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This article was published in 1971
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Diseases Associated With Lot-Feeding Of Cattle

P. J. AHRENS, Veterinary Inspector, Molong

The purpose of this review is to draw attention to the problems that can arise from manipulating cattle nutrition to gain better production. Most of the information has been obtained from the fattening industry in North America and the barley-beef industry in the United Kingdom.

One of the criteria widely accepted for profitability in opportunity feeding units is minimum-cost construction. No doubt this will sometimes be associated with minimum-cost management to the detriment of the health of the stock.

We are fortunate in this country to be free of the Shipping Fever complex. However, there are many other viral and bacterial infections which are aided by the close proximity of the animals and stress factors within the feedlot yard. In addition, there are various "social diseases" which can be manifested as a result of population pressure and boredom. These include navel sucking, rail-chewing, riding and being ridden, shy feeding and "feed tiredness".

This paper is confined to the diseases actually associated with heavy cereal feeding especially of diets with a high percentage of grain. These diseases are:—

Other conditions related to grain feeding but not dealt with are Telangiectasis and Sawdust Liver which are probably caused by a rapid rate of fattening; and Polioencephalomalacia, which although it does occur in cattle at pasture, is more severe in lot-fed cattle. Enterotoxaemia is another feed related disease.

Despite all those possibilities, the percentage mortality in Australian feedlots is probably fairly low. Pryor (1970), states that it is less than ½ per cent. Beeby (pers. comm.), also says that ½ per cent is a realistic figure to budget against. Individual losses have at times been much higher but management faults are largely responsible.

Lactic Acidosis

Grain poisoning or "grain overload", as it is also termed, is created in a rumen which is not accustomed to the quantity of grain ingested, or more accurately the quantity of freely fermentable carbohydrate ingested.

The disease is caused by the excessive production of the D isomer of lactic acid by a suddenly altered rumen microflora. Lactic acidosis can also result from ingestion of other highly fermentable feeds such as beet crops or silage when the microbial population is not adjusted to it.

In a study of naturally induced lactic acidosis, Brawner et al (1969) found the increase in rumen lactate to be of the order of 0.33 m. moles to 99.41 m. moles.

Absorption of lactate into the bloodstream caused the pH of the blood to fall from 7.4 to 7.28. (Working with a small number of Bos indicus and Bos taurus animals, these workers found that Bos indicus absorbed the lactate more rapidly and exhibited lower tolerance to biochemical change).

Clinical Signs

Sudden loss of appetite is the first sign. This can happen as early as 12 hours after engorgement, but may take as long as 36 hours. Body temperature remains normal but ruminal movements cease and at this stage one might suspect simple indigestion.

The rapidity of development of more severe signs is a guide to the prognosis which in any case is not easy.

Acceleration of the heart rate and respiratory rate indicate that severe acidosis is occurring and small samples of rumen liquor should be obtained for pH estimation and for smears on glass slides. The smears can be used to demonstrate the alteration of rumen microflora to a predominance of Streptococci (Str. bovis).

"Combistix" indicator strips show the pH to be between 4 and 5 and sometimes even lower.

As haemoconcentration and acidaemia develop, the affected animal becomes very depressed and weak in the muscles. A staggery, drunken gait may cause it to bump into things, and in recumbency can look very much like hypocalcaemia.

Death occurs in 24-72 hours. If death is not the result at this stage, the pulse rate subsides to normal, the temperature rises and the return of ruminal activity promotes a copious grey mucoid diarrhoea. It is not uncommon for some animals to then die of gangrenous rumenitis.

Post-Mortem Signs

If the post-mortem delay is less than one hour, estimations of rumen pH may be of value in confirming a diagnosis (Blood and Henderson, 1963). Smears of rumen liquor from different locations may be useful specimens to take. Affected areas of epithelium are seen as dark brown irregular patches of swollen, friable villi which wipe away easily, revealing haemorrhagic submucous tissues.

Congestion and inflammation may be present in the abomasum and small intestines. Serosal surfaces commonly exhibit petechial and ecchymotic haemorrhages.

An effect of the haemoconcentration may be seen as a thickening and darkening of the blood, and visceral veins stand out prominently.

