Cobalt deficiency (bush sickness)
Cobalt deficiency was the cause of bush sickness, particularly on the pumice soils of the North Island, and was widespread among livestock in the early 1930s. It was known as Morton Mains disease in Southland, and Glenhope ailment in Nelson. The condition still occurs, particularly in lambs, and results in appetite loss, poor growth, wasting, failure to thrive and eventual death. Ruminants need cobalt for the production of vitamin B12 by micro organisms in the gut. This vitamin is then absorbed and stored in the animal’s liver. Vitamin B12 is needed for energy and protein metabolism – so cobalt deficiency is really a vitamin B12 deficiency. Lambs seem to need more cobalt than cattle and deer.
Since many New Zealand soils are deficient in selenium, so are the plants that grow in them. Selenium is one of the antioxidants that enhance immune responses and protect against toxic metabolites. A deficiency causes white muscle disease (muscular dystrophy), poor growth in lambs, calves and fawns, low fertility in ewes, and poor milk production in cattle.
Selenium deficiency can be corrected by using fertilisers containing selenium at the rate of 1 kilogram per hectare. A pour-on animal treatment is also available.
Copper levels in pasture are lowest in winter and animals are often tested at this time.
Animals will be deficient if their feed is low in copper, or suffer induced deficiency when copper intake is high but there is high molybdenum content in the feed – the molybdenum interferes with the absorption, use and storage of copper. Cattle and deer are more sensitive than sheep to induced copper deficiency because their requirements are about twice that of sheep.
Copper assists in the formation of the myelin sheath around nerves, and in bone development. Some copper enzymes have antioxidant properties. Copper deficiency causes a nerve disorder (enzootic ataxia), weak bones (osteoporosis) and poor growth in lambs and calves. Fewer lambs and calves are born, and adult cattle can lose weight and suffer bad diarrhoea (peat scours). Livestock can suffer copper deficiency in spring on peat soils when the molybdenum concentrations in pasture are at their highest.
In the 1920s and 1930s people in much of New Zealand had mild to moderate iodine deficiency. In some areas up to 30% of schoolchildren had goitre. The introduction of iodised salt in 1939 helped to eradicate this by the 1950s. In the 1960s, milk-equipment cleaners contained iodine, which was absorbed by the milk. These are no longer used, and salt intake has also diminished. Recent studies show that adults may be becoming mildly deficient in iodine again.
Iodine deficiency causes an enlarged thyroid gland (goitre) in the neck of newborn animals, particularly lambs. Goitrous thyroid glands grow larger to compensate for insufficient iodine in the blood. Humans show the same effects of iodine deficiency.
Most iodine deficiencies occur when brassica crops are fed to pregnant ewes during the second half of their pregnancy. These crops are low in iodine and contain chemicals which interfere with the use of iodine by the thyroid gland. Deficiency results in lower lambing and a higher death rate of newborn lambs. Adding iodine to the diet corrects the problem.