CHAPTER 25

Rapidly growing, very young grass causes excessive production of ammonia in the rumen

An opinion widely held to date has been that, in the case of ruminants, there is no point in paying too much attention to the composition of the nitrogenous fraction, particularly the amino acids, of the ration. What happens is that the micro-organisms (that is, the microflora of the rumen) utilize these various nitrogenous substances to synthesize microbial proteins that have a high biological value for the ruminant. This opinion is perfectly correct and in agreement with a phenomenon actually taking place in the rumen. Another contrary phenomenon, however, has been overlooked:¹ the microorganisms of the rumen are equally capable of breaking down the nitrogenous substances and converting them to ammonia (and various nitrogenous compounds). This ammonia can be absorbed directly into the rumen and passes into the portal blood, whence it is transported to the liver to be converted to urea.² These breakdown phenomena are particularly important and dominate those of synthesis when the ration has the following three characteristics:

1.	Excess of nitrogenous substances over carbohydrates.
2.	Insufficiency of crude fibre.
3.	Presence of nitrogenous substances which, because of their constitution, are rapidly broken down.

In such cases the production of ammonia in the rumen is considerable.³

Excess ammonia in the rumen favours hypomagnesaemia

What will be the consequences of this excess of ammonia in the rumen for the metabolism of magnesium and the animal organism?
Excessive ammonia in the rumen reduces the latter's mobility, with the result that the animal's appetite is diminished. It is not impossible, however, that the inadequate quantities of dry matter "harvested" by the cow when it is put out to graze help to reduce the quantities of magnesium it ingests. It could be, therefore, that the excessive amounts of ammonia produced by young grass in the rumen accentuate this under-feeding ⁸ by reducing the cow's appetite.
Excess ammonia in the rumen, moreover, has been seen to diminish considerably the resorption of magnesium in the digestive tract, which will promote a reduction in the magnesium content of the blood serum. As has just been said, the more protein the herbage contains, the greater the amount of ammonia produced in the rumen.

Application of nitrogenous fertilizers to young grass favours hypomagnesaemia

In certain cases, as when increasing quantities of nitrogenous fertilizer are applied, the following converse variations can be followed:

	crude protein content of the herbage;
	magnesium content of the blood serum.

This is obvious in Table 20. Following dressings of sulphate of ammonia,⁹ the crude protein content of the herbage increases from 14-9 to 23-8% and, at the same time, the content of ammonia in the peripheral blood is doubled ¹⁰ while the magnesium content of the blood serum is reduced by almost half (1-00 instead of 1-90 mg./100 c.c.).

Excessive production of ammonia in the rumen adversely affects the liver

There is another consequence of excessive ammonia production in the rumen: part of the excess thus produced is absorbed in the rumen and transported by the portal vein to the liver, which must very rapidly convert to urea and similar substances) this ammonia that is so toxic to the organism. If these quantities of ammonia for conversion are excessive there is the risk that the liver in the long run will become exhausted ¹¹ and deteriorate. It is then affected by granulo-fatty degeneration,¹² which is almost always to be found in the livers of cows that have died from tetany. Such degeneration, having become more or less necrotic, appears to be no longer capable of being reabsorbed ¹³ despite the unbelievable capacity of the liver for regeneration.

Table 20: Influence on hypomagnesaemia of increasing dressings of nitrogenous fertilizers

Liver and individual susceptibility of the animal to tetany

It is obvious that cows whose livers have gradually deteriorated in the course of previous sojourns on very young grass or under the influence of a winter ration excessively rich in nitrogen will be particularly predisposed to tetany because they are able only slowly, and even with difficulty, to convert the urea ¹⁴ the excessive quantities of ammonia passing into the blood in the wake of an exclusive diet of very young grass.
Moreover, depending on the character of the cows and particularly, no doubt, on the capacities of their liver, different and more or less rapid increases in the ammonia content of the peripheral blood are observed when these animals are suddenly put out to graze young spring grass after their diet in the stall. It has been established, for example, that from the very first day in some cows the ammonium content of the peripheral blood was multiplied ¹⁵ by 8, whereas in other cows it takes several days on a pasture before an increase of any significance at all can be determined in the ammonium content of the peripheral blood. It is probable that in the first case the liver of the cows had only a limited capacity for converting ammonia to area, whereas in the second case the organ was in good condition and was able to convert large quantities of ammonia to area, at least over a certain period of time.

