In a particularly extensive subject, this article is confined to the elements calcium, magnesium and phosphorus; with special reference to disease syndromes as they occur in New South Wales and recommendations that can be made in the light of more recent published research.
MAGNESIUM METABOLISM.
The occurrence of hypomagnesaemia constantly occurs in southern New South Wales, especially throughout the South-west Slopes, in cattle, also in parts of the Hunter River Valley, but only recently was it diagnosed in the County of Cumberland at Minto.
In the latter case, April, 1954, an incidence of over ten per cent. occurred in an Ayrshire herd with varying degrees of nervous irritability which in some cases simulated "Stringhalt". The subjects were dull-eyed and had difficulty in walking over obstacles. The majority affected were heifers and the condition itself in both incidence and appearance was similar to that of nervous acetonaemia; though levels of blood and urinary ketones would not substantiate this diagnosis. The subjects were fed 5 lb. of proprietary concentrates containing 15 per cent. protein; together with grazing on oats and paspalum-love grass paddocks.
Clinical cases examined gave blood analyses as follows:—
| Ca. | Mg. | |
|---|---|---|
| Affected seven days | 12.00 | 0.5 |
| Affected seven days | 9.6 | 0.36 |
| Affected seven days | 10.8 | 0.4 |
| Affected three days | 11.4 | 1.4 mg. % |
Apart from the affected cattle, random sampling of the same herd after three deaths over 12 days in the following year (June, 1955) indicated that four cows ranged from 0.45 to 1.9 mg. and the remaining nine 2.0 to 2.6 mg. per cent. Therapy of magnesium injections was disappointing in that no marked responses were obtained; the condition tending to persist for several days afterwards.
Another outbreak of hypomagnesaemia occurred recently in the Kangaloon-Bowral area on highly improved winter rainfall rye grass-clover pastures. In this instance it occurred for the most part with hypocalcaemia in newly-calved cows. The pasture growth was lush following heavy and consistent rains coupled with long periods of warm humid weather in the autumn. It is estimated that over 30 head were lost over a period of three months. The clinical picture of the subjects varied somewhat from a typical milk fever attack followed by constant relapses; with indifferent results to calcium, magnesium and dextrose therapy. Trembling, stiffness of the limbs and bellowing were seen constantly in the recumbent subjects. Other subjects exhibited paddling, stamping and falling over with a chronic hyper-excitability. An odd history was that of a subject which took a "fit" in the paddock, with severe tetany and death within a few minutes. This condition is tentatively referred to as peracute hypomagnesaemia; a form rarely recorded in the State. Blood serum samples collected from cases indicated a range from 0.4 to 1.7 mg. per cent. magnesium.
Recent overseas research has indicated that ruminal ammonia has a bearing on the magnesium balance of cattle. The excretion of magnesium and serum magnesium levels were depressed when cows were changed from dry feed to cut spring grass despite the adequate magnesium level in the grass. Spring grass is associated with high ruminal ammonia. When ammonium acetate or ammonium carbonate were fed to cattle receiving hay and concentrates the serum magnesium and urinary magnesium were similarly reduced.
Treatment consists of subcutaneous injection of 200 ml. 25 per cent. solution of magnesium sulphate, combined with daily drenching with either 2 oz magnesium oxide or calcined magnesite.
The evidence is not at all satisfactory that fertiliser treatment will prevent hypomagnesaemia, although it is known that the magnesium values of pastures decline in spring to values of 0.16 per cent., rising in summer to 0.30 per cent. Dressings with magnesium limestone (15 per cent. MgO and 43 per cent. CaO) can increase the magnesium content of pasture over 75 per cent. Most probably the basic problem is that of absorption from the gut rather than a deficiency in the plant, and the ruminal ammonia theory is one of the most promising approaches to the basic cause of the condition.
MILK FEVER.
If any broad conclusions can be drawn from specimens received at Glenfield, it can be stated that its incidence and complexity varies between the northern part of the State, where the biochemical picture is the classical hypocalcaemia linked with hypermagnesaemia, and the southern half, where hypomagnesaemia can occur with hypocalcaemia as well as in the classical form. The coincidental occurrence of hypomagnesaemia with milk fever is, one considers, the factor making the syndrome so complex in the southern parts during particular seasons. In all forms there is a depression of the whole blood inorganic phosphorus values.
Various preventive measures have been developed in recent years and are on trial at this and other laboratories.
