Amaranthus retroflexus
Sometimes called redroot (nb. A. powellii is also called redroot). Pigweed is the American name, but the plant came from there so it seems sensible to use this name.
This is a herb with green to reddish stems growing up to 1m (less fleshy than A. powellii), depending on situation. The pale green leaves are oval, with the upper ones being more lance like or tapering. The flowers are in an open branched inflorescence both at the ends of stalks and in the axils. The sepals taper to a point in A. powellii, but are truncate in A. retroflexus. The plant bears a dry fruit.
Redroot (10 other naturalised species of Amaranthus)
Introduced from America in the 19th century, now all over in waste ground. A. retroflexus can grow in drier ground than A. powellii.
The toxic component that causes perirenal oedema/nephrosis of pigs and cattle has yet to be identified. There is a high oxalate level found in A. retroflexus. Oxalates that are soluble and absorbed into the blood may cause hypocalcaemia and hypomagnesaemia by reacting with calcium and magnesium. They may also crystallise in vessels resulting in vascular necrosis and haemorrhage. If these crystals were to lodge in renal tubules, they would cause anuria, uraemia and electrolyte disturbances. In many cases of suspected poisoning of pigs, oxalate crystals were not found in renal tubules and there was no evidence of hypocalcaemia, casting aspersion on the suggestion that high oxalate content is the toxic principle, as nephrosis caused by plant oxalates is usually characterised by large amounts of oxalate crystals in the kidneys. Amaranthus species may accumulate nitrate to potentially lethal levels. This ability is affected by the stage of development and plant growth conditions. The nitrate content of A. retroflexus specimens analysed was highly variable. Whether rumen microflora are given time to acclimatise to the plant would also seem to determine the toxicity. Oxalates may be detoxified by the rumen microorganisms and chronic oxalate exposure enhances this ability.
Pigs most commonly (overseas), also cattle in NZ. There are reports of toxicoses in sheep, goats and, rarely, horses. Although a pet rabbit was diagnosed as having pigweed poisoning, laboratory trials showed that rabbits did not develop the renal lesions reported in other species.
Signs appear within 5 - 10 days of exposure to the plant, with morbidity ranging from 5 - 40% and mortality from 50 - 100%. The animals originally present as weak, depressed and ataxic, with posterior incoordination, progressing to flaccid hindlimb paralysis, resulting in a peculiar crouching gait. Muscle tremors and knuckling at the pasterns also often occur. Although quite often in sternal recumbency, the animals remain alert and retain their appetite. Affected animals usually die from renal failure within 48 hours of the first clinical signs. Other signs sometimes seen include loss of weight, mild serous nasal discharge, foul smelling liquid faeces tinged with blood, subcutaneous dependent oedema (especially in the ventral abdominal wall, making the animals appear bloated), decreased ruminal movements, ascites, polydipsia, polyuria, anuria. There may be ulcerative lesions in the alimentary tract which are attributable to uraemia. An ECG reveals a wide and slurred QRS complex, increased T wave amplitude and Q T interval. P wave is either absent or has a diminished amplitude. With acute renal failure, potassium intoxication may lead to cardiac arrest, a major lethal factor. Haematology reveals hypocalcaemia, hypomagnesaemia, hyperkalaemia, azotaemia and elevated blood urea nitrogen, creatinine phosphokinase and serum glutamic oxalacetic transaminase. The increased BUN content and proteinuria are suggestive of severe renal disease.
The connective tissue surrounding the kidneys always exhibits oedema and the kidneys themselves are slightly swollen and pale, with petechial haemorrhages on the surface and subcapsular haemorrhage. Oedema may also be present in the subcutaneous tissue especially on the ventral abdomen, caudal thigh and around the vulva or scrotum and may also involve the superficial muscle planes. The epicardium and endocardium may display paint brush haemorrhages and ulceration may be present in the gut, nasal turbinates, dental pads, cheek and oesophageal mucosa, tongue, rumen pillars and at the omasal abomasal junction. There is ascites, hydrothorax and hydropericardium with the fluid being straw coloured or blood tinged. Histopathology reveals extensive hydropic degeneration and coagulative necrosis of both proximal and distal convoluted tubules and dilatation of the Bowman’s capsules. The tubular lumens may also contain a granular acidophilic material. The arteriole walls in the gastrointestinal tract, lung and myocardium may show hyalinisation.
Epidemiology, clinical features, and gross and microscopic lesions can be used to make a presumptive diagnosis, with the presence of perirenal oedema being highly suggestive of A. retroflexus poisoning. The presence of the weed in recently grazed pasture is also an important clue. There may be seeds in the rumen.
Hypocalcaemia, hypomagnesaemia, hyperkalaemia (the ECGs are very similar), and toxicoses from oak (Quercus species), Cassia species, oxalate from Aspergillus species, other oxalate containing plants such as Halogeton glomerulatus, Oxalis species, Rumex species and Setaria species, mycotoxicoses, lead, arsenic or insecticides. Fat hen, Solanum rostratum (buffalo burr), black nightshade and thorn apple are other plants that may cause perirenal oedema in pigs. Those viral infections which result in ulceration of the alimentary tract should also be ruled out based on epidemiological and post mortem findings. The histopathology is almost identical to that seen with oak poisoning, although with oak the renal medulla is relatively unaffected.
Response to treatment is limited. Calcium glucose preparations, lactated Ringer’s solutions, B complex vitamins, electrolytes, vitamins A, D, E, selenium and antibiotics, have all been attempted, but affected animals have responded poorly to such therapy. Calcium and magnesium therapy may clinically correct some of the signs, but will not prevent the disease progressing and removal of animals from the source will also not halt the condition. Access to water is vital to speed up the urinary excretion of oxalates, thus preventing their deposition as crystals.
Affected pigs often die within 48 hours of ingesting Amaranthus, although the clinical course may last for up to 10 days. In a recent case in the Wairarapa, 8 of 30 heifers were affected, of which 6 died.
Denying access to pigweed, removing the plants, ensuring the animals have sufficient good quality feed and supplying them with dicalcium phosphate are all good preventative measures. The plant is unpalatable, and large amounts must be ingested to cause toxicity, so toxicoses are more common under drought conditions, as the hungry animals are forced to eat it.
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4 October, 2007