In cases of gangrenous rumenitis, a thickening of affected areas is caused by severe haemorrhagic necrosis which may show on histological section invasion with fungal mycelia.

Treatment

The best treatment in early acute engorgement is emergency rumenotomy. The offending ruminal contents are replaced by some hay. water and fresh supplies of normal rumen micro-organisms. Since the lactic acid destroys so much of the normal microbial populalation, a rumen transplant should be administered to any convalescent prospect.

A commonly used treatment for engorgement has been magnesium sulphate but some Queensland experiments by Lainberth (1966) showed that in fact the hypertonic situation in the rumen is exacerbated by the epsom salts, further embarrassing the animal's fluid dynamics.

The approach to the circulatory problem should be parenteral administration of 2 gallons and even more of isotonic electrolytes. To this could be added calcium borogluconate and possibly 12 gm. of sodium bicarbonate, as part of a slow intravenous injection on the first occasion.

A decision as to what home treatments to advocate is always unsatisfactory with lactic acidosis. But, of course, even with the best attention many cases will die, having wasted hours of care and great quantities of drugs. Nevertheless, there is no doubt that in many cases, thorough treatment can be well worthwhile.

A basic difficulty with therapy to combat the ruminal acidity is the atonic rumen which does not mix the drench treatment adequately through rumen contents. Stomach tubes offer some advantages over drench bottles.

Magnesium oxide ("Causmag"), hydroxide of carbonate in quantities of 1 lb. twice daily are effective antacids for the purpose. Calcium carbonate as ground limestone has also been used in conjunction.

Sodium bicarbonate should be given with caution since distressing alkalosis may occur (dose 4 oz.).

Antihistamine and antibiotic injections are also strongly advocated in therapy of this condition to prevent development of founder and liver abscesses respectively.

Prevention

Buffer mixtures of alkaline aperients have been included in change-over rations to meet the stress of new carbohydrate components. Culhoun and Shelton (1969) found that a 2:1 mixture of magnesium hydroxide and potassium bicarbonate at the 3% level effectively prevented feedlot lambs from going off feed when rolled sorghum was suddenly introduced to a ration. The buffer mixture only needed to be fed for 6 days.

As to whether buffer mixtures should be permanently included in feedlot rations to guard against acid diseases is open to argument.

Rumen Parakeratosis

This is a very common condition in lot-fed cattle and 100 per cent incidence has been observed in cattle fed on all-concentrate diet. The name has been coined to denote the common rumenitis induced by feed.

Rumen parakeratosis has been defined by workers in North Carolina (Wise et al, 1968) as an increase in the thickness of the cornified portion of the ruminal epithelium with a persistence of nuclei in most of the cornified cells. Some cells have vacuoles which contain a watery fluid. The papillae become firm, leathery, enlarged, and dark in colour and often adhere together to form clumps. The mucosa has an unhealthy appearance and the site of the lesion varies from a few affected papillae in the anteroventral sac, to most of the papillae on the entire ruminal surface with the anteroventral sac being the worst affected.

Perhaps dealing with a somewhat different condition, workers at the Rowett Research Institute in Scotland (Kay et al, 1969) described a rumenitis affecting barley-beef calves 200 lb. in weight. The disease characteristically found in these animals involves the lamina propria so that rugae are formed.

The thickening of the epithelium, the crowding together of the papillae, the underlying stromal proliferation result in the formation of rugae which in turn leads to the trapping of debris.

Hairs caught in the debris tend to irritate the tissues by penetrating the epithelium, thus aggravating the situation. The ridges become stiffened by the dense carpet of papillae and some fuse together. Food particles and matted hair are locked in and ulcers start to form.

Aetiology

Despite an obvious relationship between these two conditions, some considerable variation of opinion exists as to the aetiology. Probably multiple factors are involved.

By buffering a pelleted barley ration with sodium bicarbonate at the 0.75 per cent level, the British workers were able to prevent the pathological changes in the rumen wall. They postulated that the acidity of the rumen ferment modified the mucosal structure by increasing the blood low and expanding the vascular bed. Further progression of the condition naturally followed from the superimposed inflammatory changes.

