SOME MINERAL DEFICIENCIESAND EXCESSES IN CATTLE AND

SHEEP IN BRITAINBy RUTH ALLCROFT, Senior Research Officer,Veterinary Laboratory, Ministry of Agriculture,Fisheries and Food, Weybridge, Surrey, England.

Although the production of good pasture is astarting point, one end point is a prime, healthy animal.

lemsAt Weybridge, we have many animal health prob-associated wrth the grazing of apparently good

pastures, and it is some of these problems that I pro-pose to discuss this afternoon: Because some of thesedisorders are not associated with a deficiency of miner-als in the herbage itself, it may be misleading to referto them merely as “trace element” or “mineral defici-ency” diseases, which usually implies a deficient intakeof some essential dietary constituent rather than adysfunction of the mineral metabolism of the animal.Magnesium

Hypomagnesaemic tetany, commonly referred toas “grass tetany,” “‘grass staggers,” or “lactation tet-any,” is usually included in the so-called “metabolicdisorders” such as milk fever and ketosis, but it is dis-cussed here, not only because it is a disease of consid-erable economic importance in Britain and otherEuropean countries as well as in New Zealand, but alsobecause there is growing evidence that some forms of$he disorder are related to dietary factors (Blaxterand McGill, 1956).

Most investigators agree that the disorder is notcaused by deficiency of magnesium in the classicalsense, since pastures on which it occurs show a magne-sium content as high and sometimes higher than pas-tures on which it does not occur; even on soils whichrespond to magnesium fertilisers, -the incidence ofhypomagnesaemic tetany appears to be no greater thanon soils rich in magnesium. Nevertheless, there is agood deal of evidence which shows that an increase inthe magnesium intake of cattle can prevent, or at leastmitigate, the fall of serum magnesium levels (Allcroft,

, 63

1953 ; Stewart, 1954 ; Blaxter and McGill, 1956). Theuse of oral supplements of magnesium oxide haveproved to be very effective under certain conditions(Allcroft, 1954) and this has been widely confirmed byfarming experience in Britain.

Swan and Jamieson (1956) have shown that adeficient food energy intake is one cause of hypomag-nesaemia in lactating cows. Clinical cases of grassstaggers were produced by underfeeding alone, butoccurred more readily when thryroprotein dosing wassuperimposed on the underfeeding. Norwegian work-ers have also demonstrated that hypomagnesaemiacould be induced in stall-fed lactating cows on a lowmagnesium/low energy diet (Breirem, Ender, Halse,and Slagsvold, 1949). Some trials at Weybridge, how-ever, showed that even lower magnesium intakes didnot produce significant hypo-magnesaemia in 2-year-old stall-fed heifers whether on high or low energydiets, but these animals were not subjected to theadditional strain of lactation as were the Norwegiancattle.

The evidence, so far, indicates that there are twomain types of the disease in the bovine ; one is arapidly developing type most commonly associated witha flush growth of grass in spring and autumn, whilethe other is a slowly developing or seasonal type(Green, 1948). The first is most prevalent in dairyanimals, and although most common during spring andautumn and least common during the summer, the con-dition can occur at any time in cattle in Britain, eitherat grass or on stall feeding. It is not confined to anyparticular age, sex, or breed, but the incidence is lowin Jersey cattle and is practically unknown in thisbreed in their native island. This seems to be an inter-esting contrast to the incidence of the disorder in Jer-sey cattle in New Zealand.

The slowly developing or seasonal type is mostprevalent in beef cattle, dry cows, and young stock,and occurs more frequently during the winter thanduring the season of rapid growth of grass. A markedassociation has been reported (Allcroft, 1947) betweenlow serum magnesium values in out-wintered beefcattle and wet, cold, windy weather. In beef cows thehighest incidence usually occurs a few weeks afterwinter calving when pasture growth is very slow andconsequently when the plane of nutrition is generallypoor. It is often at this time, especially, that a sud-den, wet, cold spell of weather may precipitate clinicalcases ; that is, at a time when the animal is subjected

54

to heavy stresses, such as lactation, low plane of nutri-tion and high loss of body heat.

