Senecio vulgaris
Subsucculent, annual herb up to 60 cm tall. Leaves are oblong and sharply toothed. Flowers are pale yellow florets in drooping clusters.
A member of the ragwort family. There are many similar species, eg, shore groundsel (S. lautus) on beaches (probably not toxic).
Common in gardens, cultivated land and waste areas of both islands.
Pyrrolizidine alkaloids.
One case reported in calves ingesting hay with 5% groundsel.
Liver failure. The animals may, be dull, have an increased pulse rate, have an increased respiration rate, show weakness, have colic, perhaps show signs of jaundice. Horses may show great nervous excitement and violence. Usually the animal will die within a few days or weeks.
Chronic weight loss and poor doer. Early clinical signs include: a loss of body condition, and inappetence and constipation. Later on animals may have pallid mucous membranes, signs of jaundice may be visible, photosensitisation and abdominal pain. Cattle often show persistent straining (no diarrhoea), with some occasional nervous signs in the form of mania. Horses may also have nervous symptoms such as yawning, drowsiness and a staggering gait.
A grossly enlarged, cirrhotic liver due to centrilobular necrosis and portal fibrosis (especially in horses and cattle, uncommon in sheep). Some endothelial cell damage leading to vascular leakage and thrombosis (especially cattle), large nodules in the liver due to proliferation of intra hepatic biliary tissue and parenchymal cell regeneration. Generally the liver is atrophic, fibrotic and distorted with irregular nodules of regenerated tissue. Histologically the architecture of the organ is completely disrupted.
Lung may have endothelial damage resulting in fluid leakage, fibrosis and thrombosis, pulmonary hypertension with cardiac hypertrophy, pulmonary oedema and hydrothorax (due to progressive vascular damage)
Kidneys glomerular vascular lesions and tubule epithelial megalocytosis, congestion and perhaps fatty degeneration of the kidneys.
Gut atrophy of the intestinal villi (which results in decreased absorption and digestion and thus loss of body condition during life), perhaps some early ulcers, petechial haemorrhages of the small intestine, gastroenteritis and oedema of the wall of the abomasum may also occur.
Ascites, petechial haemorrhages of the heart and serous membranes may be seen.
History, clinical signs and pm. Biochemistry serum protein, bilirubin, BUN, any enzymes relating to liver function, however the results need to be carefully interpreted with the history. Liver biopsy as the damage is usually well distributed look for megalocytosis (may/may not be present) and acute haemolytic necrosis (however this can be caused by many other toxins/infections) if non grazing animals show this it is probably due to heavy feed contamination with PAs. Clinical signs of liver insufficiency as animals will less frequently show respiratory damage and occasionally renal insufficiency.
Anything that causes signs of liver failure, but narrowed down by the history.
These could include such things as facial eczema, and liver fluke.
There is no specific treatment. Remove the source of the toxin and feed the animal a highly digestible diet that is high in energy and low in protein. High protein diets seem to exacerbate nervous signs. Other treatment is symptomatic.
The appearance of clinical signs indicate a poor prognosis as clinical signs are only seen once a considerable amount of toxin has accumulated in the body. If well established the liver damage is permanent and further progression will occur. Affected animals may have their survival time prolonged, but there is a decreased capacity to cope with the demands of production or the stress of work. It is therefore recommended where possible to cull the animals affected.
Susceptible animals should not graze heavily infested pastures and care should be taken that supplementary feed such as hay and grain also do not contain the alkaloid. The level of toxin is lowered by ensiling, but not by the hay making process. Feed bought on to the farm should come from a reputable dealer. The plant should be sprayed and removed from the pasture as the dead leaves are still toxic and become more palatable to stock. Sheep and goats have been used as a control as they are relatively resistant.
Connor, HE, The Poisonous plants in New Zealand, 2nd ed.,1977, Government Publications Ltd., Wellington
Parton K, Bruere A.N. and Chambers J.P. Veterinary Clinical Toxicology, 3rd ed. 2006. Veterinary Continuing Education Publication No. 249
