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This article was published in 1962
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INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.
Grass Tetany in Cattle
R. P. HERD, B.V.Sc., District Veterinary Officer, Benalla, Victoria
INTRODUCTION
It is important, at the outset, to differentiate between the two conditions, Grass Tetany and Hypomagnesaemia.
Hypomagnesaemia is a condition which frequently occurs in clinically normal animals in which the serum Mg. is less than the normal range of 1.8-4.0 mg. per cent.
Grass Tetany, in contrast, is the clinical state of excitement and tetanic spasm which is precipitated in a hypomagnesaemic animal by a hypothetical stress factor.
It must be appreciated that a marked hypomagnesaemia may exist in a herd for considerable periods, with individual animals showing serum Mg, as low as 0.3 mg. per cent. without developing any clinical signs of Grass Tetany.
Although hypomagnesaemia alone is not enough to cause Grass Tetany, there is now a great deal of experimental and field evidence to show that if the hypomagnesaemia is prevented by feeding extra Mg. Grass Tetany will not occur.
HISTORY
The earliest reports of Grass Tetany in England and Europe date from the 1920's, but it is probable that some of the unexplained sudden deaths of cattle previously encountered and labelled as Eclampsia, Brain Fever and Bovine Hysteria were, in fact, Grass Tetany.
The association of a hypomagnesaemic condition with cattle in tetanic spasms was first recognised by Sjollema in Holland in 1928. This occurred in dairy cattle in the first few weeks after being turned out from Winter stalls to lush Spring pasture.
Soon afterwards it was observed also by Dryerre in Edinburgh and Blakemore and Stewart at Cambridge in both beef and dairy cattle. Blakemore and Stewart also demonstrated the potential usefulness of dietary Mg. compounds as a prophylactic measure against G.T., a potentiality which more than a quarter of a century later is still not fully utilised.
Grass Tetany occurs in most European countries, North America, Australia and New Zealand. In all countries it is associated with improved pastures, and there is evidence of an increase in its incidence.
Early published records of the condition in Australia are rare, but some information is to be gained from N.S.W. and Victorian Department of Agriculture records.
Rose established definitely the presence of hypomagnesaemic tetany in the Cootamundra district of N.S.W. in 1934, although he had suspected the condition previous to this. He initiated treatment with 15 gm. MgCl2 and 40 gm. CaCl2 in about 6 oz. Water i/v, found this fairly satisfactory, and later prevented the condition in both cattle and sheep by feeding magnesium phosphate.
From 1938-39, Gorrie surveyed the incidence of Grass Tetany in the Western District of Victoria and ruled out the possibility of Enterotoxaemia as a cause of deaths by obtaining completely negative results.
Lloyd and Snowdon did a considerable amount of investigational work in North-East Victoria during 1953-57 and demonstrated a seasonal hypomagnesaemia and hypocalcaemia in beef cattle. Limited pasture analyses failed to show any significant relationship between pasture Mg and the occurrence of the disease. Lloyd also investigated the possibility of Enterotoxaemia deaths and, like Gorrie, got completely negative results.
INCIDENCE
In Victoria, G.T. occurs in all the major beef breeding areas, but the incidence is greatest in the North-East. Last year was a particularly bad year in the Benalla, Mansfield and Wangaratta areas, where deaths occurred over a more prolonged period than usual.
It was estimated that 1,000 breeding cows died from April to September, and losses of up to 25 cows occurred on individual properties. This represented a loss of about £50,000, not to mention the orphan calves which either died or received a setback in their development.
In the North-East of Victoria it is primarily a disease of well conditioned, lactating beef cattle. Losses also occur in dairy cattle and sheep, but the incidence is not nearly as high as in beef cattle.
Third-calf cows and older are affected most commonly, but it is not uncommon for deaths to occur in first and second-calf heifers as well. There is evidence that the better producing cows are the most susceptible, as there is usually a good, fat vealer running with the affected cow. Cases have occurred in dry cows and bullocks, but these are rare.
Beef cattle are calved in the Autumn and Winter in the North East and the majority of losses occur in the Winter months, June, July, August, when the calves at foot are one to three months old, but there is no close association with the lapse of time after calving as in Milk Fever and cases may occur any time from one day to eight months post-calving in Autumn,Winter or Spring.
Most losses occur on young, actively growing, improved pastures or green oat crops. Grass dominant pastures are more commonly associated with G.T. than clover dominant pastures, but heavy losses do at times occur on the latter. Last year a particularly mild Winter was experienced in the North-East with very few severe frosts or water logging and consequently, there was continual growth of pastures throughout the winter. This may have been one of the reasons why G.T. losses occurred over such an extended period.
