CHAPTER 33

The character of the individual animal and grass tetany

1.	for an identical ration, the tendency of the animal towards hypomagnesaemia is more or less marked;1
2.	for a certain degree of hypomagnesaemia, that is, for an identical, low content of magnesium in the blood serum, certain animals in a herd will be attacked by tetany while others remain normal.2

Consequently, it appears as if another explanation will have to be sought. This may perhaps be furnished by the thyroid. In effect, lactation corresponds with increased thyroid activity, and it has been seen that the secretion of large quantities of thyroid hormone may, in certain circumstances, assist in lowering the blood serum magnesium content.

Are very high yielders more susceptible to tetany?

Although lactating animals are infinitely more susceptible to grass tetany, there is no certain proof that very high yielding cows are more susceptible than average yielders. Neither has any correlation been observed between the daily milk yield of a cow and the magnesium content of its blood serum. However, let us assume, as some authors do,⁸ that very high yielders are particularly susceptible to hypomagnesaemia and tetany. A high milk yielding capacity is known to correspond, above all, with certain hereditary characteristics of the endocrine system, particularly the thyroid gland. These hereditary dispositions in favour of high milk production may also, therefore, sensitize" the animal to tetany.
But another factor, non-hereditary this time, can help to make very high yielders susceptible to grass tetany: this is the particular feeding the cows receive. To maintain such a high milk production, the cows must be fed a diet very rich in protein, which, in the long run, may adversely affect the liver and render the animals susceptible to tetany. Moreover, as PETERS emphasizes, high-yielding cows have particularly high requirements of vitamins and mineral elements; if these requirements are not satisfied the result may be internal disorders predisposing to tetany. In other words, past feeding can "sensitize" high yielders to grass tetany. The role of the animal's "dietary record", that is, the role of acquired characteristics, in grass tetany will now be studied in greater detail.

Anatomical and biochemical lesions give expression to the "dietary record" of the animal

As was described previously the animal that has died of tetany presents various anatomical and biochemical lesions, the principal and most common among which are:

a.	Granulo-fatty degeneration of the liver;
b.	calcification of the kidneys (more exactly, of the renal tubules);
c.	hypertrophy of the adrenal glands.

These lesions,⁹ as has just been said, may be favoured by certain hereditary predispositions, but they express, above all, the "dietary record" of the animal, which starts not at the latter's birth but at its conception.¹⁰
An old proverb runs: "Man is what he eats." The animal, too, is "what it eats", although an even better expression of the influence of the "dietary record" on the present condition of the animal would be: "The animal is what it has eaten" (and also what its mother ate while carrying it).
If, in the course of its dietary history, a cow has often consumed a ration too rich in nitrogenous substances, especially rapidly decomposable nitrogenous substances that lead to the production of excessive quantities of ammonia in the rumen, it will be the victim of degeneration of the liver.¹¹ This is what happens with a cow that each year, for a large part of the season, grazes very young grass that has received very large dressings of nitrogenous fertilizer.¹² In the same way, a cow that has frequently been kept on a diet giving rise (directly or indirectly) to magnesium deficiency will suffer from calcification of the kidneys which will go far towards preventing the excretion in the urine of the excess of potassium supplied to the organism by tetanigenic herbage. Finally, regular feeding with a ration containing too much potassium and too little sodium will cause deterioration of the adrenal cortex, with the result that the hormonal secretions of the cortex will no longer be able to regulate adequately the mineral metabolism of potassium and sodium: not to mention a possible direct influence on the metabolism of magnesium.
In summary, a cow that, because of its past feeding history, has had its various metabolic mechanisms upset to a greater or lesser extent, will be more sensitive to tetanigenic factors than another cow whose mechanisms are in good order.
It was likewise seen that female rats fed in their youth on a ration moderately low in magnesium were not affected by convulsions. But when they had dropped their young and were lactating these females suffered from convulsions if they received this same magnesium-deficient diet, although the latter triggered no convulsions in females that had received normal magnesium feeding in their youth.

Short-term experiments do not take the cumulative effects of dietary history into consideration

