Senecio jacobaea
Tansy ragwort, Saint James’ wort
Herbaceous biennial, perennial or annual with a diffuse root system. In the first year the plants are usually present as a rosette of leaves arising from the crown. Multiple crowns with several rosettes are often formed. The flower stalks of ragwort, which develop during the spring, are single or multiple, up to 1m. Flowers are conspicuous yellow daisy type. Seeds have a downy pappus for wind distribution. Ragwort plants in various stages of growth may be present at the same time in the field, because germination can occur at different times of the year. Ragwort spreads rapidly and once established eradication is difficult and grass and legume production is reduced. The persistence of ragwort has been encouraged by a farming system based on continuous grazing without periods of cultivation. It is a problem on properties where cattle graze, in particular dairy farms, as cattle avoid eating ragwort. This selective grazing encourages its development and spread. Palatability but not toxicity is increased when cured in hay or wilted. All parts of the plant are toxic and stock will eat the green plant if forced, by lack of other food.
Some alpine daisies have similar flowers, but nothing which looks similar is likely to be seen in pasture in NZ. There is a large range of introduced and native species of Senecio, many of which are poisonous.
Abundant in pasture on both islands, especially where rainfall is high.
Usually horses and cattle, but can include sheep, goats, pigs, chickens and sometimes humans. Sheep appear resistant to ragwort toxicity (perhaps due to the PAs being detoxicated by bacterial enzymes in their rumens), so they have been used to clean up ragwort infested pasture. However, there is some evidence that sheep can have chronic liver toxicity and delayed mortality without showing early signs of disease. If given a choice, grazing animals tend not to eat ragwort, unless there is more ragwort than grass in the pasture. They will eat wilted plants or hay. Pigs and poultry are usually only affected if their feed is contaminated with PAs, they will not choose to eat ragwort. Humans can also suffer from ragwort toxicity from ingesting disguised plant material present in cereals, herbal tea and milk products. There is also evidence for milk products becoming contaminated after lactating animals have eaten ragwort. Honey produced from ragwort nectar is also toxic, however it is usually too off coloured and bitter to market.
Acute PA toxicity is rare but may occur if stock have been eating feed heavily contaminated with PAs. The animals may be dull, have an increased pulse rate, 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 PA toxicity results from an accumulation of toxins over weeks to months, thus the clinical signs will be delayed. Early clinical signs include a loss of body condition, inappetence and constipation. Later on animals may have pallid mucous membranes, signs of jaundice may be visible, photosensitisation, abdominal pain. Cattle often show persistent straining (no diarrhoea), with some occasional nervous signs in the form of mania. Horses may also develop hepatic encephalopathy and show nervous symptoms such as yawning, drowsiness and a staggering gait. Sheep may not show any signs, but all sheep fed ragwort showed marked liver dysfunction in one experiment.
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 intrahepatic 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 endothelial damage resulting in fluid leakage, fibrosis and thrombosis. Cardiac hypertrophy may have resulted from pulmonary hypertension, 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 also be seen.
History, clinical signs, serum biochemistry for liver function (eg. bromosulphothalein clearance), however the results need to be carefully interpreted with the history. A liver biopsy can be taken 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 nongrazing animals show this it is probably due to heavy feed contamination with PAs.
Anything that causes signs of liver failure, but narrowed down by the history. These could include such things as facial eczema and fascioliasis.
There is no specific treatment for ragwort toxicity. Animals with PA induced liver damage should be removed from the source of the toxin and fed 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. Horses with hepatic encephalopahty have a grave prognosis.
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. In the case of ragwort, the plant should be sprayed and removed from the pasture as the dead or wilted leaves are still toxic and become more palatable to stock. Sheep and goats have been used as a control as they are relatively resistant to ragwort toxicity. Cinnabar moth caterpillars are being tried as a biological control.
Conner H.E. The Poisonous Plants In New Zealand. 1992. GP Publications Ltd, Wellington
Cooper M R, Johnson A W. Poisonous Plants and Fungi in Britan: Animals and Human Poisoning. Her Majesty’s Stationary Office. London. 1998
Dewes, H.F. and Lowe, M.D. (1985). Haemolytic crisis associated with ragwort poisoning and rail chewing in two thoroughbred fillies. N Z vet J. 33: 159 160.
Elcock, L. and Oehme, F.W. Senecio poisoning in Horses: A Summary. Vet Hum Toxicol. 24:122-123
Hill F. (1998). Plant poisonings in cattle. Vetscript XI. 9:14-15.
Johnson, A.E. Molyneux R.J. & Ralphs, M.H. 1989. Senecio: A Dangerous Plant for Man and Beast. Rangelands. 11(6).
Mortimer, P.H. and White, E.P. 1975 Toxicity of some composite (Senecio) weeds. Proceedings of the 28th NZ Weed and Pest Control Conference, 88-91
Parton K, Bruere A.N. and Chambers J.P. Veterinary Clinical Toxicology, 2nd ed. 2001. Veterinary Continuing Education Publication No. 208
Seawright, A.A. (1982). Animal Health in Australia. Vol. 2. Chemical and Plant Poisons. Australian Bureau of Animal Health, Canberra, Australia.
Surveillance (1974) 1(5):24 Ragwort poisoning in Otago and Southland (Cattle and Sheep)
Surveillance (1976) 3(1):18 Ponies, summer camps and Ragwort poisoning.
Surveillance (1980) 7(1):15 Ragwort poisoning (sheep, deer, cattle)
Surveillance (1981) 8(3):20 Ragwort poisoning in deer.
Surveillance (1981) 8(3):26 Ragwort poisoning in horses.
Surveillance (1983) 10(1):26 Ragwort poisoning in deer.
Surveillance (1983) 10(4):15 Ragwort poisoning (cattle).
Surveillance (1992) 19(1): 4 Ragwort poisoning in cattle.
Surveillance (1993) 20(3) 28 Ragwort poisoning in calves.
Surveillance (1994) 21(3) 31 Ragwort poisoning in sheep.
Surveillance (1996) 23(2): 4 Ragwort poisoning in horses.
Surveillance (1996) 23(4): 3 Ragwort poisoning in cattle.
Surveillance (1997) 24(2) 22 Ragwort poisoning in cattle.
4 October, 2007