In the colder hill country to the East there is usually a more prolonged Winter, with little pasture growth, followed by a later Spring. G.T. losses often occur later in these areas and coincide with the renewed growth of young grass about September.
SEASONAL HYPOMAGNESAEMIA
Regular blood samples taken from Hereford and Aberdeen Angus cattle on two affected properties in the North-East last year showed that a seasonal Hypomagnesaemia was present on both properties.
On the property of Mr. G. T. Lack, near Wangaratta, samples were taken fortnightly from the same 12 cows from August, 1960, to September, 1961, during the danger period and at monthly intervals during the rest of the year.
Blood samples were also taken from 12 Hereford cows on three occasions in July and August, 1961, on the property of Mr. H. W Lester at Mansfield. This work was specifically aimed at testing the use of a cheap magnesium oxide supplement in the prevention of G.T., but the results also gave further evidence of a seasonal hypomagnesaemia.
Further, a hypomagnesaemia was present for quite an extended period and a hypocalcaemia was evident also to a less extent on both properties. Overseas workers have frequently shown an associated hypocalcaemia in 70-80 per cent. of cases of Hypomagnesaemia, and it is possible that the role of calcium has not been appreciated fully.
Two of the experimental cows at Wangaratta died during August, and these two had consistently shown very low serum Mg levels. Cow No. 8, an Aberdeen Angus, developed clinical G.T. on 19th August, responded to Ca and Mg therapy, but was found dead 10 days later. At her routine blood sampling 10 days before the clinical attack, her serum Mg was 0.5 mg. per cent. with normal Ca. During the attack, her serum Mg was 0.6 mg. per cent. and Ca was 7.0 mg. per cent. Four days after the attack, the Mg level was again 0.6 mg. per cent. and Ca was back to normal Cow No. 11, also an Aberdeen Angus. was found dead on 5th August after showing a serum Mg level of 0.9 mg. per cent. and normal Ca 10 days earlier. It was not possible to do a P.M. examination in either case.
AETIOLOGICAL FACTORS
Ever since G.T. was found to be associated with a hypomagnesaemia, there has been endless argument as to whether G.T.is a deficiency, or metabolic, disease. The disease occurs under a wide variety of circumstances and it appears that many factors, dietary, metabolic and stress are all important in the development of the condition. The major contributing factor may vary from district to district, farm to farm, or cow to cow.
Dutch workers claim that there is a significant positive correlation between pasture Mg and serum Mg and that G.T. losses will not occur when the pasture Mg level is above 0.2 per cent. DM. They also found a significant negative correlation between both K and crude protein content of herbage and serum Mg. Nevertheless, G.T. often has been known to occur on pastures higher in Mg than safe pastures, and, although nitrogenous and potash-rich fertilisers are notoriously dangerous, G.T. is not always associated with their application. Under some conditions, botanical composition of pastures may play a part as there is a big species variation in Mg, the clovers and broad-leaved species being much higher than the grasses. The fact that heavy losses sometimes have occurred on clover dominant pastures only emphasises the fact that pasture Mg content is not the whole story.
Many research workers appear to have seized upon one individual factor associated with G.T. as the complete answer to the problem, whereas there is now evidence that a whole range of both plant and animal factors may be involved.
Although many pasture and topdressing trials have been carried out, little is known of the availability of Mg in that pasture and this could be influenced by both plant and animal factors. Work by Field (1960), and others, has indicated that availability is extremely low and that about 80% of the dietary Mg is excreted in the faeces. Not only is availability low but it varies considerably from cow to cow on the same diet. This is of the greatest importance as it implies large individual differences between cows in their efficiency to utilise dietary Mg and may help to explain why some cows are more susceptible to G.T. than others.
There is further evidence that storage of readily available Mg in the cow's body is very limited. Although there is a considerable storage in bone, this becomes increasingly static and immobile with advancing age, so that a cow may die of G.T. and yet still have a big supply of Mg in her bone. This may also explain why most G.T, losses occur in older cows.
Thompson (1960) stresses that there is a very precarious balance between the amount of Mg available from the metabolic pool and the cow's daily requirements for maintenance and lactating cow then becomes very dependent on her daily intake. If we accept this view, it is then easy to realise that it is only necessary for a small upset in Mg intake or absorption to occur and the balance will be tipped to the negative side with a hypomagnesaemia resulting.