(1) The feeding of 30 million units of Vitamin D per day for not more than seven days before calving is recommended by American workers. The form fed is as irradiated dry yeast (64 million units per pound) or Viosterol, an oil-concentrated irradiated ergosterol (1 million units per gram). There is a danger in that prolonged feeding is definitely dangerous, bringing about deposits of calcium in the heart and blood vessels; hence the limitation to 5 to 7 days prior to calving. In the commercial forms available here, the cost of the preparation is approximately £3 per head per day, and with an expenditure up to £21 per cow it cannot be recommended unless a cheaper form is forthcoming.
(2) Dihydrotachysterol. This is available commercially as an oily preparation produced from irradiated ergosterol. The preparation has been used for over 20 years in the treatment of hypoparathyroidism in humans and is effective in elevating the serum calcium levels. The dose may be administered orally or by injection some 24 to 96 hours before calving, depending on the mode of administration. Trials at Glenfield to date have failed to show a significant rise in serum calcium in normal animals, but this may not be so in the parturient subject.
(3) Phosphorus Supplementation. This development by Boda and Cole consists in feeding a high phosphorus low calcium diet prior to calving with the object of inducing hyperfunction of the parathyroid glands and so mitigating the physiological fall in serum calcium immediately post calving; at least to prevent the exaggerated fall seen in milk fever.
The method has been under trial at Yanco Experiment Farm, where there was a high percentage of milk fever. A supplement of 21b./day of concentrates plus 20 per cent monosodium phosphate was fed for the fortnight prior to calving. The results indicate that a higher proportion of milk fever occurred in the control, i.e., untreated group), but aged cows in both groups were affected. One might postulate that the parathyroid glands were partially or completely incapable of response; in fact, a virtual senility of the gland. This aspect is being followed up.
APHOSPHOROSIS IN CATTLE
Diagnosis in this condition depends on clinical symptoms and determinations of whole blood inorganic phosphorus. Stunting, narrow chests, shoulder lameness, low production and high incidence in cows with calves af foot are frequent. The condition also shows up in late gestation.
Determinations of whole blood inorganic phosphorus from field collections, in the main, are far from satisfactory. 5 ml. of whole blood is added to 20 ml. of 2.5 per cent. trichloracetic acid in normal saline and the mixture quickly despatched to the laboratory. For some reason the contents are received in a whipped cream consistency which is impossible to filter. Again, the filtrate itself is opalescent; making the solution unsuitable on a photometer after colour has been developed. Probable causes are that under summer time conditions the acid solution is too warm, and further that the bottles are not carefully shaken after the blood has been added. Delay in transit under ordinary temperatures can result in the organic phosphoric esters breaking down and producing elevated (and fictitious) values.
It should be realised that whole blood inorganic phosphorus values are very variable and can be affected by handling the animals, watering, feeding and other external factors. Values below 3 mg. per cent. are considered to indicate aphosphataemia. It is preferable to collect at least 12 samples from affected and apparently unaffected subjects in the herd at the same time; making a judicious selection of the late pregnancy, early lactation and dry cows. For example, one collection from a herd with 4 clinically affected animals out of five sampled, returned values such as 1.9, 2.2, 2.8. 3.1, 3.2 mg. per cent. Here the issue is clear-cut. The second herd sampled where there was no apparent lameness at the time of collection indicated a relative aphosphorosis:
5-6 year old, calved 3-4 months-2.9, 2.5, 2.5, 2.7.
6 year old, calved 4 months, on better pastures 3 months-5.2.
3-4 year old on improved pasture-5.2, 5.2.
Aphosphorosis is known to occur in parts of the South Coast and Northern Tablelands, and often is associated with hypocuprosis on the North Coast. Often the pastures in such regions are poor; with species (eg, Native Tussock (Poa caespitosa)) containing 0.07-0.09 per cent. phosphorus on a dry matter basis as opposed to values of 0.3-0.5 per cent phosphorus in good, green leafy pasture. It is considered that herbage containing less than 0.1 per cent. phosphorus will induce aphosphorosis.
However, as Snook in Western Australia has indicated, there is no justification for the assumption that phosphatic supplements are unnecessary where pastures have been heavily top-dressed with superphosphate or lime, as high producers cannot eat sufficient to satisfy their phosphorus requirements. It well may be that apart from a simple phosphorus deficiency in the poorer grasslands mentioned previously, a phosphorous deficiency exists in some of our high producing herds: leastways the possibility should not be overlooked.
The use of superphosphate in drinking water is now generally accepted; at the rate of 3 lbs. per 100 gallons. With a consumption of 10 gallons per day this is equivalent to an intake of 3½ oz. bonemeal per day.