DISTRIBUTION:
Mostly found in the central and eastern parts of the country. In open veld on mountain slopes and in marshy areas. Often invasive.
BOTANICAL DESCRIPTION:
Senecio latifolius
General: The species that cause the most problems are robust herbs with annual aerial stems ±1 m high that grow from a stout perennial rootstock. The stems are mostly smooth, but typical small pads of woolly hair are found at the bases of the stems. About 300 different Senecio spp. are growing in South Africa. Worldwide about 2000.
Leaves: Alternate, leathery, blue-grey or grey-green without leaf stalks. The base is heart-shaped. Venation very conspicuous when leaf is held up to the light. Margins have short rectangular prickly teeth, evenly spaced at about 3 mm.
Flowers: Stems unbranched before the inflorescence. Numerous yellow flowers in spreading, much branched, terminal clusters. September - December.
Fruit: Seeds are about 2 mm long, each with a crown of hairs.
TOXIC PRINCIPLE:
Pyrrolizidine alkaloids, i.e. sceleratine and retrorsine. S. latifolius is the most toxic plant of the Paucifolii group. Important hay contaminant. (remains toxic when dry).
SYNDROMES:
Dunsiekte (horses)
Molteno straining disease (cattle)
Hepatotoxic syndrome without photosensitization.
SYSTEMS AFFECTED:
Liver.
CLINICAL SIGNS:
Acute syndrome:
• Die within a few days (sheep even within 24 hours, but usually 1-4 days).
• Loss of appetite
• Depression
• Apathy
• Abdominal pain
• Constipation (sometimes diarrhoea)
• Rumen stasis (ruminants)
• Icterus (longer living cases).
Chronic syndrome:
• Long latent period (even up to 9 months).
Horses - Dunsiekte
• Yawning.
• Unthriftiness, ematiation.
• Heads kept low, sleepy, tame.
• Gait abnormalities, walk aimlessly, staggering (sleepy staggers).
• May become frantic (violent staggers).
Cattle - Molteno Straining Disease• Progressive weight loss, unthriftiness, staring coat.
• Severe tenesmus (straining) associated with continuous bloody diarrhoea.
• Eversion of the rectum.
• Dehydration.
CNS:
• Delirious,
• belligerent,
• ataxia followed by drowsiness (due to hepatic encephalopathy).
NECROPSY:
Acute deaths:
• Severe liver damage• Liver swollen, necrotic, congested
• Gall bladder oedematous and haemorrhagic
• Haemorrhages in body
• Oedema of caecum and colon (horses) or abomasal folds (ruminants)
• Mild to moderate icterus
Chronic seneciosis:• Emaciated carcase• Hepatic fibrosis or cirrhosis
• Icterus• Effusion into body cavities (ascites, hydrothorax)
• Oedema of abomasal folds.
• Perirectal oedema (cattle).
HISTOPATHOLOGY:
• It is basically a hepato- and endothelial toxin
Acute:• Necrosis of centribular hepatocytes and haemorrhages
Chronic:• Damage leads to fibrosis• Bile duct proliferation
• Megalocytosis and karyomegaly of hepatocytes• Hyperplastic islands of regeneration
• Veno-occlusive lesions - endothelial cells of veins undergo metaplasia plus
the fibrosis around the veins leads to occlusion of the vessels - hydropericard,
hydrothorax, ascites, generalized oedema
• Also hepatoencephalopathy due to NH3.
DIAGNOSIS:
• Liver sample in 10% formalin for histopathology - typical lesion• Presence of plants that have been eaten. (Acute cases)
• Remember the long latent period in chronic seneciosis.
TREATMENT:
• Symptomatic treatment, liver supportive therapy.
• Activated charcoal.
Prophylaxis:
• Prevent excessive trampling of veld.
• Provide sufficient food.• Utilize infected camp in winter (aerial parts dead).
• Herbicides (very expensive).
• Activated charcoal before grazing in camp.
