The toxicity for cattle of bufadienolide cardiac glycosides from Bryophyllum tubiflorum flowers.
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Biomedical subjects
Publications and source records attributed to P J Dunster.
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Two calves given a mean of 16.1 g and 16.4 g ripe Castanospermum australe seeds/kg body weight daily for 13 and 16 days respectively developed haemorrhagic gastroenteritis. The first calf died. The second calf had mild myocardial degeneration and necrosis and mild nephrosis at necropsy. Two calves given a mean of 16.8 g unripe C. australe seeds/kg body weight daily for 18 days remained clinically normal and had mild gastritis at necropsy. The activity of alpha-glucosidase was reduced in the mononuclear cells of peripheral blood and in skeletal muscle. This was attributed to the presence of the indolizidine alkaloid, castanospermine, in the seeds. The toxin causing the gastroenteritis and other lesions is unknown.
Twenty-six Hereford heifers died after eating mostly ripe fruit of Cucumis myriocarpus growing in a fallowed cultivation paddock. Four affected cattle were dehydrated and apparently had abdominal pain. Necropsy of three revealed intense congestion with haemorrhage of the alimentary tract, numerous C. myriocarpus seeds in ruminal contents, pulmonary congestion and oedema and, in two, swollen livers. Midzonal swelling and vacuolation of hepatocytes occurred in these two. C. myriocarpus fruit (83% by weight ripe) were dosed to two calves at 60 g wet weight/kg live weight. Both collapsed with tachycardia and dyspnoea and died within 6 h. Their packed cell volumes just before death had increased to 0.7. They had hydropic degeneration and necrosis of the ruminal mucosa, intense congestion and oedema of the rumen, abomasum and intestines, swollen and vacuolated hepatocytes and foci of myocardial degeneration and necrosis. Two other calves were dosed daily with 20 g fruit/kg for three days, then 40 g/kg for three days. One calf received a further 40 g/kg next day. Both calves developed persistent diarrhoea and neutrophilia, and their plasma gamma glutamyltransferase and bilirubin concentrations increased. Necropsy revealed necrosis and oedema of the rumen and swollen degenerate hepatocytes.
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Cardiac glycoside poisoning was produced in calves given (in descending order of toxicity) flower heads of the hybrid Bryophyllum (Kalanchoe) daigremontianum x B. tubiflorum, of B. pinnatum, of B. tubiflorum (from previous work), whole plant of B. fedtschenkoi, flower heads of B. daigremontianum and whole plant of B. proliferum. For each plant (except B. tubiflorum), 2 calves were each given a single dose of 20 g wet weight per kg bodyweight. By using high performance liquid chromatography, the bufadienolides (cardiac glycosides) bryotoxin A, B and C were detected and assayed in the flower heads and leaf plus stem of B. tubiflorum and in the roots of B. tubiflorum, the hybrid and B. pinnatum. Only bryotoxins B and C were detected and assayed in the flower heads and leaf plus stem of the hybrid, B. daigremontianum and B. pinnatum. No bryotoxins were detected in B. fedtschenkoi. Bryotoxin A and a mixture of bryotoxins B and C from B. tubiflorum flowers were used as standards in the chromatographic assay. Comparing the results of the calf toxicity experiment with the amounts of bufadienolide measured in the plants suggests that bryotoxins A, B and C probably account for the observed disease, but that B. pinnatum and B. fedtschenkoi contain at least one other cardiac glycoside.
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A slurry of activated carbon (activated charcoal) in electrolyte replacement solution given by stomach tube and antiarrhythmic drugs given parenterally cured 9 of 11 calves dosed 7 to 24 h previously with a lethal amount (20g/kg) of Bryophyllum tubiflorum flower heads. Two of another 4 calves treated 26 to 36 h after dosing with flowers survived. B. tubiflorum toxins are bufadienolides (cardiac glycosides). Activated carbon was effective at a single dose of 5 g/kg. Calves were rehydrated with oral electrolyte replacement solution at 150 ml/kg in divided doses over 24 h. Tachycardia was treated with intravenous lignocaine (200 mg doses) or propranolol (5 mg doses) and atrioventricular block with atropine (0.5 mg/kg).
Findings from natural cases and experiments with cattle emphasise that flowering plants are the most important form of Bryophyllum (Kalanchoe) spp in poisonings in Australia. The main life-threatening lesion is myocardial. The effects on the alimentary tract are less important than was believed previously. B. tubiflorum, B. daigremontianum x B. tubiflorum, B. pinnatum and B. proliferum caused 41 recorded poisoning incidents affecting 379 cattle in Queensland between 1960 and 1984. Poisoning occurred between May and October--the flowering season of these plants. Experimental B. tubiflorum poisoning and natural poisonings produced anorexia, depression, ruminal atony, diarrhoea, heart rate and rhythm abnormalities, dyspnoea and death. Increased plasma concentrations of urea, creatinine and glucose and decreased chloride were measured experimentally. Both natural and experimental cases had myocardial degeneration and necrosis with haemorrhages of the heart and alimentary tract. Cattle with severe dyspnoea had atelectasis and emphysema of the lungs. Some cattle had mild nephrosis. The median lethal doses of B. tubiflorum flowers, roots and leaf plus stem were 0.7, 2.3 and 5.0 g dry matter/kg liveweight respectively (7, 7 and 40 g wet weight/kg). Bufadienolides have been isolated recently from B. tubiflorum flowers and the syndrome is consistent with cardiac glycoside poisoning.
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