Hypomagnesaemia: Are Fertilisers Really to Blame?

Several early studies of hypomagnesaemia in dairy cows in the 1950s involved the use of extraordinarily large applications of fertiliser potassium and nitrogen to spring grazing to induce the condition so that preventive magnesium supplementation methods could be evaluated. In one such study 4 cwt potassium sulphate per acre was given in two successive years to a cocksfoot/clover sward and a hormone weed killer was used to suppress the resulting profusion of clover growth! Other plots were given up to 6 cwt per acre of ammonium sulphate. Cows were withdrawn from the fertilised plots for 'safety' reasons when serum magnesium concentrations fell below the then accepted 'normal range' (for housed cows given mixed diets) of 2.0-2.8 mg Mg/100ml. There was no justification other than potential cost for such caution and when these two or three cows were either transferred to magnesium-fertiliser supplemented grazing or given daily oral calcined supplementation, all the 'low' values returned rapidly to normal. Subsequent surveys (e.g. Hemingway and Ritchie, 1964) have shown the plasma Mg values for cows experiencing clinical tetany; 52% were below 0.5 mg/100ml and a further 40% of cases were between 0.5 and 1.0 mg/100ml. Severe accompanying hypocalcaemia was present in 80% of clinical cases. The Netherlands MAFF (1973) considered that herbage with over 0.20% Mg, and especially over 0.25% Mg was 'safe' even when herbage K and crude protein contents were as high as 4% K and 25% CP. Nevertheless, it is sensible to restrict the spring use of K fertiliser and slurry to grass to be mown for silage or hay rather than for grazing.

In a 5-year study (Coombe and Hood, ICI, Jealott's Hill, 1980) when groups of 21 cows were allocated to separate areas fertilised as described in Table 1, mean plasma Mg concentrations were similar for both contrasting fertiliser rates and only one case of clinical tetany developed (for the 750 kg N/ha area). There was no difference in the overall herbage K contents of the contrasting regimes and the grass from the 750 kg N/ha regime contained rather more magnesium and less sodium. Importantly, for the grazing area, potassium chloride was applied in mid-season.

Table 1. Annual fertiliser applications (kg/ha) and mean herbage composition (% dry matter). (Coombe and Hood, 1980).

The normally increased amounts of nitrate-nitrogen and urea-nitrogen and potassium in rapidly growing herbage have not been implicated as causal agents for clinical hypomagnesaemic tetany; phosphorus is without effect. Frequently, potassium fertilisers depress the sodium content of grass. The high incidence of clinical tetany (2212 cases over a 13-year period in 35 dairy herds in Hampshire operated by the late Rex Paterson in the 1950s) was reduced by a combination of feeding sodium chloride, eliminating spring fertiliser K applications and using more fertiliser nitrogen.

Clinical tetany incidence in cows at spring grazing has not been related to earlier plasma Mg concentrations when housed. Prior magnesium supplementation can not be stored to give some initial protection. Neither age of cow nor milk yield are related to incidence. Onset of clinical tetany has been associated with a range of factors which reduce normal intake patterns, even on a very short-term basis. e.g. sudden unexpected cold, wind and rain and various factors such as change of grazing, oestrus or lameness and even disturbing factors such as dogs and flies can all affect full herbage intake. There are unknown palatability aspects. Adequate daily magnesium intake in an available form is the key; both dry matter intake and magnesium content of the dry matter are equally involved.

Dietary magnesium intake must be continually maintained for dairy cows. An adult cow contains about 250 g Mg; 150 g in the bones with about 100 g in the soft tissues. Bone Mg cannot be mobilised and feeding magnesium in advance of known critical periods gives no protection. Milk production of 30 litres requires about 3.7 g Mg/day, but only about 3.0 g is present in blood plasma. There is very little margin for safety if for any reason magnesium intake is not maintained.

An adequate soil magnesium status is desirable, and in addition dusting pastures with fine particle magnesium oxide or, more recently, the use of magnesium hydroxide-containing sprays which ensure good adhesion to herbage, ensure Mg intake by the whole herd. Provision of magnesium-rich mineral mixtures, magnesium-containing feed blocks and molassed magnesium liquids rely on regular consumption of appropriate amounts by all individuals. Cows do not have exceptional wisdom to seek out such sources; adequately dispersed feeding points and some prior training are desirable. Magnesium chloride in drinking water is a possibility, but intake depends on weather conditions. Wet grass alone may provide adequate water to cows unless they give more than about 20 litres milk/day.

Continuous magnesium intake throughout the day is desirable. Clinical tetany is often discovered when cows are collected in the field for morning or evening milking. This suggests that giving magnesium-supplemented feed twice a day in the milking parlour may not give full 24-hour cover. It is not practically possible to check by taking blood samples from cows just prior to milking. Individual administration of magnesium alloy rumen boluses gives continuous 24-hour release for four weeks and is the only product with a Veterinary License against clinical tetany.

Appropriate magnesium supplementation can reduce the incidence of clinical hypomagnesaemic tetany. It is not caused directly by fertiliser use.

Professor Gordon Hemingway.
Glasgow University Veterinary School, Bearsden, Glasgow G61 1QH

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Potash Development Association

update: March 2005