Hypomagnesaemia is most likely to develop following the onset of lactation in ewes, and those bearing twins are most vulnerable (Sansom et al., 1982).
Subnormal serum calcium values usually accompany the low serum magnesium and shifts in the balance between hypocalcaemia and hypo- magnesaemia can influence clinical manifestations; no other inorganic blood constituent is consistently affected. Severe hypomagnesaemia inhibits the customary PTH response to mild hypocalcaemia and fasting has a similar effect (Littledike and Goff, 1987); it is therefore possible that the inappetence associated with severe hypomagnesaemia is responsible for inhibiting PTH secretion. There are parallel reductions in magnesium concentrations in other body fluids (e.g. vitreous humour, CSF), but the magnesium concentrations of the milk (Rook and Storry, 1962), soft tissues and bones of affected cows and ewes remain within normal limits. In contrast, calves chronically depleted on a low-magnesium diet reduce the magnesium reserves in their skeletal tissues and Ca : Mg ratios increase from a normal 50 : 1 to 150 : 1.
Despite a great volume of research in many countries, the aetiology of grass tetany remains incompletely understood. Influences of herbage constituents, such as citric and aconitic acids (Bohman et al., 1969), the higher fatty acids (which cause magnesium soaps to form in the rumen) and aluminium (really a soil contaminant) have been proposed (Grunes et al., 1970; Suttle, 1987).
The organic acids are unlikely aetiological factors, because they are destroyed in the rumen and cannot complex magnesium or reduce its availability and the role of aluminium has been discounted (see Chapter 18). Numerous studies have demonstrated a positive relationship between the incidence of tetany and fertilizer treatment of the pastures with nitrogen (N) and Fig. 6.4. Plasma magnesium concentrations can decrease markedly with age in a beef suckler herd but cumulative nutritional deficits may contribute to the apparent ‘age’
effect (from Suttle et al., 1980).
Blood biochemistry
Pasture biochemistry
potassium (Kemp et al., 1961). Thus ’t Hart and Kemp (1956), in a study of 3942 cows on Dutch farms, found the incidence of grass tetany to be 0.5% on pastures low in potassium; 5.2% with excess potassium; 4.3% on pastures treated with more than 50 kg N ha21; and 6.5% with excess potassium and nitrogen; such fertilizer treatments with N and K also decrease herbage magnesium concentrations (see Chapter 8). Signs of grass tetany have been induced by increasing the intake of potassium in sheep (Suttle and Field, 1969) and in cattle (Bohman et al., 1969). Dutch workers brought the hypothetical influence of ammonia formation into their prediction of serum magnesium concentrations by incorporating dietary CP concentrations in a manner which treated the influences of both factors sensibly as continuous variables (Fig. 6.5), but the basis for their predictions was never shown. High nitrogen and potassium concentrations have also been implicated in the disorder which occurs when cereals are grazed as forages (Mayland et al., 1976), but the two factors are confounded and potassium is by far the more influential. Pasture potassium and nitrogen concentrations rise rapidly in spring in response to rises in soil temperature, but the patterns of change in soil temperature and therefore potassium : magnesium ratios in herbage will vary greatly from week to week and year to year.
Fig. 6.5. Risk of hypomagnesaemia in the Netherlands has been predicted from the magnesium, crude protein (CP) and potassium concentrations in pasture (Netherlands Ministry of Agriculture and Fisheries, 1973): note the use of a marginal range for serum Mg within which onset of tetany is uncertain.
The transition from winter rations to spring grass is accompanied by marked changes in the rumen (raised pH, NH4+, insolubility of magnesium) and these have been linked to the development of hypomagnesaemia. The magnitude of the changes eventually diminishes (Johnson et al., 1988; Johnson and Aubrey Jones, 1989) and may contribute to a gradual recovery in plasma magnesium. A change of diet can depress plasma magnesium even when the change is from grass to hay (Field, 1983). A fall in plasma magnesium can be associated with delayed rumen contractions in response to feeding and with impaired motility in the lower intestinal regions (Bueno et al., 1980).
Intravenous infusions of magnesium sufficient to restore normal plasma con- centrations do not immediately restore normal intestinal motility. Such responses may explain the loss of appetite for roughage which can be seen in recently calved cows on low-magnesium diets (Braak et al., 1986). Loss of appetite compounds the problem of low absorbability by lowering magne- sium intake and plasma magnesium further (Herd, 1966). These changes are usually taking place at a time of increasing milk yield, associated with increases in the quality and quantity of digestible organic matter on offer from spring pastures. Close correlations between dietary composition and incidence of tetany are unlikely to be found in such circumstances and a fur- ther search for missing dietary factors in the aetiology of the disease is unlikely to pay dividends.
The initial signs of hypomagnesaemic tetany in cattle are those of nervous apprehension, with ears pricked, head held high and staring eyes. At this stage, the animal’s movements are stiff and stilted, it staggers when walking and there is a twitching of the muscles, especially of the face and ears. Within a few hours or days, extreme excitement and violent convulsions may develop; the animal lies flat on its side, the forelegs ‘pedal’ periodically and the jaws work, making the teeth grate. If treatment is not given at this stage, death usually occurs during one of the convulsions or after the animal has passed into a coma. The presence of a scuffed arc of pasture by the feet of a dead animal is an important diagnostic feature. However, the subclinical stage may be followed by spontaneous recovery from hypomagnesaemia and does not invariably progress to the acute disorder.
Preconvulsive clinical signs in sheep are less clearly defined than in cattle and can be confused with those of ‘hypocalcaemia’ or pregnancy toxaemia.
Affected ewes breathe rapidly and their facial muscles tremble; some ewes cannot move, while others move with a stiff, awkward gait. Eventually, they collapse and show repeated tetanic spasms, with the legs rigidly extended.
The roles of dietary change and anorexia