The Americans on the other hand felt that no clear cut conclusions could be drawn about the protective action of buffering agents. They state that no product other than roughage has yet been discovered which will prevent rumen parakeratosis.

Depending on the nature of the roughage, probably 10-15 per cent is necessary. Whether it is the physical qualities of coarseness, bulkiness or abrasiveness, or whether there is a lack of some metabolite not yet identified, has not yet been determined.

It should be remembered that these two approaches to the problem started from different basic feed types.

Clinical Signs

No particular clinical changes have been attributed to rumen parakeratosis alone. No altered efficiency of digestion has been found and no reduction of appetite has been related to the simple rumen pathology However, its close association with liver abscesses makes it undesirable.

Of course, deep ulcerative rumenitis might be expected to have systemic repercussions, but locally the scarring, depigmentation and devillation have not in themselves crippled a surviving animal (despite the popular image of a foundered beast when it is described as "burnt out').

Treatment

Complete reversal of rumen parakeratosis was achieved in 12 days by Cunningham et al (1969), who fed a high roughage mixture for various periods. Cure was rated on the suitability of the rumen wall to be cleaned for tripe.

Liver Abscesses

In 1954, Jensen et al published figures correlating abscessed livers with inflammatory lesions in the stomachs. After experimentally reproducing the disease by intraportal innoculation with F. necrophorus, Jensen suggested that penetration of epithelium by these bacteria occurred after erosion of ruminal villi by chemical irritation or foreign bodies.

Incidence

In the U.S., groups of heavily fattened cattle have recorded up to 95% of livers condemned for abscessation. Surveys have shown that 8% of all cattle slaughtered in that country have abscessed livers.

In Britain, up to 40% of "barley-beef" calves have been found affected. A feedlot in Australia recently reported 80% of individual lots of cattle with hepatic abscesses (Thompson, pers.comm.).

AETIOLOGY

Usually the abscesses take several weeks to develop after change over to a high concentrate ration, especially if the changeover had been too rapid or the ratio of concentrate to roughage too high.

Careful bacteriological investigations show nearly all abscesses to be infections with F.necrophorus, though a small per centage of other bacteria may be involved (Jensen and Mackey, 1965), notably some C. pyogenes in some Barley-Beef units (Rowland 1966).

It is slated by Rowland (1966), that the Barley Beef system in Britain is "sufficiently different from the feedlot methods of America, in respect of refinement of managemental techniques, to reduce considerably the insult to the rumen mucosa following the establishment and maintenance of these animals on high energy diets".

He could find no evidence of a direct relationship between obvious lesions of rumenitis and hepatic necrobacillosis, and felt that the aetiology was not so simple.

CLINICAL SIGNS

In the common chronic form, large numbers of 15-20mm diameter abscesses can be present throughout the liver substance without any detectable symptoms. However, a number of studies have been conducted in recent years demonstrating slower bodyweight gains in affected animals.

The following figures are quoted from Wise et al (1968):—

Daily Growth Rate of Cattle
Found Affected at Slaughter No Abscesses Found
Garrigus et al (1967) 1.13 kg/day 1.29 kg/day
North Carolina State University 1.10 kg/day 1.19 kg/day
North Carolina State University 1.19 kg/day 1.34 kg/day

Sporadic cases of the acute form of liver abscess disease occur during fattening, either from rupture of an abscess with subsequent peritonitis, or in the cases described by Jensen and Mackey (1965), from acute necrobacillosis of hepatic tissue resulting in hepatic insufficiency, jaundice and death.

PREVENTION

The use of antibiotics such as chlortetracycline and zinc bacitracin have been favourably reported on occasions. Other workers attempting to confirm such effects have repeatedly failed.

In the event of treatment being undertaken of cases of lactic acidosis, parenteral antibiotics would appear to be indicated to prevent liver abscesses.

The level of roughage required to keep rumen parakeratosis at bay has been mentioned and the prevention of pH drop by means of buffering agents also deserves consideration. A good measure of ground limestone in the ration is suggested for its antacid properties; and perhaps ½ per cent. magnesium oxide may prove useful under certain circumstances.