Even though there appears to be no associationwith soil type, and no correlation between the magne-sium content of the soil or pasture and the severity ofthe disease, the condition does appear to be more pre-valent on some farms than on others. The increasedincidence is often associated with improvement ofgrassland and/or the adoption of an intensive systemof rotational grazing where’application of artificial fer-tilisers is heavy.

Collaborative work at Shinfield and Weybridge(Bartlett et al., 1954) indicated a greater incidence of

the disease on a cocksfoot and clover sward which hadbeen given a heavy dressing of sulphate of ammoniathan on a similar sward which had no nitrogenousdressing that season. When a heavy application of acommercial grade of magnesium oxide was given beforethe sulphate of ammonia, the magnesium content ofthe pasture was doubled and little hypomagnenaemiaand no clinical cases of tetany occurred. The occur-rence or absence of hypomagnesaemia in the cowsgrazing the various experimental plots could not, how-ever, be correlated with pasture magnesium values andthe possibility must be considered that the beneficialeffect of the magnesium oxide dressing may have beendue to an alteration in soil conditions resulting in theabsence of “tetany-producing” factors in the pasture,rather than to an increased magnesium contentper se of the sward.

The application of magnesium compounds to ex-perimental plots was studied in New Zealand by Cun-ningham (1936)) who used dressings of both magne-sium sulphate and dolomite. Although these dressingsappreciably increased the magnesium content of thesward, it was not considered that the intake of magne-sium by the grazing animal could be increased economi- ’tally by these methods. More recent investigations byScottish workers (Stewart, 1953 and Stewart andReith, 1956) have also shown increases in the magne-sium content of pastures dressed with magnesiumlimestone, and this effect was correlated with the main-tenance of normal serum magnesium levels of cattlegrazing the treated pastures. Work is now being car-ried out at Weybridge to study the value of magnesianlimestone dressings under controlled conditions and tocompare it with the use of magnesium oxide, whichis too expensive for large scale application. The resultsso far obtained (Parr and Allcroft, 1956) confirm that

55

the magnesium content of pasture can be raised bymagnesium manures and that this has a beneficialeffect on serum magnesium levels in cattle. They alsoindicate that the uptake of magnesium can be influ-enced by other manurial treatments, particularly thoseinvolving the use of calcium. The use of magnesianlimestone on soils which have a definite lime require-’ ’nient seems justified as a step toward the control ofhypomagnesaemia, but it is unlikely that it would be ofvalue on soils with an already adequate lime status.Magnesium oxide or other magnesium rich compoundsare likely to give better results on such soils, but muchwork remains to be done on this aspect of prevention aswell as on the metabolism of magnesium in the animalitself.

The incidence of hypomagnesaemic tetany in thecalf appears to have increased during the last fewyears. Blaxter and Sharman (1955) have suggestedthat the disease is due to a simple dietary deficiencyof magnesium. associated with the liberal feeding ofwhole milk. Evidence from field reports collected atWeybridge indicate that although it is frequentlyassociated with a high milk intake, it can occur incalves under all conditions of feeding and management.

Although this disease is much more prevalent incattle than in sheep, Weybridge records show thatclinical symptoms associated with hypomagnesaemiaare fairly common in both hill and lowland flocks. Theincidence ,of clinical cases is highest during the 4-weekperiod after lambing, the peak usually occurring atlo-14 days after parturition. In some lowland flocksthe disorder has been associated with improvement ofpastures, with the use of simple seeds mixtures, andwith increased use of artificial fertilisers; nevertheless,the incidence in hill flocks on poor grazing is not neg-ligible in some seasons.

Copper and MolybdenumSo much has already been reported on the meta-

bolic inter-relationship of copper and molybdenum inruminants, that it will be more convenient to dealbriefly with related aspects of copper deficiency andmolybdenum excess in cattle and sheep in Britain thanto discuss them separately.