Histamine and grass tetany

Another consequence of this excess of ammonia in the rumen is interference with the fermentations taking place. This may result in the production of toxic substances,¹⁶ contributing towards the triggering of grass tetany. Certain toxic amines may form, for example, especially histamine ¹⁷ the content of which in the blood of cows suffering from tetany appears to be higher than in that of normal cows. It has been seen that this histamine, directly or indirectly (particularly by sensitizing the muscles to the potassium ions), can help to bring on grass tetany. It has also been said that anti-histamines are sometimes used successfully to treat this tetany.

Does rapidly growing young grass contain a particular factor that will promote the occurrence of tetany?

Many investigators have wondered whether young grass in rapid growth might not contain a particular factor favouring hypomagnesaemia and tetany.
It has likewise been thought possible that a graminaceous species, when it first grows after sowing, may contain this factor, since, as will be seen below, green corn seems often to have marked tetanigenic characteristics. It might even be wondered if this particular tetanigenic factor does not persist throughout the first years of the life of the Gramineae following sowing, tetany appearing to be more frequent on temporary than on permanent pastures.
BARTLETT is of the opinion that very young grass contains a tetany producing factor and that the application of magnesium fertilizer to the soil reduced the herbage's content of this factor. WALSHE, for his part, has advanced the hypothesis that the simultaneous application of nitrogenous and potassium fertilizers leads to the development in grass of a factor of this nature that conditions the appearance of hypomagnesaemia. The Irish worker is of the opinion that it is still impossible to state whether this factor present in young grass is mineral or organic in nature. He considers that all that can be said is that the application of magnesium fertilizers, simultaneously with nitrogenous and potassium fertilizers, neutralizes or suppresses the tetanigenic factor present in rapidly growing young grass.
Another opinion expressed has been that it is possible that "tetanigenic" herbage contains too many nitrates; but the results are too variable for a verdict to be given.
Some American workers ¹⁸ have thought that very young grass in the rapid growth phase might contain a chelating agent ¹⁹ which could affect the metabolism of magnesium. Very recent experiments carried out by PULSS at the University of Kiel would appear to confirm the existence of a particular tetanigenic factor of this nature in such herbage. The German worker extracted juice by pressure from a tetany- producing herbage and added it to the ration of female rats. He found the result to be a marked reduction of 20% in the basal metabolism, whereas the juice of grass not producing tetany reduced the basal metabolism by only 6%. Following other experiments with yeasts and thin liver slices, PULLS put forward the hypothesis that this particular factor in tetany-producing herbage was an inhibitor ²⁰ of certain enzymes. He did not think that the factor exercised a direct influence on the nervous or hormonal system.

Grass tetany prevented by an application of cobalt to the soft

The hypothesis of the presence in young grass of a tetanigenic factor, resulting from a lack of magnesium in the soil, assumes a greater degree of probability when one remembers that there is a special grass tetany which is prevented by an application of cobalt to the soil. This is Phalaris tuberosa tetany,²¹ a plant very widely grown in Australia.
In certain regions it was noticed that sheep grazing Phalaris ²² suffered from convulsions ²³ that almost always led to death after a period. No therapeutic method proved effective,²⁴ and the only means of controlling this disease was to practice "protective medicine".
This protective medicine turned out to be very simple: buccal administration of cobalt ²⁵ is enough, or, better, the application of a fertilizer containing cobalt ²⁶ to Phalaris pastures. This application of cobalt to the soil is sufficient to more than double the cobalt content of the plant,²⁷ and the tetany disappears completely.
This is a typical case, therefore, of a deficiency of some element ²⁸ in the soil or herbage being sufficient to lead in a rapidly growing plant to the presence of a neuro-toxic factor.²⁹ Data may perhaps become available on this point in future, with a bearing on hypomagnesaemic grass tetany.³⁰ This information however, is of an even more general nature: PULSS' theory and Phalaris tetany prove that mineral imbalances in the soil (and plant) can upset the metabolic mechanisms of the plant in such a way that the latter synthesizes ³¹ substances ³² which themselves upset the metabolism of the animal consuming such a plant.