The extra limestone demands trace supplementation with zinc.

LAMINITIS

The appearance of laminitis or founder in cattle which have been on a high grain diet for a period is not uncommon. These animals are unable to maintain growth rates and actually lose condition to a marked degree if they are left in the same pen as healthy cattle. Often, if nursed along in individual pens, they may still gain weight slowly.

Generally the condition is irreversible and affected animals remain permanently crippled, hobbling around in a dejected fashion.

The syndrome is divided by Nilsson (1963), into 3 stages:—

Acute — The first 10 days.

Sub-acute — 10-45 days.

Chronic — After 45 days. (Nilsson 1963, quoted by Maclean, 1966).

CLINICAL SIGNS

(a) Acute Phase. The stance is fairly typical. The back is arched, the head is held low and extended, and the animal is not too willing to move. In all cases, all four feet are equally painful so that the beast wishes to walk on its heels. This means that all legs may be placed ahead of their normal position and the toes tend to point upward. Beeby (pers.comm.). describes forward movement as looking like walking on glass. Paddling may be a feature in the very early stages. Much time, however, is spent lying down, and if forced to rise, the animal does so clumsily. Muscular tremors may be seen. There may be sweating, respiratory rate may be elevated.

Heart rate is raised.

Appetite is normal.

Temperature is normal.

Rumenal movement is normal.

The feet are warmer than normal but this is difficult to detect. There is no change in the form of the hooves, but internally there has been severe congestion, haemorrhagic oedema and early deviation of the third phalanx.

It should be possible to feel an increased and powerful pulsation in the volar digital artery just above the accessory digits. Also the superficial veins of all four legs are distended. The most obvious are the volar metacarpal as it crosses the postero-medial aspect of the carpus, and the internal saphenous vein of the hind leg.

(b) Sub-acute Phase. General symptoms are somewhat less severe. In the sub-acute cases, the hoof has much the same appearance except for a deep transverse line just below the coronet which is obvious in comparison with the normal shallow transverse lines.

On paring the sole, there are signs of haemorrhage and discolouration in the horn tissue especially at the toe and at the heel-sole junction.

(c) Chronic Phase. Movement is very awkward. The feet become markedly overgrown. Transverse lines are well marked. There are signs of old haemorrhage in the feet horn and the sole. Internally the third phalanx has become deviated and atrophied and epidermal horn formation is altered. Pathological changes are described in detail by Maclean (1965 and 1966), who studied the disease in dairy cows and 4-6 month old "barley-beef" calves.

AETIOLOGY

Theories on the pathogenesis of laminitis involving sensitisation phenomena, mast cells and the mystical histamine are still surrounded with great confusion.

However, the aetiology appears to be associated in lot-fed animals with mild degrees of lactic acidosis. Ahrens (1965), quoted by Sanford (1966), found that the animals which foundered had shown few toxic signs of the engorgement syndrome. The rumen contents had developed an acidity of pH4-5 for 24-48 hours but the forestomachs had not lost their motility for long. Under these conditions histamine can be produced by an altered rumen microflora from protein sources in the ingesta, no doubt including the bacterial fermentation of killed microbes.

Maclean (1966), postulated that the continued motility allows the histamine to be carried on to the intestines for absorption.

Whether this is the correct explanation or not is open to argument. It should be noted that silage can contain quite high levels of histamine, Researchers have found a great deal of individual variation between animals.

DIFFERENTIAL DIAGNOSIS

Differentiation of laminitis from S.B.E., tetanus, ephemeral fever and traumatic reticuloperitonitis can present considerable difficulty at times.

TREATMENT

An energetic therapeutic regimen with antihistamines in the first 24 hours might be expected to block the progress of the disease, but once physical damage has occurred in the hoof it will progress to the chronic stage unimpeded. Antihistamines are indicated in all cases of mild to moderate lactic acidosis if laminitis is to be avoided. Although incidence of laminitis as a sequel is relatively low, it can be serious in individual outbreaks.

Phlebotomy has been used with success for acute cases of the disease, its action possibly depending on the stimulation of histaminase production. Corticosteroids are also good. The administration of normal rumen liquor to re-establish the microbial population is enormously helpful and should not be forgotten.