The peculiarity of copper deficiency in Britain isthat the condition occurs on pastures normal or evenhigh in copper content and is therefore an “induced”or “condjtioned” deficiency. Low copper values in pas-ture grasses have, so far, been found only for short

SE

periods during spring growth in a few isolated areas,chiefly in East Anglia, and also in a few cereal andother crops.

Historically, the associated clinical disorders wereobserved in Britain, first in sheep, and then in cattle,but economically, the disorder is now of greaterimportance in cattle.

The chief manifestation of copper deficiency insheep in Britain is the occurrence of “swayback” orneonatal ataxia in lambs, which is pathologically simi-lar to “enzootic ataxia” which occurs in Australia andNew Zealand.. Apart from the well-known symptomsand pathological lesions which characterise this dis-order in lambs, no other abnormality has been associ-ated with a low copper status of sheep in Britain.Although there is ample proof that administration ofcopper to the ewe during the gestation period willprevent the occurrence of swayback in lambs andalthough low blood and liver copper values have alwaysbeen found in affected lambs and their mothers, manyliver samples have shown equally low copper valueswithout any evidence of demyelination or of clinicalmanifestations of swayback in the flock. It wouldseem possible, therefore, that a low copper status alonedoes not necessarily produce the lesions of swaybackand that another factor may also be concerned which

Copper deficiency in ‘Aberdeen Angus cattle. Calves showsevere symptoms of copper deficiency while the mother appears

clinically tiormal.

67

Effect of intravenous administration of 50mg of ,copper to calfon right. Calf on left, which is same age, is untreated;

operates to produce -demyelination of the nervous sys-tem of the lamb only when the copper status of bothewe and lamb is low.

Copper deficiency in cattle is reflected by a .widevariety of non-specific clinical manifestations, “thechief of which is progressive loss of condition. Diar-rhoea is not always present; in some cases it is severewhile in others it is absent. Concurrent anaemia isuncommon. Adult as well as young stock are affected;but frequently, especially in beef herds, the calves arese,verely affected, while their mothers appear clinicallynormal, even though the copper status of both may beveryilow. Administration of small quantities of copper‘Gially, gives a spectacular response in increase ofgrow.th in these cases.: I. 1 &pocuprosis in cattle has’ been observed in many&fferent areas widespread throughout the country.

,I,Our:evidence does not indicate that it is confined to any-,particular soil type, and alth,ough it is usually found invarying degrees of severity in cattle grazing peatyareas, it is by no means confined to these. , .

‘Its occurrence on pastures of normal or even highcopper content obviously suggests the presence of

58

other constituents in the herbage which interfere withthe utilisation of copper in the animal.

The harmful effects to ruminants of a relativelyhigh molybdenum/copper ratio are well known andhave been demonstrated in several parts of the worldsince Ferguson, Lewis and Watson (1943) showed thatthe scouring and unthriftiness that occur in cattle onthe “teart” pastures in Somerset were directly relatedto the water-soluble molybdenum in the herbage. Cun-ningham (1950) has shown that a relatively. high in-take of molybdenum can reduce liver copper storagein cattle and sheep, can reduce growth rate in calves,and produce a clinical picture of scouring and unthrifti-ness similar to natural cases of “peat scours.” Ourexperimental observations agree with his findings asfar as the bovine is concerned and in some areas, espe-

. cially on peat soils, the relative amounts of copper andmolybdenum in the pastures fall, within‘ the rangewhich he has shown to be harmful for cattle (1950 and1955). In many other areas, however, this does notappear to be the explanation, since copper deficiencysymptoms are by no means always associated withadverse copper/molybdenum levels and have beenobserved on pastures with values similar to those foundfor many “healthy” pastures. Also, there appears tobe no relationship between the copper and molybdenumcontent of pastures and the incidence of swayback.