1. See Grass Productivity, pp. 116-22. *

2. In other words, all this fraction of the nitrogen is lost from the point of view of the animal's nutrition. As MEYER so aptly reminds us: "The actual value of a protein to the ruminant depends on the rate of that protein's decomposition." *

3. Ammonia production appears to be assisted, moreover, by any sudden change in diet compelling the animal to feed exclusively on young grass. The rumen microflora does not have time to adapt itself to this new food so different in character from its previous diet (stall-feeding, hard hill grass, etc.). The result would be accelerated decomposition of the protein to ammonia. *

4. The nitrogen of which will be badly utilized and "valorized" by the animal. *

5. It was seen elsewhere (Fig. 7) that this rapid breakdown of the crude protein in very young grass also leads to excessive production of hydrogen sulphide in the rumen, which may also perhaps favour tetany. *

6. The physical structure of the grass also appears to play a part in tetany. LARVOR reports having put three groups of cows out to graze:
   (1) A control group;
   (2) a group receiving 41 lb. [2 kg.]meadow hay per cow per day;
   (3) a group receiving this same hay supplement finely ground.
   The normal hay was found to have prevented in part the drop in blood serum magnesium recorded in Group 1, whereas the ground hay did not exercise this protective effect. It should be borne in mind that some authors have shown that, in cows, the digestibility of hay is diminished by grinding owing to the acceleration of its passage through the digestive tract. *

7. Experimentally HEAD got the same result by introducing starch through a fistula into the rumen of a cow consuming very young grass. The ammonia content of the rumen became twice as low. *

8. hypomagnesaemia caused by under-nourishment. *

9. Sulphate of ammonia will be seen to appear to favour hypomagnesaemia (see Table 18). *

10. In the present state of our knowledge it is impossible to state to what extent this increase in the ammonia content of the peripheral blood might possibly contribute towards upsetting the endocrine mechanisms that control the magnesium content of the blood serum.
    Note only that it has been possible to produce nervous disorders by increasing sufficiently the ammonia content of the blood: for example, by the introduction of an aqueous solution of urea into the rumen through a stomach tube. But this effect was obtained only when the nitrogen (N) content of the ammonia was 2 mg. (or 2000 microgrammes) in 100 c.c. peripheral blood. With the cows concerned in Table 20 this content reached only 40.8 microgrammes, and it seems to be exceptional that, under actual grazing conditions, contents (127) of more than 150 microgrammes ammonium nitrogen (N) have been observed in 100 c.c. peripheral serum. This is far from the toxic 2000 microgrammes.
    However, as CORNETTE reminds us, the content of ammonia in the blood serum provides no indication of the percentage of ammonia that can be fixed in the nerve centres.
    Moreover, this does not make it impossible for this increase, even though moderate, in the ammonia content of the peripheral blood to exercise a direct or indirect action on the neuro-muscular system. It is known, in particular, that alkalosis of the blood can help to increase neuro-muscular excitability. *

11. In the same way as the liver of an alcoholic is affected by cirrhosis. *

12. The toxic amines produced in the liver when the fermentations are upset by the excess of ammonia may contribute to the hypertrophy and deterioration of the organ. *