BLOAT

The complexities involved in the bloat-producing potential of foodstuffs are far from understood, and research has been directed more towards legume bloat than to the factors in concentrates. An example of the delicate physical properties in grain when it is foam producing is given by King (1966). He states that rolled barley should be rolled properly at a moisture content of 18% otherwise bloating occurs.

The rapid formation of a stable foam may result from an acid shift to pH 6, when carbon dioxide is evolved from fermentation and salivery bicarbonate.

Foam stabilisers in lucerne hay are also suspected to contribute where this is included in the ration.

ANIMAL FACTORS

Lindahl et al (1957), noted that quite marked differences existed between animals in their predisposition to bloat. They fed 20% soybean oil meal und 80% barley to 6 steers and regularly caused bloating in 3 of them. Ruminal atony was not responsible since the frequency of contractions was actually found to increase as the animals began to bloat.

Lack of roughage no doubt predisposed to the condition but was not the cause.

Bloat susceptibility is not necessarily inherited since it has been observed in pasture studies that there can be a significant difference between identical twins.

TREATMENT

Chronic severe bloaters in a feedlot are best treated with a small surgical fistula at the top of the rumen to protect them to slaughter weight.

Frequently the insertion of a stomach tube (through the nose) to deflate a bloated animal is all that is necessary, which means that much of the foam has broken down prior to attention being given. The presence of the stomach tube usually serves as an enticement to pump in a gallon of paraffin oil and some antiferments.

PREVENTION

Bartley and Meyer (1967), studied the protective value of poloxalene against feedlot bloat and deduced that 10 gm. per day afforded useful control. However, fistulated observations showed that even at 20 gm. per day, bloat foam was not completely eliminated. Therefore poloxalene can be used in the feedlot but it does not in theory afford the degree of control that can be obtained with its use with legumes.

VITAMIN A DEFICIENCY

It is now well recognised, that vitamin A is required in greater quantities by high-cereal diet animals. Spralling et al (1965), suggests that the critical level of vitamin A between health and deficiency is 40 i.u. per 100 ml. of plasma. However, it can be difficult in the field deciding if the vitamin A supplement provided is inadequate or not.

Tables have been published by various authorities but Jordan et al (1963), and others, claim that the standard recommendation e.g. 750 i.u. / lb. of feed; 25,000 i.u. per 1000lb. steer—N.R.C.) are grossly insufficient for grain fed or cereal silage fed cattle. The amount of vitamin A supplement that should be added has not been accurately determined because of varying rations and circumstances.

CLINICAL SIGNS

Reduced appetite is an early sign of avitaminosis A but papilloedema is of great diagnostic significance and has been described in detail by Spratling et al (1965).

These authors at Cambridge studied the syndrome in twin calves and found inappetence and therefore reduced growth rates to be an early symptom. Optic disc changes lead to night blindness and there is a change in demeanour, described as a "slouching posture", apathy, dull coat and pityriasis. In addition to these signs a wide variety of secondary effects can take place, understandable in terms of the vitamin's accepted role in maintaining the integrity of epithelia. These include lachrymation, keratitis, diarrhoea, coughing nasal discharge and notably a lowered resistance to parainfluenza 3 virus and pasteurella pneumonia, (Booth 1966).

An interesting symptom appearing on warm sunny days is an intolerance to heat manifested in high body temperatures and respiratory distress (Seawright 1966).

Also, a peculiar phenomenon mentioned by all these authors and not uncommon in lot-fed cattle is that of startling convulsive episodes.

Individuals or even groups of animals can become triggered by even minor stimuli into tonic convulsions like a fainting fit but associated with clonic movements and nystagmus of varying direction. The teeth may grind and death may appear imminent. However, after 30 seconds or so, the affected animal will rise and walk away in a dazed fashion.

TREATMENT

It has been recommended by Beeson (1965), that 3 million international units of vitamin A be given by intramuscular injection, but subsequently the oral route has been advocated as being more effective.

Even under the demanding conditions of high cereal diets, the liver storage of this dose should be enough to last 6 weeks.

