DISTRIBUTION:
Sorghum is cultivated mostly in the drier parts of the summer-rainfall areas such as Mpumalanga, Free State and the Northwest. Grain sorghum is cultivated for human consumption, while various feed sorghums have been selected for their low prussic acid potential.
BOTANICAL DESCRIPTION:
A robust tufted grass with thick culms and wide leaves. It does not have rhizomes.
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 20mg % (200 ppm) HCN, 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 occur.
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, nitrate/nitrite poisoning.
SYSTEMS AFFECTED:
Haemopoietic system.
CLINICAL SIGNS:
In practice a problem in cattle, sheep and goats.
Peracute:
• Death in few minutes - usually found dead.
• Transient convulsions progressing to paralysis, stupor.
Acute: (usually)
• Respiratory distress - dyspnoea (gasping), polypnoea, cyanosis.
• CNS excitement and tremor - convulsions, paralysis and stupor.
• G.I.T.: Bloat, frothing at mouth and salivation may occur.
NECROPSY:
• 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 frequent.
• 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 possible
2. 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.