Many factors could influence the amount of Mg reaching the metabolic pool and hence the Mg balance. These include soil Mg. botanical composition of pastures, stage of growth, fertilizer treatment, daily intake, gut absorption, renal excretion, bone Mg mobility or immobility, maintenance, and milk production requirements. At present little is known about the mechanisms of absorption or excretion or the influence of the endocrine glands on Mg homeostasis.
An important point appears to be the large variations which can occur between cows on the same pasture in feed intake and availability, rate of immobilisation of bone Mg, and maintenance and milk production requirements. It is then not surprising that some cows appear to be much more susceptible than others to G.T. and will consistently show very low serum Mg levels and suffer repeated clinical attacks. Nor is it surprising that many cases occur in good producers at the time of peak milk production.
The factors mentioned above are those thought to play some part in the development of Hypomagnesaemia. Certain stress factors, some of them yet unknown, are believed to trigger of a clinical attack of G.T. in a hypomagnesaemic animal
In North-East Victoria, excitement, oestrus and adverse weather appear to be the three most important precipitating factors, although there are numerous cases where there is no obvious explanation. There have been many cases of cows going into tetanic spasms when chased by a dog, yarded or handled roughly. On the other hand, one cow put in the crush and bled from the jugular at Mansfield showed a serum Mg of 0.3 mg% at the time and remained perfectly normal.
Other cases have occurred the day after a cow was in oestrus. or oestrus has occurred three weeks after a cow had survived a clinical attack. The fact that her muscular activity is increased while her grazing and ruminating time is decreased, may be significant. In all parts of the world G.T. is a disease of low temperatures, usually occurring in the temperature range of 40-60 deg. F.
Cold, wet, windy weather is considered more dangerous than cold, dry weather, but if the temperature drops too low or severe frosts inhibit pasture growth, G.T. losses are not likely to occur. Heavy losses in the North-East have frequently been associated with cold, wet, windy weather, but deaths also occur on mild, sunny days, without any obvious explanation. Last year a wave of deaths followed one of the few severe frosty spells in Benalla, but there was never any cessation in pasture growth.
Temperature probably acts in two ways, firstly, by providing suitable conditions for the growth of young, lush feed and, secondly, by causing increased heat loss and shivering in the animal, with a corresponding increase in Mg requirements. It has been claimed that a cow's Mg requirements can be increased tenfold during cold weather.
SYMPTOMS
Close on 50% of cases are found dead, but in other cases the animal is usually found lying flat on her side with head and legs extended. Attacks of acute muscular tetany are interspersed with periods of relative quiet and it is during a spasm that death frequently occurs. An accelerated and pounding heartbeat, rolling of the eyeballs, marked trembling of the eyelids and grinding of the teeth are often observed during a spasm, while a semi-circle of grass is often eroded by the violent leg thrashings.
Early symptoms are not often observed except in the case of dairy cattle, but these include increased nervousness and hyper-excitability, with the whole body taut, head held high, muscle tremors, dilated pupils and a wild look in the eye. There are jerky movements of the limbs which are often lifted in an exaggerated manner and the cow may stumble or stagger. The slightest stimulus is sufficient to provoke an acute attack of tetany with possible fatal results or the cow may go down, struggle up again and career of only to go down a second time, followed by death in a few minutes or hours. Very high temperatures up to 110 deg. F. are recorded frequently and this is due probably to the violent muscular activity.
An interesting point is that there is no correlation between the severity of symptoms and the degree of hypomagnesaemia, One cow with a serum Mg level of 0.3 mg.% which appeared perfectly normal, has already been mentioned. On the other hand, one clinical G.T, case showed a normal serum Mg level of 2.8 mg. %. but a low Ca level of 4.5 mg. %. and yet this was a definite clinical case of G.T.
This brings up the possibility of other serum constituents such is CA, Na and K affecting the development of G.T. But it must be stressed that the blood picture during an attack of G.T. does not give a reliable indication of the ionic concentrations preceding the onset of symptoms, because of the changes due to muscle catabolism during tetany.
Nevertheless, the importance of Ca must not be underrated when it is considered that there is a considerable loss of Ca in milk. Serum Ca is often low in both hypomagnesaemic and clinical cases and in some cases Ca therapy alone will save a cow. There is often a close association between Ca and Mg in body metabolism. In the nervous system, Ca and Mg both play a role in the production and destruction of acetylcholine, the substance necessary for the transmission of impulses at the neuromuscular junction. According to Douglas (1960) both Ca and Mg are necessary to activate the acetylcholine-splitting enzymes. Their absence would have serious consequences on the nervous system.