Dick (1953-54) has demonstrated that the inor-ganic sulphate content of the diet can influence theeffect of molybdenum on liver copper storage in sheep,but a difference in the sulphate content of healthy andaffected pastures does not appear to be a significantfactor in the occurrence of hypocuprosis.

Table I shows some mean values of copper, molyb-denum and inorganic sulphate contents of pastures onwhich hypocuprosis in cattle and swayback in lambsdoes and does not occur (Allcroft and Lewis -1956).

These data, then, suggest that there are factorsother than (1) a dietary deficiency of copper; (2) anexcess of molybdenum relative to copper; or (3) adifference in the sulphate content of the pastureswhich can cause copper deficiency in cattle and sheep.Nor do these factors appear to be the only ones whichinfluence accumulation of copper in sheep, since deathsdue to chronic copper poisoning have occurred in stalledsheep at Weybridge on diets supplying approximatelynormal concentrations of these three constituents (12p.p.m. Cu, 1 p.p.m. MO, and 0.7 g. per cent inorganicsulphate). It would seem, therefore, that there are

59

I

TABL& I.-Copper, molybdequm, and inorganic sulphate content, of pastures on which copper, deficiencyin cattle and sheep has and has not occurred.

Description

Cattle Pastures1. No copper deficiency

(a) Non-industrial areas(b) Industrial areas .

2. Copper deficiency(a) Non-industrial areas(b) Industrial areas .

Sheep Pastures1. No swayback . .2 . S w a y b a c k .

7

.-

-

No. ofSamples

.y

CopperI

Molybdenump.p.m./D.W.i

Mean Range [ Mean Range

;56.2-2115-35

li:13-1813-37

18 6.2-35'14 8.4-20

i::0.32-2.1.2.0-7.5

2.1 1.1-4.3 0.72 0.44-0.827.0 1.5-15 0.58 0.24-1.10

[norganic Sulpliate

Mean

1

0.67 0.49-0.900.83 0.40-1.3

1.2 0.39-2.5 0.61 0.23-0.911.6 0.46-3.6 0.68 0.45~(I.95,1..

other factors, as yet unknown, which can profoundlyinfluence copper metabolism in cattle and sheep.

C o b a l tCobalt deficiency does not appear to be of such

economic importance in Britain as it is in New Zea-land and Australia. The disorder is less common inEngland than in Scotland where systematic mappinghas been carried out and cobalt deficient areas werereported by Stewart, Mitchell, and Stewart (1946).Patterson (1946) has described cobalt deficiency insheep on the granite and sandstone soils of Devon andCornwall and later observations by Osborne, Feather-stone and Herdan (1954) indicate that marginal andseasonal deficiencies of cobalt occur in Herefordshireand Worcestershire.

FluorineThe problem of fluorosis in farm animals in Britain

is not due to the high fluorine content of rock phos-phate deposits, volcanic soils, or water supplies, butarises from the emission of fluorine containing gasesand dusts from industrial plants. If the density of ourindustrial areas is considered in relation to the rela-tively small area of the whole country, it can be readilyunderstood that a great deal of agricultural land mustbe adjacent to industrial works.

The chief sources of fluorine contamination ofgrassland and crops are: (1) steel and metal workswhen the method of production involves the use oflarge amounts of fluorspar as a flux ; (2) brickworks,where the source is usually the local clay, although coalis sometimes a contributory factor; (3) production ofaluminium by the electrolytic reduction of alumina;(4) glass, enamel, and colour works where fluorinecompounds are often added to facilitate melting and togive the finished products certain properties ; (5) thecalcining of iron-stone where the sourtie is mainly thefluorine-rich ore itself; (6) potteries and other ceramicindustries where the materials used in manufacture arehigh in fluorine; (7) collieries, power stations andother industries which consume large quantities ofpulverised low-grade coal with a high fluorine content.

