Zamia staggers in cattle
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Grazing cattle in cycad(zamia)-infested country can become costly for some graziers due to annual losses from poisoning. Zamia, zamia palm or burrawong, as the plants are often known as, grow mostly in eastern Queensland and inland to the Central Highlands. The cycad genera in Australia likely to be involved in this condition are Cycas, Macrozamia and Bowenia.
The syndrome is seen in cattle and rarely in sheep. Water buffalo (Bubalus bubalis) are also reportedly susceptible. The neurotoxin responsible for this condition (staggers) has not been identified; however, these plants also contain a chemical known as MAM, which can be damaging to the liver. (Sheep are more likely to suffer from this toxin.)
The seeds and young fronds appear to be quite palatable and are readily eaten, especially when other feed is scarce. This can occur commonly with regrowth after bushfires. These are also the most toxic parts of the plant.
After eating the young leaves for some time (generally more than 14 days), the animal loses coordination of the hindquarters, staggers about and eventually falls. This is sometimes mistakenly referred to as 'rickets', a name used for the condition of softening of the bone due to vitamin D deficiency.
The posterior paresis and ataxia is the result of degeneration of nerve fibres in the spinal cord. Additionally, signs of liver or alimentary tract damage, such as jaundice and diarrhoea, by the co-occurring MAM toxins may be seen in cattle showing zamia staggers.
Experimental reproduction of toxicity occurred frequently from the 1890s through to late 1900s.
Feeding calves on young leaves at 1.8 kg daily for 11 days or 2.7 kg daily for 7 days reproduced the disease.1
It was reported the first signs of the paralytic condition generally appear after about 14 days´ zamia feeding - when 0.9-1.8 kg of any part of the plant are consumed per day.2
Posterior ataxia (´rickets´) was produced in cattle fed 0.9 kg daily for 31 days.3 Similarly, neurotoxicity was produced in a 320 kg heifer fed 24 kg4 and in a 176 kg steer fed 4.3 kg over 20 days (1.2 g/kg/day), producing the first signs on Day 18.5
In other trials, neurological disease was not always reproduced. Two calves were fed 3.6 kg of leaves daily for 3 days and one other calf 2.7 kg daily for 6 days. All died with severe gastroenteritis, but no neurological signs were seen.6
An 8-month-old steer was fed 0.9 kg daily for 28 days, then 1.8 kg daily for the next 28 days without producing illness,7 while two steers, each weighing 357 kg, ate 2.8 kg in 7 days and 5.3 kg in 20 days with no ill effect.8
Recovery of affected stock
Cattle that develop neurological signs and are subsequently removed from the zamia do not improve. They remain in that condition for the rest of their lives. Related deaths frequently occur through misadventure when cattle fall down banks and breakaway gullies.
The rickety condition of affected cattle makes them difficult to market, as they are likely to fall down in transit and cause other sound stock to go down and become injured. As the condition is nervous, the quality of the meat is not affected.
One control method for the grazier is to fence off the zamia country and only graze it for short periods when feed is plentiful (and/or supplementary feed available), and young shoots and seeds are not evident.
Chemical control of cycads is difficult. Reshooting from the base of the plant will occur if treatment is not thorough. The use of Tordon 75D injected into the stem is effective and is registered for this use. However, chemical control of zamia is usually uneconomic because it grows in lower carrying capacity country.
Be aware of legal requirements for the conservation of cycads. Consult your state government nature conservation authorities for up-to-date and accurate advice.
1 Edwards, HH 1894, 'Report of the Government Veterinary Surgeon, Mr. H.H. Edwards on the disease known as "rickets" or "wobbles"', The Journal of the Bureau of Agriculture of Western Australia, vol. 1, no. 18, pp. 225-234.
2 Hunt, JS 1899, 'Rickets in cattle', Annual Report of the Department of Agriculture, Queensland, 1898-1899, pp. 120-122.
3 Stewart, JD 1900, New South Wales Department of Agriculture, Report of the Chief Inspector of Stock, p. 20. [cited by Hurst, 1942, p. 3]
4 Hall, WTK 1964, 'Plant toxicoses of tropical Australia', Australian Veterinary Journal, vol. 40, pp. 176-182.
5 Hall, WTK & McGavin, MD 1968, 'Clinical and neuropathological changes in cattle eating the leaves of Macrozamia lucida or Bowenia serrulata (Family Zamiaceae)', Pathologia Veterinaria, vol. 5, pp. 26-34.
6 Lauterer, J 1898, 'New investigations on rickets and Macrozamia', Proceedings of the Royal Society of Queensland, vol 14, pp. 1-9.
7 Bennetts, HW 1934-35, The Journal of the Royal Society of Western Australia, vol. 21, p. xxi.
8 Hall, WTK 1961, In correspondence with LG Newton, 28 February 1961. (Original in former DPI&F Natural Toxicants Database files.)