Post-mortem findings
There are few constant lesions to be seen on autopsy, the most consistent being ecchymoses of the epicardium and endocardium which may be very severe and there is often emphysema of the lungs, presumably due to the agonal struggles.
This raises the problem of P.M. diagnosis as G.T. cannot be diagnosed on this alone. At present there is a lot of circumstantial evidence to indicate that G.T. is the major cause of deaths in the Winter, but other conditions such as Enterotoxaemia must be kept continually in mind. The fact that the incidence is confined almost exclusively to lactating cows with a higher mortality in older cows, the finding of a seasonal hypomagnesaemia in the district and the highly successful treatment of hundreds of clinical cases each year with Ca and Mg therapy, as well as the apparent success obtained in the prevention of the condition with daily MgO supplements, leaves little doubt of the importance of G.T. in beef cattle in NorthEast Victoria.
TREATMENT
Considerable success has been obtained in the treatment of clinical G.T. and last year it appeared that treatment for G.T. gave better results than treatment for Milk Fever.
Treatment in the North-East usually consists of i/v Ca borogluconate and i/v or s/c Mg sulphate or hypophosphate. If Mg is injected i/v, it is advisable to do this slowly and to auscultate the heart at the same time. Although 2 oz. MgSO4 is often an adequate dose, some practitioners have had to inject up to 6 oz, before getting the cow on her feet. Success has also been obtained with 1 oz. chloral hydrate or 10 ml Sparine i/v in combination with Ca and Mg therapy, and it appears that with this method the dose of Mg can be considerably reduced.
A British practitioner, Mr. Steele-Bodger (1960), says that the rational treatment would be chlorpromazine to control the spasms and Ca to get the animal on to her feet. He has used this treatment for several years with excellent results. Dr. Seddon has described some cases treated successfully with 10 ml. Sparine i/v and nothing else, but he did mention they were not completely typical G.T. cases. It is quite conceivable that the symptoms of a Mg lack can be controlled by other drugs and this fact does not detract from the etiological importance of Mg. But such cows would still be very susceptible to further G.T. attacks and it would be advisable immediately to initiate daily MgO supplementation.
Usually, if a cow gets straight up after Mg therapy or soon after a chloral hydrate sleep, the prognosis is good. But in any recovered case, there is a likelihood that she will not be back to normal health for some weeks, and it is advisable to put her on oral Mg supplements straight away. Some cows appear to be particularly susceptible to G.T. and a second and sometimes fatal attack often follows in a few weeks.
In some cases, a cow will remain down for a week or more after treatment for G.T. symptoms; the tetany is controlled, but she is unable to rise. The prognosis is usually poor in these cases, but if she is feeding, there is some hope. These complicated cases are not fully understood and, when occurring after calving, may be associated with Milk Fever and other post-calving troubles. Blood samples from one such case, four days after treatment, showed a serum Mg level of 1.2 mg. % but normal calcium.
Quiet handling is always essential in the treatment of clinical cases, as excitement can stimulate a further convulsion.
PREVENTION
The high mortality rate of this disease has already been mentioned. This emphasises the need for an effective, practical and economical method of prevention and work in the North-East is being concentrated on this aspect.
In the past, prevention in the North-East consisted mainly of feeding hay during the danger months, and, provided sufficient good quality hay was fed, this appeared to have some preventive effect. However, it was not effective under all conditions and losses still occurred.
Other graziers found the disease could be prevented by moving breeders off improved pastures to rough hill country during danger months, but many properties have only improved paddocks and the unimproved areas can support cows and calves for only a very limited time. Spring calving may be another line of approach, but it is not very practical in the North-East.
Although there are many aspects of G.T. still not understood, it has been known since the 1930's that the condition can be prevented by feeding luxury amounts of Mg supplements.
Work by Allcroft (1960) in England has now established 2 oz/day of magnesium oxide as the minimum effective prophylactic dose which will offer almost complete insurance against Hypomagnesaemia and G.T. under all conditions. This must be fed daily during the danger period, since serum Mg levels may fall dangerously low within 48 hours of ceasing supplementation. There is no benefit in feeding MgO during pregnancy or prior to the danger period as the cow has no readily available storage of Mg. which can be drawn upon when needed, Up to date, there are no authentic reports of harmful effects from the prolonged feeding of MgO at the 2 oz/day level.
