F.R. Emmerson and R.A.McKenzie, Biosecurity
Pigweed (Portulaca oleracea) is a succulent annual plant which can be excellent stock feed. It grows throughout Australia in coastal and inland areas. It responds rapidly to rain and can dominate previously bare patches and stock yards, especially after a dry period. However, oxalate and nitrate compounds in pigweed are potentially lethal.
Droughted, hungry or travelling cattle and sheep are at risk when pigweed suddenly becomes a major part of their diet. Sheep are more likely to be poisoned.
Poisoning can be due to the toxic effects of both oxalates and nitrates.
Oxalate is normally metabolised and rendered harmless in the rumen by bacteria, but high oxalate intakes cannot be metabolised fast enough and the oxalate is absorbed. Oxalate binds calcium in the intestines and the blood, lowering serum calcium levels.
Nitrates in plants are gastro-intestinal irritants. However in cattle and sheep, nitrates are readily reduced to more lethal nitrites by the action of rumen bacteria.
Nitrites, on absorption into the bloodstream, convert blood haemoglobin, which conveys oxygen to the tissues, into methaemoglobin. This deprives the animal of oxygen.
The concentrations of both oxalate and nitrate in pigweed are boosted by growing in soil with a high nitrogen content. Manure and urine are very good sources of nitrogen, so pigweed in and around stockyards is likely to contain large amounts of these toxins.
Clinical signs of pigweed poisoning are often a mixture of those of oxalate and nitrate poisoning.
Oxalate hypocalcaemia produces signs similar to milk fever. In early cases the animal may be excitable and want to charge. Muscular tremors (twitching), staggering and `proppy' movement lead to lying on the side with legs extended and lying on the sternum with the head forward, or turned back along the side.
Bloat, lowered temperature, rapid shallow breathing and fast, weak heart rate are common signs.
Animals usually lapse into a coma and die within 12 hours of ingesting the plant.
Nitrites deprive the animal of oxygen, inducing rapid gasping breathing, rapid weak pulse and cyanosis or bluing of the mucus membranes.
As with the oxalates, there is likely to be muscular tremor, staggering and finally collapse.
Temperatures are usually normal or low. Convulsions usually precede death, which is within 24 hours.
Oxalate poisoning has no characteristic post mortem signs, but kidneys are usually swollen and pale and some animals will have severe fluid accumulations in the lungs with froth flowing from the trachea (windpipe). A typical chocolate brown blood discolouration is the main post mortem finding in cases of nitrate-nitrite poisoning.
Samples can be collected from sick or dead animals to confirm the field diagnosis.
To help confirm oxalate poisoning in live animals, blood from the jugular vein can be analysed for its calcium content (very low in oxalate poisoning) and for indicators of kidney damage. In nitrate-nitrite poisoning, this blood sample will be tinted brown.
Post mortem samples should include at least aqueous humour (the clear fluid from chamber of the eyeball immediately behind the cornea) for nitrate assay and a sample of kidney preserved in 10% formalin for microscopic examination for oxalate crystals.
Samples of the plants should be collected for oxalate and nitrate assay. These should be packed in paper (not in plastic bags).
All samples should be sent to a veterinary laboratory for processing.
Perhaps the best diagnostic indication is a positive response to treatment.
Oxalate - Intravenous calcium borogluconate (CBG) is recommended. Because oxalate poisoning damages kidneys, treatment will not always be successful and some deaths will occur in spite of it.
Warning: Overdosing with CBG can be fatal to stock. Inject slowly and monitor the pulse rate. As the pulse starts to slow, cease the injection.
Dosage for a 25% solution of CBG
cattle 300-500 mls
sheep 50-100 mls
Check the concentration and adjust the dose rate accordingly.
Nitrite - Methylene blue as a 2-4% solution in water injected intravenously is the antidote for nitrite poisoning.
Dose rate: 2mg/kg B.W. Repeated doses may be required if nitrite continues to be absorbed from the rumen.
If in any doubt, consult your veterinarian.
Avoid access to substantial quantities of pigweed, especially by hungry or stressed animals.
Stock watered and fed roughage such as hay before access to pigweed are at less risk because their rate of intake of the pigweed will be reduced and rumen bacteria will have a better chance of dealing with the toxins.
Should stock have already gained access they should be denied water for at least two hours and watched carefully.
In danger areas, such as trucking yards, it may be possible to control pigweed by scarifying or spraying with herbicide. It has been suggested that keeping stock moving for a period after introduction to yards carrying a heavy growth of pigweed to thoroughly trample it may significantly reduce intake.
Last updated 09 June 2005