Even with the deficiency overcome, repair processes are gradual. Spratling et al (1965), found that the demeanour, appetite and hair coat showed remarkable improvement within 10 days but the papilloedema regressed only slowly. Night blindness was still present at 123 days.

Vitamins A, D, and E are thought to be best in combination.

PREVENTION

Beeson (1965), recommends 1 million units of vitamin A to be given to feeder calves on arrival at the feedlot and a daily supplement of 30,000 i.u. to be included in the ration.

UROLITHIASIS

The propensity for urinary calculus formation in feedlot steers is partly explained by a couple of dietary effects of grain feeding. One is a urinary phosphate level for phosphatic calculi and the other is renal mucoprotein production for organic substrate.

AETIOLOGY

The genesis of uroliths is complex. It is believed that magnesium and ammonium phosphate ions are bound to mucoprotein to form a highly insoluble organic matrix. Cornelius et al in 1959 showed that mucoprotein in urine is significantly increased when there is a sudden change in nutrition from a roughage diet to high concentrate. Also, King (1966), observed a degree of renal necrosis in Barley Beef animals and Vasudevan and Dutt, (1969), demonstrated a relationship between vitamin A deficiency and calculus formation.

Tiny centres of organic matrix act as a nidus for the accretion of minerals. One type of calculus commonly formed is composed of silicates and these are characteristically irregular and spiny. Another type, moro likely to be found in grain fattened animals, are the phosphate stones which are usually smooth surfaced. These grow readily in the high urinary phosphate levels promoted by grain feeding. (Hoar et al, 1970).

CLINICAL SIGNS

Calculi as small as 2 mm. in diameter can become firmly lodged in the hypoplastic urethra of steers, often in the region of the sigmoid flexure. Abdominal pain is manifested, accompanied by unsuccessful efforts to urinate, a pulsation of the urethra at the ischial arch, and characteristic twitching of the base of the tail.

Incomplete blockage delays the progress of the clinical cause, and a small rupture of the bladder or upper urinary tract prolongs it. However, a large rupture of the bladder provides symptomatic relief and appetite is regained. Differential diagnosis of this event may present problems. Abdominal centesis is a useful aid. In the case of rupture of the urethra, diagnosis is simplified and prognosis is brighter.

TREATMENT

Some ingenious surgical approaches have been developed to salvage cases of both internal and external "water-belly" to get them to slaughter weight.

PREVENTION

Weaver (1966), quotes Crookshank (1963), as recommending 1.5 ozs. ammonium chloride daily in the concentrate ration for steers as an effected protection against the problem. Diuresis alone does not explain its preventive action. Probably the chloride ion displaces magnesium and phosphorus from the centres of nucleation.

Working with lambs, Hoar et al (1970), found that 2 per cent. ground limestone in the diet improved weight gains and reduced calculi formation.

The effect claimed was reduction of urinary phosphorous excretion. Ioar et al (1969), found that a low calcium to phosphorous ratio in the feed did not lead to a build up of urinary calculi unless the phosphorus content was high (around 0.55 per cent).

ABOMASAL DISPLACEMENT

Where recently calved cows are being grain fed to promote milk production or fertility to the extent that excessive acidity is produced in the rumen, the occurrence of mechanical displacement or torsion of the abomasum is greatly increased. More than 80 per cent of cases surveyed in New York State in 1967 were cows which had given birth to a calf within 30 days prior to the catastrophe. About 75% of the displaced a abomasa were displaced to the left.

AETIOLOGY

Svendsen (1969) and Svendsen and Stevens (1969), reproduced the disease experimentally by infusing 300 ml. of rumen fluid containing excessive volatile fatty acids, into the rumen of a cow. This appeared to decrease the abomasal motility. The researchers then insufflated nitrogen gas into the abomasum, which caused typical displacement of that viscus und the clinical course of the disease could then be followed. Under natural conditions large amounts of gas would be produced in the abomasum 5 hours after feeding 15 lbs. of concentrates, the escape of this gas into the forestomachs apparently depending on abomasul muscular activity

CLINICAL SIGNS

A useful list of clinical signs is given by Whitlock (1969).

