From late June in their second year, the ragwort plant produces 30 - 100 cm flowering stems. Flowers are bright yellow and daisy-like in appearance, often about 2cm in diameter. The flowers are arranged in dense, flat-topped clusters. The leaves on the stems are heavily divided into lobes, with only their bases attached to the non-woody stem. These stems die back into the rosette shape again, after the seeds have been produced, usually in September. The massive number of seeds produced by a single mature plant is such that the population increases at a rapid rate.

The toxin involved in Ragwort poisoning is called a pyrrolizidine alkaloid (PA). Senecio jacobaea is not unique in producing this toxin as it naturally occurs in a number of other plant species such as Common groundsel (Senecio vulgaris) and Fiddleneck (Amsinckia intermedia). Indeed, it is not only livestock who are at risk from PA poisoning either, as there have been a number of outbreaks of PA poisoning in humans where they have eaten contaminated foods. In humans, the condition is called venoocclusive disease (VOC).

Pyrrolizidine poisoning primarily affects the liver but in some animal species it may also affect the lungs and kidneys but to a lesser extent. The pathological changes in the liver are unique to PA poisoning and include cell necrosis, sinusoid distension and megalocytosis (enlarged cells). Perhaps the most devastating effect of PA poisoning is that it inhibits the regeneration function of the hepatocytes, so that while the damage continues, the repair mechanisms are not able to cope. Even for patients who recover from poisoning, the liver damage is permanent.

Horses and cattle are the most sensitive animals to PA poisoning and serious toxicity can be seen after 5-10% of their own bodyweight is ingested. PA poisoning produces a chronic delayed toxicity, which means that clinical signs of poisoning are not seen until long after the PA has been absorbed. The length of time between absorption and response are proportional to the concentration of PA absorbed over time, and therefore a horse that has received a large dose of PA in one go, will show a response more quickly than a horse that receives the same amount of PA but over a longer period of time.

As ragwort is digested in the small intestine, the pyrrolizidine alkaloid is absorbed straight into the portal vein that enters the liver. In theory, ragwort poisoning can be easily recognised by the damage caused, but a biopsy is required to confirm this. Unfortunately, during the early stages of PA poisoning, the biopsy is only a small piece of a large organ and damage may be missed, not to mention that the process involves invasive surgery that is always a risk in itself. By the time that enough clinical symptoms of liver damage have become apparent to diagnose liver failure, 75% of the organ will already be irreparably damaged. This is a good indicator of the massive functional reserve of the liver.

Clinical diagnosis of liver damage can be based on some/all of the following symptoms:

Weight Loss
Lethargy
Depression
Blindness
Diarrhoea
Abdominal Swelling
Jaundice
Photosensitization

Although it is near impossible to detect liver damage in its early stages by clinical symptoms alone, if a horse is suspected of having eaten ragwort, the extent of liver damage can be measured by taking a simple blood sample. Newly damaged liver hepatocytes leak enzymes into the blood stream, which under normal circumstances would not be there in such abnormal amounts. Such enzymes include: gama-glutamyl transpeptidase (GGT) and alkaline phosphatase (ALP).

Bearing in mind that the clinical symptoms of liver failure develop only after 75% of the liver is irreparably damaged; it is unsurprising to find that the prognosis is poor and the horse will probably not survive for much longer.

There is no known cure for pyrrolizidine poisoning.

If liver failure is detected early on in its course and the horse is no longer exposed to the source of the poison, the condition may not be fatal as there will be enough reserve cells to allow the correct functioning of the liver. Careful dietary management (which allows the liver to carry out as few functions as possible) has been found to be helpful but this is by no means a cure. Such diets must be low in protein, high in carbohydrate and supplemented with vitamins A, D, E and B. This means that newly cut hay, clover and cereals must be avoided and molassed sugar beet pulp is advised.

Advanced liver failure is often not treatable. Diets that avoid extensive hepatic function are, as before, helpful and some success may be gained by prescribing corticosteroids, antibiotics and/or steroids, but it is debatable as to whether their administration actually helps, or hinders the liver as they pose another demand on the liver functions.

It appears then, that the only way to ’treat’ ragwort poisoning is to prevent it in the first place. The only, truly successful method of disposing of these ragwort plants is by pulling them up by their roots and burning them. The ragwort plants must be removed before they go to seed as one plant can shed up to 100,000 seeds. There are a number of suitable herbicides available, but these must be administered at certain times of year and the pasture must not be grazed on in the following six weeks as the toxins will still be present in the dying/dead plants.

There are increasing concerns about the safety of baled hay or haylage, both of which form the bulk of a domestic horse’s food in the winter. Unfortunately, no farmer can go around checking each bit of a hay field for unobvious ragwort as it is impractical. Therefore, it is not unlikely for a small amount of ragwort to be present in a bale of hay. Unlike other poisons, drying has no effect on the lethal nature of pyrrolizidine alkaloids so it is just as harmful dry, as it is fresh, bringing to light the hazards of long-term damage again.

Thankfully, horses will only eat growing ragwort if there is little other palatable food available. Once it is dry however, ragwort becomes much more palatable to the horse and he will find it harder to detect.

There is evidence proving that pyrrolizidine alkaloid poisoning can also affect humans and has also been shown that the toxin may be absorbed through the skin into the blood stream: the use of thick gloves or a rag fork is therefore essential when pulling out the plant.

The growth of Common ragwort is governed under the Weeds Act 1959 and The Ragwort Control Act 2003. If seen on private land you can take action by alerting the landowner, on motorways and major roads by contacting the Highways Agency, and on other roads or council land by contacting the local council and if spotted on railway embankments contact Network Rail (0845 711 4141).

Author: Zoe Ong