13. CORNETTE gives the following description, taken from LABIE, of the sequence of this degeneration of the liver: "First of all there is a granular degeneration, detectable only by microscopic examination; then fatty degeneration, characterized on post-mortem by the presence of yellowish areas on the normal brown background of the organ; the fats are no longer capable of conversion and accumulate in the hepatic cell. At this stage, however, the lesions are still reversible and it is sufficient to supply the organ with the lipotropic factors it lacks. At a more advanced stage the fatty degeration gives way to necrosis: the liver, yellowish in colour, becomes flaccid and friable. Haemorrhagic necrosis is sometimes present; a sheet of blood takes the place of the hepatic tissue. These necrotic lesions are irreversible." *

14. It is apparently being assumed more and more that the neurological phenomena accompanying these serious liver diseases in humans (tremors, lack of direction, etc.) are due to an increase in the ammonia content of the blood. Note also that in humans cirrhosis of the liver causes a drop in the magnesium content of the blood serum. *

15. It rose from 12 microgrammes ammonium nitrogen (N) in 100 c.c. peripheral blood to 95 microgrammes. *

16. FERRANDO considers that the excess of potassium manuring may perhaps facilitate the formation of these toxic substances. *

17. DAIN has noted the presence of histamine and tyramine in the ingesta of the rumen of ewes suffering from indigestion following over-feeding. He found up to 70 mg. histamine Per litre ingesta. *

18. BARRENTINE. *

19. This would be a chelating agent that would form organic compounds with magnesium and other mineral elements. *

20. He is of the opinion that in normal grass, on the other hand, there is a factor that favours these enzymes. *

21. Or: long reed Canary grass. *

22. The disease has also been observed on Ronpha in South Africa. *

23. It was not hypomagnesaemic tetany that was involved. Note that the post-mortem anatomical lesions are different from those observed in the case of hypomagnesaemic grass tetany. The principal lesion in Phalaris tetany is a degeneration of the spinal marrow, apparently due to a neuro-toxic substance destroying the myelin. (See also Soil, Grass and Cancer, pp. 73-6.) *

24. Magnesium or calcium injections in particular had no effect. *

25. Each week per sheep 28 mg. cobalt in the form of cobalt chloride (CoCl₂.6H₂O). Weekly administration of this kind obviously presents tremendous difficulties in a herd of sheep. *

26. The recommendation is to apply 120 gm./acre [300 gm./ha.] sulphate of cobalt (CoSO₄). The effect of a cobalt application lasts one year only.
    Note that this dressing of cobalt represents a content of 1/10 p.p.m. in the upper soil layer. This difference of 1/10 p.p.m. in the cobalt content of the soil is sufficient for the stock to be either perfectly healthy or affected by an incurable, fatal disease. This explains how the least upset in the balances of the soil can affect animal health. *

27. 2-21 lb. [1 kg.] dry matter of normal grass is estimated to contain 100-300 microgrammes cobalt, whereas deficient herbage (causing "pining" or pernicious anaemia) contains only 10-50 microgrammes.
    In the case of Phalaris, tetany has generally been observed when the plant contains 8-36 microgrammes in 1 lb. dry matter [20-90 microgrammes in 1 kg. dry matter]. Application of a fertilizer with cobalt raises this content to 52-92 microgrammes/lb, [130-230 kg./].
    In South Africa, with Ronpha, tetany was observed when this species contained 70-200 microgrammes cobalt per kg. dry matter. The application of a cobalt fertilizer raises this content to 150-250 microgrammes and the tetany disappears.
    In both cases, however, the contents are erratic. *

28. Available element, naturally. *

29. It is possibly hydrocyanic acid that is involved. Vitamin B12 (which contains cobalt) seems to play an important part in the detoxification of hydrocyanic acid and its conversion to thiocyanate. *

30. It would be interesting in any case to study the cobalt content of tetanigenic herbage. The author is unaware of any such determinations having been made. *

31. It was seen in Soil, Grass and Cancer (p. 64) that a deficiency of superphosphate in the soil causes subterranean clover to synthesize an oestrogen (isoflavone) that is extremely dangerous to the health of the sheep. *

32. The author calls these substances "anti-factors". These may possibly help to explain the geographical distribution of certain diseases affecting Man, among them goitre and cancer. (See Soil, Grass and Cancer (pp. 225 and 257). *