It is generally accepted that the fluorine con-tent of most plants, with the exception of the roots, isnot readily affected by the amount of fluorine in thesoil. There seem to be a few exceptions to this, not-ably the tea plant. and the camellia, which appear tobe fluorine collectors, but common fluorine values for

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The chief chemical sign of fluorosis in severely affected cattleis lameness, which is frequently associated with marked skele-tal abnormalities such as an increase in diameter of bones andwell defined exostoses. Enlargement and gross exostoses inbovine limb bones (left) compared with normal bones -(right).

uncontaminated animal foodstuffs lie between 1 and10 p.p.m. on a dry matter basis. Excessively highvalues’ up to 2000 p.p.m. have been reported (Green1946) on herbage near sources of emission of fluorinecompounds. Herbage and soil samples provide usefulcorroboration, but are not suitable alone for assessing

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degree and extent of contamination, since results willdepend on climatic conditions around the time ofsampling, on the direction of the prevailing winds, andon the topography of the surrounding terrain. It isdifficult to suggest a minimum fluorine value for con-taminated pastures at which clinical cases of fluorosiswill occur, because of the variable factors first men-tioned, and because the all-important factor is thelength of time over which the foodstuff is consumed at

,any particular level of contamination. And since devel-opment of clinical sympt,oms is slow, a pasture analysisonly demonstrates that contamination is present; it

‘cannot give a direct correlation of the degree of fluor-osis in the animal.

Present evidence suggests that the order ,of sus-ceptibility of farm animals to fluorosis is calves, dairycows, other bovines, sheep, pigs, horses, and poultry,but this order may be revised when comparative testson a known and comparable body weight intake havebeen carried out, The chief clinical ,symptom in sev-erely affected cattle is lameness, and it is this whichusually suggests the possibility of fluorosis and leadsto a closer investigation of the herd. The lameness isfrequently associated with marked skeletal abnormali-ties such as an increase in diameter of limb bones andwell-defined exostoses. Dental lesions in the perman-ent teeth of cattle reared on affected farms are one ofthe best indications of the presence and degree offluorosis. They include loss of lustre, pitting, stainingin parts of the defective enamel, and excessive andirregular wear. Clinical diagnosis can be confirmed bydetermination of the fluorine content of urine and bonesamples.

Although the total economic loss due to fluorosisis not great when considered in relation to that.causedby the major transmissible diseases, it is a matter ofserious concern in affected .areas and methods of con-trol are being studied both by industry and agriculture.Reduction of emission can be achieved to some extentin some industries by trapping and washing the dustsand gases, but in others the practical difficulties andthe costs would be so great that it is unlikely thatefficient devices could be installed. Some degree ofagricultural control can be achieved by farming withthe fluorine hazard in view, e.g., improvement of pas-ture management, limitation of grazing periods; keep-ing pigs and poultry instead of cattle and sheep, orusing the land for production of crops only. The pos-sibility of alleviating the effects of fluorosis in cattle

63

by feeding certain mineral supplements is also beinginvestigated by the Ministry on an experimental farmon which fluorosis occurs.

IodineIt has been thought that typical iodine deficiency

in farm stock in Britain is rare, but thyroid hyper-plasia in new-born calves occurs not infrequently andhypothyroidism in cattle and its possible relationshipwith reproductive disorders have been reported (All-croft, Scarnell, and Hignett, 1954). There are reportstoo of congenital goitre in lambs. Jamieson and Har-bour (1947) recorded its occurrence in lambs fromewes running on grassland, while Shand (1952) des-cribed an outbreak resulting from excessive feedingof kale to pregnant ewes. Subsequent investigation ofthe goitrogenic factor in kale showed that it could be,overcome by feeding additional iodine to the ewes dur-ing gestation (Shand, Allcroft, and Hignett, unpub-lished data). Analysis of food samples has shownsome low iodine values and there appears to be a pos-sibility that thyroid hyperplasia in cattle and sheepmay be associated with marginal intakes of iodine aswell as with other goitrogens, but much work remainsto, be done before the nature of these antithyroid fac-tors is understood.

