Panicum miliaceum
Broom corn millet, common millet, French millet, proso millet, Russian millet
Productive grass / seed crop grown world wide for both animal and human consumption. The leaves are long, thin and slightly hairy and branch out from the main stems. During early summer, the plant dries off from a deep green colour to a golden brown. Large clumps of seeds are produced at the tips of the stems. The seeds produced are small spherical, 2 3mm and golden brown.
Millet is uperficially similar to maize. There are over ten different species of Panicum grasses that have been implicated in poisonings in animals. Millet is grown as an annual cereal crop. P. dichotomiflorum (smooth witchgrass, fall Panicum), is a weed encountered during turf establishment in the USA. Is it a sprawling to erect summer annual, with stems bent and branched outwards. Leaf blades are smooth, occasionally hairy on the upper surface, with distinct broad, light green midrib. Ligule fringe of hairs. Seedhead purplish coloured at maturity, open, freely branched. Toxicosis caused by P. coloratum (kliengrass) (not in NZ) and P. antidotale (giant or blue panic grass) is a common problem in many parts of the U.S.A. and South Africa. They are similar to smooth witchgrass.
Millet is occasionally grown as a cereal crop in intensive cropping areas of NZ, including Canterbury, Hawkes Bay and Marlborough. It is also sometimes grown for silage. Other panicum species are found growing in pasture, along roadsides and amongst lawns. Many of these grasses are rare in NZ.
May contain sufficient nitrate, cyanide or oxalate to cause poisoning. Some species are also involved in hepatogenous photosensitisation. The main toxic principle are believed to be saponins (glycosides). They are broken down by the liver to form saponinogens.These are then precipitated in the bile ducts as crystals. This results in irritation and obstruction of the bile ducts. The resultant cholestasis causes jaundice, increased blood ammonia levels (may lead to hepatic encephalopathy) while the reduced breakdown of phylloerythrins by the liver (a photodynamic substance) leads to hepatogenous photosensitisation. Young growing plants seem to be the most hazardous due to their high saponin content. The toxin remains even when dried, but is also concentrated with drying, therefore, panicum hay can be particularly dangerous. The most common time of year that poisoning occurs is form late spring to early autumn.
Horses and ruminants are the most common species likely to be grazing Panicum pastures, released onto millet crops or given Panicum hay to eat. Rare in NZ.
Can include icterus, photosestivity, intermittent colic and fever, weight loss and neuroloical signs (hepatic encephalopathy). Lameness may occur due to photosensitisation around the coronary bands. Affected animals seek shade from the sun. Clinical signs can develop anywhere from three days to several weeks of the animals grazing the pasture.
Lesions include: hepaic and portal fibrosis, billiary hyperplasia, severe jaundice, photosensitisation of the face, ears and coronary band and subcutaneous oedema. Histologically, birefringent crystals are usually seen in the bile canaliculi and macrophages of the liver. These crystals accompany bile duct fibrosis hyperplasia and consequent cholestasis. Necrosis of the heart, liver, adrenal and kidney can also occur.
Jaundice and photosensitisation lead to the suspicion of liver disease. Presumptive diagnosis of plant induced hepatopathy is based on the history of exposure to plants and multiple animals on a farm or in as area affected. Post mortem of affected animals with detection of birefringent crystal in the small bile ducts canaliculi, kupffer cells and renal tubules will ensure diagnosis.
Other causes of photosensitisation: facial eczema but disease usually occurs later in the year than Panicum poisoning, usually in mid to late autumn, when the level of plant dead matter is high, and the temperature and humidity levels are still high. Clinical signs are very similar but with no crystals in bile ducts. Other causes of secondary (hepatogenous) photosensitisation include; lupinosis, congenital photosensitivity of Southdown and Corriedale sheep, ngaio poisoning, ragwort, blue green algae, phosphorus and carbon tetrachloride poisonings.Primary photosensitisation can also be due to the ingestion or direct absorption through the skin of a photodynamic substance such as that from St John’s wort, parsnip and parsley. In these cases, icterus is usually not observed.
Affected animals should be removed form the toxic source, fed good quality hay and protected for the sunlight.
Mortality can be high, reaching 100% in animals not removed from the pasture. Prognosis depends on the intake of Panicum and the concentration of the saponins within it. Provided animals are removed from the source of poisonings before clinical signs have progressed too far, the liver will regenerate and the animal will recover. However, in very acute cases, the disease may have progressed too far for recovery.
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