We commenced the investigation in the North-East using imported calcined Magnesite which contains at least 90% MgO and is the supplement most commonly used in England and Europe. It was soon found that cattle would readily eat this at the 2 oz/day dose rate when mixed with water and sprayed on good quality hay with a watering can. A mob of 50 cows would require approx. 6 lb/day and it was found best to mix this with two gallons of water, spray it on two broken-up bales and feed this treated hay to the mob before putting out the rest of the hay. The cattle are then sure of getting the total MgO supplement.
This procedure was carried out throughout the winter on the experimental property at Wangaratta and the calcined Magnesite was fed daily to approx. 70 breeders, while the 12 experimental cows were kept separate and unsupplemented. No deaths occurred in the supplemented group of 70 cows while two deaths occurred in the 12 unsupplemented experimental cows.
Early in July 1961, we heard of a much cheaper Australian produced MgO, named "Causmag", produced by the "Causmag" Ore Coy., Young, N.S.W. and sold as an industrial chemical. This cost 4d/lb, or only 2/- /day to feed 50 cows as compared with 1/8 /1b for imported calcined Magnesite. "Causmag" is almost identical with the imported product, containing 90-94% MgO and in this respect is far superior to other Mg compounds such as Epsom Salts, Agramag and Dolomite which may have a MgO content as low as 16%. There is reason also to believe that there is a better assimilation from the gut with the oxide. Epsom Salts feeding has been used in the past by various graziers and the variable results are easily understood.
A trial to test the "Causmag" was immediately commenced on a property at Mansfield which had already lost 14 Hereford Cows from presumptive G.T. The two experimental groups were limited to six cows each, due to the difficulty of getting Mg determinations done and these two groups were run in two adjoining paddocks where heavy losses had previously occurred. Both groups were showing a hypomagnesaemia at the commencement of the trial and thereafter the serum Mg levels of the "Causmag" group rose to a mean of 1.8 mg/S, while the control group still remained dangerously low. No deaths occurred in either group. The results were statistically analysed and found to be significant at the 5% level.
Following the promising results at Mansfield, the "Causmag" Ore Co., sold 20 tons of "Causmag" to graziers and we have heard of no reports of G.T. losses in cows being fed "Causmag", although there were several reports of graziers who had further losses when they ceased supplementation too early.
There is always the possibility with beef cattle that some cows will not get their full share of supplement and odd losses are to be expected, but with dairy cattle fed in the bail, this should not be a problem, Overseas work also indicates that blood levels do not rise for 3 or 4 days after the commencement of supplementation, deaths could still occur in this period.
Further experiments were carried out by the Department Fodder Conservation Officer, Mr. E. K. Simmons, at Werribee Research Farm and on a private property last Spring, in an attempt to incorporate "Causmag" into the hay at baling time and thus save the daily labour of spraying hay during the danger months. In one trial a modified "Sunprong" fertilizer box mounted on the baler and used fairly successfully as a dispenser of dry "Causmag" while in another trial, the windows were sprayed with a suspension of "Causmag" before baling. Various chemical stickers have been added to the "Causmag" suspension, with the object of improving spreading and adhesion of the "Causmag".
Finally, brief mention will be made of Mg topdressing and licks. Experiments by Alleroft and others have shown that Mg topdressing at rates of 5-10 cwt, of calcined Magnesite/acre will prevent hypomagnesaemia and G.T. for several years. Magnesium oxide, in the form of calcined Magnesite, has also proved superior to other Mg compounds, even when those compounds are used at correspondingly high rates to give the same concentration of MgO. At present it appears that this method would be uneconomical in Australia as compared with Mg feeding, but until we carry out controlled top dressing trials in this country, we will not know what rates are necessary. A trial now in progress at the Levington Research Centre in England has indicated that topdressing levels as low as 50lb. MgO/acre may be effective under some conditions. There appears to be little place for Mg licks as the daily intake of Mg would be far too small to ensure complete protection.
In conclusion, the results, up to date, have been most encouraging and it appears that "Causmag" may be an effective, cheap and practical method of preventing G.T. under conditions of beef cattle husbandry in the affected areas of Victoria and N.S.W. But, the investigation is far from complete and work has already commenced this year to repeat and expand last year's work. On the property of Mr. T. H. Collins, "Fairfield Park," Greta South, the effect of both daily and every second day supplementation with MgO is being assessed. If every second day supplementation is found effective this will halve the labour involved. A topdressing trial was also organised for 1962, but this had to be abandoned owing to lack of finance.
REFERENCE
- British Veterinary Association Conference on Hypomagnesaemia (1960)