"Grass Tetany" is a highly fatal disease; not particularly common to cattle in this area, but during the latter part of the winter and spring of last year, many cases did occur. The condition affected both beef and dairy cattle, and whilst in the former it usually was acute and uncomplicated, most cases in dairy cattle were complicated by acetonaemia and hypocalcaemia.
Generally speaking, response to treatment was not good, although in some cases of the acute form, rapid and uneventful recovery followed subcutaneous or intravenous injection of magnesium sulphate. These cases were in beef cattle and treatment was effective even though the beasts appeared very close to death.
It appears that Hypomagnesaemia is more widespread now than earlier and that the incidence is greater. It could be that this is due to failure to recognise the condition in the past, although it is believed that pasture improvement may play a role; while in dairy cattle, workers in the United Kingdom believe that due to the elimination or reduced incidence of certain diseases - T.B., C.A.B., Mastitis, Infertility, etc. - there has been an actual increase in the proportion of older animals. There is definite age incidence. Older cows, ie, those which have had more than six calves, are much more susceptible; in fact 14 times more susceptible than cows on their first lactation. The economic importance of Tetany would appear to lie in its high mortality rate, rather than a high morbidity. Its incidence is very much lower than that of Milk Fever or Acetonaemia.
Hypomagnesaemia affects both lactating cows and calves on whole milk alone, or whole milk supplemented by lush spring pasture, or hay, or concentrates low in Magnesium.
In cows this disease is not associated with parturition, but does occur only in lactating animals. It is associated mainly with the lush growth of pasture in the spring, but is seen often where pasture is very short, though showing fresh growth, and no roughage is available. Placing cattle on to rapidly growing cereal crops may often precipitate an outbreak. In the latter circumstances, the disease usually appears uncomplicated and easy to treat.
In the past there have been two main schools of thought:
(1) claiming the disease is due to a metabolic disorder in which the nutritional status is of no importance.
(2) claiming that it has a complex nutritional or dietetic origin.
The correlation between the incidence of the disease and the increase in the pasture of such substances as protein and potassium, together with the fact that oral administration of Magnesium increases the serum magnesium level and can eliminate the disease entirely, lends substantial support to the latter belief.
However, it is difficult to believe that the aetiology is entirely nutritional, when one considers that the serum magnesium can drop so very sharply within a few days when an animal is placed on to lush pasture. This hardly can be due to a true dietary deficiency, as the same animal most likely will recover its normal serum magnesium even when left on the pasture which was responsible for the fall in serum magnesium.
Physiologically, Hypomagnesaemia can be divided into two types:-(a) the slowly developing type as seen in calves; (b) the rapidly developing, as seen in cattle on spring growth.
During growth on magnesium deficient diets, calves are able to transfer a large amount of magnesium from their bones to soft tissues and body fluids. Here the bones act as a very mobile reserve of magnesium in the absence of sufficient magnesium in the diet and provide a source of magnesium for soft tissue growth and the replacement of the element lost in urine and faeces.
In the young animal almost the entire skeletal system acts as a reservoir for magnesium; whereas in the adult animal a large part of the skeleton is metabolically inert, and with the advance of age even less of the skeleton becomes available to take part in magnesium metabolism. It seems logical to conclude that this impairment is largely responsible for the comparatively high incidence of hypomagnesaemia in older cows.
Analysis of the bones of adult animals dying from this disease shows no depletion in the magnesium content. In calves, however, 60% of the Magnesium component of the bones may be lost prior to death. This explains why the condition is so slowly developing in calves and rapidly developing in adult animals.
In cows, a moderate hypocalcaemia often accompanies the hypomagnesaemia.
CLINICALLY there are two syndromes-peracute and subacute.
Peracute: Death may occur without any premonitory symptoms other than signs of nervousness or excitability prior to death; or the beast may appear excitable or anxious, following which muscular twitching becomes evident. The cow may bellow and rush about wildly. It may appear blind, staggering into objects. It usually will go down and show tonic extension of legs, back and neck for short periods; alternating with paddling of limbs. The third eyelid is protruded. The animal often will lie quietly between bouts, but noise or touch may precipitate another convulsion. Death may take place in less than half an hour or may be prolonged.
Sub-acute: In this type the onset is slower and in the early stages it is noticed usually that the cow is nervous when entering the bail, throws the head up and steps high. The eyes usually close as the head is thrown back, as if anticipating a blow. There is stiffness of hindlegs and tail. The disease may progress from this; the animal finally going down and showing convulsions. On the other hand, the disease may clear up spontaneously.
When down, the eye is wide and staring; with the third eyelid projecting across the eye.
In the spring, cattle show an increase in weight and milk production due to better feed and so their demand for magnesium is greater although they receive less; since during the spring the Mg. content of pasture falls during flush growth.
Magnesium tends to accumulate in the seeds of plants, unlike Calcium, and it is low in the leaves. It is high in legumes, but low in animal products, such as meat meal and milk. Hay varies considerably; legume hays being higher in magnesium than grass hays.
It has been found that magnesium fertilisers such as dolomite increase the magnesium content of pastures, whilst potassic and nitrogenous fertilisers decrease it. High rainfall is associated with a low soil magnesium.
It has been found possible to increase the magnesium content of silage by spraying it with a solution of epsom salts as it is placed in the silo.
The writer has observed that the feeding of legume hay often prevents the onset of grass tetany in herds in which the incidence is high. However, there is no foundation for the suggestion that roughage is necessary for the effective utilisation of magnesium.
Symptoms of tetany seldom are observed under 8 weeks. In many cases the onset can be predicted by a rapid drop in serum calcium.
Nervousness is followed usually by increased hypersensitivity, flapping of ears, grinding of teeth, salivation, kicking of abdomen, loss of balance, apparent blindness, with blundering into objects. Convulsions usually do not appear for a few days after the onset of symptoms.
Less than 33% of dietary magnesium is available to meet body requirements. The low availability arises from a large faecal loss of Mg. in unabsorbed digestive juices and this occurs even when there is no Mg. in diet. Lactation greatly increases Mg. requirements. The Mg. content of food is no criterion of its ability to maintain the serum Mg. as in different foods the availability of the Mg. varies. Whenever the Mg. ion is lost from bone, it is replaced by a Ca. ion, but the magnesium can be lost from bone without any loss of calcium.
The uptake of Mg. depends on the maintenance of a high concentration of Mg. ions relative to Ca. and sodium ions in the extra-cellular fluid bathing the bone crystal surface; which is the true reservoir for Mg. If the serum Ca. is maintained at high levels for long periods, then the serum Mg. falls, despite adequate Mg. in the diet.
During lactation, complete breakdown of the bone, to provide Ca. and phosphorus necessary for milk production evidently at the same time releases Mg. and the latter is excreted. Mg. can be lost from the bones without concomitant loss of Ca. or P. even though there are large losses of Mg. There is no evidence that the endocrine glands have any specific effect on Magnesium metabolism.