ReferencesAllcroft, R. Proc. XV Int. Vet. Congr., Stockholm, Vol. I,

Pt. 1, pp. 573. 1953.Allcroft R. Vet. Rec., Vol. 66, pp. 517. 1954.Allcroft, R., and Lewis, G. Proc. 7th Int. Grassland Congr., N.Z.

(in press). 1956.Allcroft, R., Scarnell, J., and Hignett, S. L. Vet. Rec., Vol. 66,

pp. 367. 1954.Allcroft, W. M. Vet. J.. Vol. 103, pp. 75. 1947.Bartlett, S., Brown, B. ‘B., Foot, A. S:, Rowland, S. J., Allcroft

R., and Parr, W. H. Br. Vet. J., Vol. 110, pp. 3. 1954.Blaxter, K. L.; and McGill, R. F: Vet. Revs. and Annot., Vol. 2,

p p . 3 5 . 1 9 5 6 .Blaxter, K. L., and Sharman, G. A. M. ,Vet. Rec., Vol. 67;‘ pp.

108. 1955.Breirem, K., Ender, F., Halse, K., and Slagsvold, L. Acta

Suecana, Vol. 3, pp. 89. 1949.Cunningham, I. J. N.Z. J. Sci. Tech, Vol. 17, pp. 775.Cunningham, I. J. N.Z. J. Agric;, Vol. 90, pp. 196. 1.955.Dick, A. T. Aust. Vet. J., Vol. 29, pp. 233. 1953.Dick, A. T. Aust. Vet. J., Vol. 30, pp. 197. 1954.Ferguson, W. S., Lewis, A. H., and Watson, S. J. J. .Agr.

Vol. 33, pp. 44. 1943.Green,-H. H. Proc. Roy. Soc...Med., Vol. 39, pp. 795. ..1946.Green, H. H. N.V.M.A. Publ. NO. 17, pp. .60. 1948.Jam?;;;, S., and Harbour, H. E. Vet. Rec., Vol. 59, pp.

G4

Agr.

1936.

Sci.,

102.

McElroy, W. D.; and Glass, B., eds. Symposium on CopperMetabolism, pp. 246-270. Johns Hopkins Press, Baltimore,1950.

Osb&& A. D., Featherstone, J., and HeVol.. 66, pp. .409, 1954.

rdan, G. Vet.

Parr, W. H., and Allcroft, R. Unpublished data. 1956.Patterson, J. B. E. Nature, Vol. 157, pp. 555. 1946.Shand, A. B.V.A. Publ. No. 23, pp. 58. 1952.Stewart, J. Guernsey Breeders’ J., Vol. 7, pp. 43. 1953.Stewart, J. Scot. Agric., Vol. 34, pp. 68. 1954.Stewart, J., Mitchell, R.L., and Stewart, A. B. Emp. J.

Agr., Vol. 14, pp. 145. 1946.Stewart, J., and Reith, J. W. S. J; Comp. Path., Vol. 66,

1956._

Swan, J. B., and Jamieson, N. D. N.Z. J. Sci. Tech. *(in II195G.

Rec.,

Exp.

PP. 1.

Iress).

DISCUSSIONCol. Stafford, Springston: You have just listened to the most

lucid speech on the deficiencies. of a number’ of elementswhich are essential to animal life. Now it has been statedthat the nH of a good nasture soil.runs between 6.5 and 7.I can oniy give you a-little .of my own experience; onceyou get the pH over 7, as you do where lime has been puton the land in excess, then you get disastrous results in ,boneformation, especially in young stock. I must congratulatethe speaker on a wonderful paper.

Q.

A.

Q.A.

Q.

A .

Q.

A.

Does Dr Allcroft know .of any cases where farmers whosestock have been affected by fluorosis obtained compensationagainst the particular industrial enterprise which has beenthe cause of it?

