Acacia species

Abstract

Acacia erioloba, Camel thorn, Kameeldoring. DISTRIBUTION: Typically found in deep sandy soil. In dry areas along river courses and other places where water is present. It is a small to medium-sized deciduous tree of up to 6m with dark grey bark and a compact rounded to flattened crown. BOTANICAL DESCRIPTION: General: A single-stemmed tree of up to 22 m, often unbranched for 1 m or more. Usually does not lose all its leaves, even in winter.The bases of the paired spines are often much swollen and fused together at the base. Leaves: The leaves, which are borne at the nodes, have 1-5 pairs of pinnae. The number of leaves per node vary from 1-7. Flowers: Flowers are in round, deep golden-yellow balls in axillary tufts, sweetly scented. Spring. Fruit: The indehiscent thick pods are large and woody, greyish-green with a dense covering of velvety hairs and shaped like the lobe of a human ear.

Acacia sieberiana, Paper bark thorn, Papierbasakasia. DISTRIBUTION: Occurs in frost-free, rather arid bushveld. BOTANICAL DESCRIPTION: General: A single-stemmed tree with an umbrella-shaped crown. The bark is corky, flaking, papery, dark grey to creamy-yellow.Twigs and young leaves covered with dense yellow hairs.The paired spines are up to 5 cm long and covered with whitish hairs when young. Leaves: The leaves are rather large. Petiole and rachis moderately hairy and leaflets closely spaced. Flowers: Sweet-scented flowers are in round cream-coloured balls. Fruit: The woody, indehiscent pods are large, thick, straight to slightly curved and pale to dark brown. Hairy when young. Open only after falling to the ground.

Acacia caffra, Hook thorn, Haakdoring. DISTRIBUTION: Widespread growing on open veld, bushveld and hillsides throughout the eastern half of the country. BOTANICAL DESCRIPTION: General: A medium-sized, single-stemmed deciduous tree of up to + 10 m tall with a rounded or irregular shaped crown. Bark dark and rough. The paired prickles are recurved and hairless. Often small and not very well developed. More noticeable on young growth. Leaves: The leaves are very variable, could be smooth or hairy, but typically with 10-18 pairs of pinnae. Flowers: Flowers are in clustered spikes, light yellow to cream and darkening with age. Spring. Fruit: The dehiscent brown pods are flat and straight, 8 - 13 cm long and usually narrower than 1,3 cm. Pointed at both ends.

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, blousuurvergiftiging.

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. PM as soon as possible. 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.