Many experiments have been concerned with cows subject for the first time to the "test" of very young grass saturated with nitrogenous and potassium fertilizers. The "real" cow, the farm cow, has been subject to this test every year since its birth, or, more correctly, since its conception, for its mother, while carrying it, was already consuming herbage of this nature.¹³ It is quite possible that the imbalances created in herbage by the methods of management studied in the course of an experiment are not sufficient to trigger off tetany in a "normal" cow, but can easily do this in the case of a cow subject to these imbalances since conception. As CHARTON writes: "The same nutritional imbalance has variable consequences depending on the neuroendocrine (or neuro-hormonal) balance of the patients which renders them more or less vulnerable to toxic attacks." And this neuro-endocrine balance depends not only on the hereditary character of the animal, but on its "dietary record."
It should be mentioned that a very recent "dietary record" can influence tetany when the stock are put out to grass: namely, the feeding in the stall during the period preceding the turning out to grass. All that has already been said about "dietary record" during the animal's lifetime holds good for this period of stall feeding in winter. All the factors that cause degeneration of the liver, damage the kidneys, upset the endocrine system, exhaust the low reserves of mobilizable magnesium in the organism, etc., will "sensitize" the animal to tetany when it is put out to graze following this period.
According to some workers, the lack of vitamins and mineral elements in winter feeding can pre-dispose ¹⁴ to tetany at the beginning of the grazing season. BECKER and PETERS, for example, of the University of Kiel, report having reduced the frequency of grass tetany in spring by administering supplements of vitamins (A and D in particular) and mineral elements to the animals during the stall-feeding period. These workers consider it to be particularly essential that large supplements of salt (sodium chloride) should be fed during the last few weeks in the stall and continued throughout the initial grazing period. The importance of this as a means of avoiding deterioration of the adrenal cortex has been described and will be dealt with again below.

Old cows are particularly susceptible to grass tetany

Another individual character that may predispose to tetany is age. Old cows are most frequently affected as is shown by Table 31.

Table 31: Distribution of grass tetany in cows according to their age

Neary half the tetany victims are 6 years old or more. This is confirmed from the U.S.A. by MERSH0N, for example, who found that of 16 cows suffering from grass tetany,¹⁵ only three were less than 8 years old.
The same holds good for ewes. HEMINGWAY, for example, found that under the same conditions, the mean content of magnesium in the blood serum was 2-26 mg./100 c.c. in young ewes against 1-62 mg./100 c.c. in old ewes; this drop in the blood magnesium level obviously renders old ewes more susceptible to tetany.
It seems that several factors enter into play in increasing the animal's susceptibility to tetany as it grows older:

	It has been seen that, for the same ration, the magnesium resorption capacity is lower in the old animal.
	The mechanisms regulating the magnesium content of the blood serum become less efficient.
	The magnesium reserves of the bones, and probably the small reserves of the muscles, become more and more difficult, and probably more and more slow to mobilize.

1. Magnesium excretion in the urine has been seen to reflect, quickly and exactly, the magnesium metabolism of the animal. Fig. 11 shows that this excretion varies in two sheep receiving identical rations. This difference in the efficiency of utilizing the magnesium in the ration admirably expresses the individual nature of magnesium metabolism in the animal. *

2. See, for example, Fig. 16. It will be seen that, for very low contents of magnesium in the blood serum, some cows are attacked by tetany and some are not. In other words, the "adaptation capacity" of some animals to a low content of magnesium in the blood serum is less good than that of others. *

3. See, for example, the article "Breeding Stock without Staggers" in the Farmer and Stockbreeder of 10th October 1961. *

4. SELLERS found, on the contrary, that Friesian cows were more susceptible to tetany than Shorthorns. *

5. Lactation has also been seen to sensitize rats to tetany caused by magnesium deficiency in the ration. *

6. Although below a certain absolute magnesium content in herbage (Fig. 16) the danger of hypomagnesaemia and tetany is very much greater. *

7. To be exact, the calculation must be made in milliequivalents. It will then be seen that when a cow loses 11 magnesium ions in 2-2 pints [1 litre] milk, it loses 354 ions of that element's antagonist, potassium. *

8. BECKER has studied farms on which, every year, 20-50% of the cows are affected by grass tetany. He found that the tetany almost always attacked the cows with the highest milk production, especially those producing 825-1525 gal. [3000-6000 litres] milk per year. *

9. Added to these, of course, are all the disorders and impairments of the digestive system that may result in diminished magnesium resorption. *

10. See Soil, Grass and Cancer (pp. 72-6). The foetus is much more sensitive to the nutrition of the mother than the adult organism to its own nutrition. *

11. It is readily understandable that, of two cows put out to grass in the spring, the one with the most impaired liver as a result of its "dietary record" will offer much less resistance to the "ammonium shock" brought on by very young grass. *

12. Feeding with too much cake can also cause wear and tear of this nature on the liver. *

13. Note that these slow and cumulative effects of the management the farmer applies make themselves felt not only on the animal but on the soil. It has been seen, for example, that, because of excessive and repeated dressings of potassium fertilizer or liquid manure, potash may accumulate in the soil in a "fixed" form, capable of subsequently becoming partly available to the plant. To list these effects once more: slow blockage of elements in an unavailable form (copper sulphide, because of repeated applications of liquid manure), exhaustion of certain elements due to leaching by rainfall, the removal being favoured by fertilizer dressings (loss of calcium following the application of sulphate of ammonia or potassium fertilizer, etc.). These slow, cumulative effects in the soil manifest themselves finally in alterations in the composition of the herbage. *

14. By creating what they call "a latent disturbance in the organism" which predisposes to tetany. *

15. This was winter tetany in cows of a beef breed suckling their calves. *