DISTRIBUTION:
E. cladocalyx is a tree of the winter rainfall area. Trees (originally from Australia) cultivated for various purposes – timber, etc.
BOTANICAL DESCRIPTION:
General: Very large trees with smooth, tan-coloured bark. Trees are fast growing and drought-resistant. Wood splits easily - can be used as firewood. Any Eucalyptus sp. is potentially toxic.
Leaves: Dark green glossy leaves are concentrated at the ends of the branches giving the tree an “open” appearance. Young leaves are round to elliptic, while the older leaves are lanceolate.
Flowers: Flowers in January and February.
TOXIC PRINCIPLE:
• Cyanogenic glycosides
• LD HCN ±2mg/kg in all species
• Monogastric animals less affected by plants with cyanogenic glycosides because HCl destroys hydrolysing enzymes
• Plants with more than 200 ppm (20mg %) or 20mg HCN / 100g potentially dangerous.
ABSORPTION AND DISPOSITION:
• CN¯ rapidly absorbed from g.i.t. and by inhalation (HCN gas)• Rapidly and very effectively detoxified in body by sulphur transferase (rhodanese) enzymes which bind it to sulphur from sulphane pool forming thiocyanate (which is excreted through urine).
Possible to ingest just less than LD continuously over extended periods without harm. If rate of liberation from glycosides in plants exceeds speed of detoxification, problems occurs.
MECHANISM OF ACTION:
• In excess situation CN¯ binds stably with Fe³+ in tissue cytochrome oxidase system and inhibits this. Thus electron transport and oxidative phosphorylation is stopped and chain of cellular respiration is halted. Results in histotoxic anoxia or hypoxia.
• Normal oxygenation of blood not interfered with. Blood stays red. (When treating, jugular blood much redder than normal.)
• CNS depression sets in (oxygen requirement of CNS high)
• Terminally respiratory depression sets in and available oxygen is utilised by uninhibited cytochrome oxidase leading to cyanosis.
SYNDROMES:
Prussic acid poisoning, geilsiekte.
SYSTEMS AFFECTED:
Haemopoietic system.
CLINICAL SIGNS:
In the western Cape a problem in cattle, sheep and goats.
Peracute:
• Death in few minutes - usually found dead.
• Transient convulsions progressing to paralysis, stupor
Acute: (usually)
• Respiratory
- dyspnoea (gasping),
- polypnoea,
- cyanosis
• CNS
- excitement and tremor,
- convulsions, paralysis and
- stupor
• G.I.T.
- Bloat,
- frothing at mouth and
- salivation may occur.
NECROPSY:
Macroscopical findings:• Cyanosis - (in peracute poisoning e.g. execution in man, may have bright red blood).
• Congestion of blood vessels (blood unclotted or clots slowly).
• Asphyxiation signs: haemorrhages in trachea, bronchi and lungs.
• Subepi- and -endocardial haemorrhages.
• Smell of bitter almonds (only some individuals can smell it)
• Rumen: Leaves and other plant residues.
DIAGNOSIS:
HCN rapidly degraded and dissipates easily. Specimens to be taken soon after death.
Degradation rapid in liver and rumen. Much slower in muscle, although HCN concentration in muscle is much lower. With long interim this is the specimen/organ of choice. Still positive next day.
1. PM as soon as possible2. Keep specimen refrigerated or frozen:
• Ruminal content
• Liver
• Muscle
• Plant material
TREATMENT:
Two Steps:
1. Remove the cyanide from the cytochrome oxidase and fix this lethal CN¯ in harmless, inert form. CN has greater affinity for tissue cytochrome oxidase Fe3+ than methaemoglobin, but can be removed from cytochrome system by large metheamoglobin concentrations. Therefore increase metheamoglobin concentration carefully and under controlled conditions with NaNO2 solution intravenously.
2. Then assist in removal of CN¯ via urine as thiocyanate. Assist sulphur transferases to inactivate cyanide by supplying sulphur in form of sodium thiosulphate (“hypo”).
PREVENTION AND AVOIDANCE:
1. Supply extra sulphur
• 5-7% flowers of sulphur in lick
• Hypo in drinking water.
2. Avoid or limit grazing of plants during danger periods - avoid wilted, frost- or hail-damaged material.