Do you mean as a result of a legal claim or do you meanas a result of private negotiations between farmer andi n d u s t r y ?

I am concerned with’ the common Iaw right.1 do know of cases. Some industries do, by private arrange-ment, pay compensation to farmers whose land is -adjacentand is severely contaminated.What is the reason for the incidence of increased grassstaggers on pastures fertilised with nitrogen in the earlyipring ?We have no explanation. The increased incidence is notonly confined to pastures treated with nitrogen. We havefound that by topdressing those. pastures with magnesiteit increases the magnesium uptake. of the pasture. Theincidence of staggers has been reduced but the incidencecannot be correlated with magnesium content alone,although it was beneficial in the cases we tried.

if crops are grown where there is fluorine contaminationdo they take up the fluorine and pass the trouble on tosomebody else ?No, it is not a case of passing it on to somebody else. Ithas been shown that most plants do not take up fluorinefrom the soil. There are two exceptions: the tea plant andthe camellia which appear to be fluorine collectors. Most

F5

Q.

A.

Q-

.4.

Q-

4.

Q.

A.

Q-

A .

grasses and root crops do not take:it up from soils. It ismostly a question of. contamination of the surface;, there-fore humans get off lightly because we do not eat grass.The inner parts of cabbages and similar. crops are not highin fluorine, only the outer coverings which are .removed.Cereal grains are also quite safe.

Is fluorine cumulative ? Can small quantities be safelyabsorbed over long periods or will they produce clinicalsymptoms ? It is sometimes the practice to add fluorine todrinking water.

Yes, it is cumulative, but if the intake is sn~all~animals orcattle do seem to be able to stand considerable amountswithout any adverse clinical symptoms at all. If they arecontinually exposed to it there will be a gradual build-upto three or four thousand parts per million. A concentrationof five to six hundred parts per million is normal. It usuallytakes several years before you get clinical symptoms, thenthey first show as dental lesions.Short of clinical symptoms such as swayback are youngsheep affected by a deficiency of copper ?I do not think so; we have not associated any. loss of con-dition in young sheep with copper deficiency. ,

How and when were the magnesites and dolomites appliedto the pastures ?The magnesite was applied during the spring. The dolo-mite we have applied on two occasions, one in the autumnand the other in the spring. We found on some plots thatjust one application in spring-February-March-was quitesufficient.

Were the copper injections to cattle as satisfactory as theapplication of copper to pasture; also if they are satisfac-tory are they satisfactory in the case of molybdenum excessas well as simply copper deficiency?

We do not usually apply copper to the pastures. It isnormally always given as oral su$plement or intraven-ous injection; in sheep always as oral supplement. Wehave tried an application of copper sulphate to cattlepasture in peaty areas in Scotland and found the effect woreoff after six months. Most farmers prefer oral supplementsor intravenous injections rather than topdressing of pas-tures. They are apprehensive about using copper for top-dressing pastures because of the toxicity to sheep. Assum-ing that all our pastures where copper deficiency occurs areused both for cattle and sheep grazing we have not pushedthe use’of copper sulphate on pastures.

H. van Rensburg: Would water containing more than 30parts per million of fluorine have detrimental effects oncattle, and how soon ? The problem occurs in Tanganyikawhere we have very high percentages of fluorine in thewater and would like to hold young cattle -on the areas for6-18 months. How long could we safely keep them there?

Dr Allcroft : With 30 parts per million in the drinkingwater you would get clinical effects if you keep them therefor 18 months. You could expect to get severe dental

66

lesions in the permanent teeth when they came through.If they were then removed and spent the rest of their livesaway from it, they might not be so bad, but still therewould be .harmful effects. Do you have to keep them therethat length of time?

H. van Rensburg: We have not kept them in this specific areafor any length of time,. but in other areas. where~there is ahigh fluorine content in the water it is very noticeableamongst stock -and humans that their teeth are severelyaffected. Conditions I am referring to would only apply tocattle afterwards drafted to market for slaughter.

ci