The rapid loss of weight and fastidious appetite (won't eat grain), suggests acetonaemia except for the following points:

(i) Slab sided on the left.

(ii) Palpation in the left paralumbar fossa reveals a hollow area between rib and rumen.

(iii) Intermittent abdominal pain caused by painful contractions of the rumen against the dilated, gas-filled abomasum.

(iv) Variable faecal consistency,

(v) Ketone test gives moderate reaction.

(vi) If pinging sounds can be heard over the left rib cage, it tends to confim L.D.A. But may not hear it.

Right-sided displacement of the abomasum (RDA) is more difficult to diagnose. Abomasal torsion is uncommon and more likely to send the animal into shock.

TREATMENT

A popular non-surgical treatment is to turn the cow on her back with the feet tied together and then rocking from side to side in a 60 degree arc, finally allowing the animal to regain her feet from the left side. This together with intravenous calcium borogluconate is said to have a 65 per cent success rate.

Various surgical techniques have been described, one author claiming 95 per cent success.

REFERENCES

General

Blood, D. C. and Henderson, J.A. (1963). "Veterinary Pathology" — Baillieve, Tindall and Cox, 2nd edition.

Jensen, Rue and Mackey, D. R. (1965). "Diseases of Feedlot Cattle" — Lea and Febiger, 1st edition.

Jones, L. Meyer, (1965). "Veterinary Pharmacology and Therapeutics" — Iowa State College Press, 3rd edition.

Maclcan, C. W., (1969), Vet. Rec. 85:208.

Morris, J. G. and Dalby, J. M., (1968). Aust. J. exp. Agric. Anim. Husb.. 8:674.

Pryor, W. J., (1970), Aust. Vet. J., Annual Conference Handbook. 46, No. 1a, page 63.

Lactic Acidosis

Brawner, et al (1969). J.Anim. Sc. (sic)

Calhoun, M. C. and Skelton, N. (1969). J.Anim. Sci., 29:154.

Kay, M., Fell, B. F. and Boyne, R. (1969). Res. Vet. Sci., 10:181.

ROY, J. H. B. (1969). Proc. Nutr. Soc., 28:160.

Taylor, D. R, Hentges, J. F. Jnr., Neal, F. C. and Moore, J. E. (1969). J. Anim. Sci., 28:126.

Rumen Parakeratosis

Cunningham, J. F. Jnr., Anthony, W. R. and Starling, J. G. (1969). J. Anim. Sc., 29:155.

Rowland, A. C., Wieser, M. F. and Preston, T. R. (1969). Anim. Prod. 11:499 - abstr. Vet. Bulletin 40:No. 1859.

Wise, M. B., Harvey, R. W., Hoskins, B. R. and Barrick, E. R. (1968) J. Anim. Sci., 27:1449.

Liver Abscesses

Rowland, A. C. (1966), Vet. Rec. 78:713.

Thompson, D. B., Veterinary Officer, Dept. Agriculture, Wagga, N.S.W. Personal communication.

Laminitis

Ahrens, F. A. (1965), M.Sc. Thesis. Cornell University, U.S.A. — quoted by Sanford (1966).

Beeby, L. D., District Livestock Officer (Beef Cattle). Dept. Agriculture, Gunnedah, N.S.W. Personal communication.

Maclean, C. W. (1966). Vet. Rec., 78:223.

Maclean, C. W. (1966). Vet. Rec., 78:572.

Maclean, C. W. (1965). Vet. Rec. 77:662

Nilsson, S.A. (1963). "Acta Veterinaria Scandinavicu", Vol. 4, Suppl. 1., quoted by Maclean (1966).

Sanford, J. (1966c). Vet. Rec., 78:321.

Bloat

Bartley, E. E., Meyer, R. M. (1967). J. Anim. Sci., 26:913.

King, J. O. L. (1966). Vet. Rec., 78:902.

Lindahl, I. L., Davis, R. E., Jacobsen, D. R. and Shaw, J. C. (1957). J. Anim. Sci., 16:165.

Vitamin A Deficiency

Beeson, W. M. (1965) — "Feed Additives for Ruminants". Animal Nutrition Seminar, convened by Roche Products Ply. Ltd., Australia.

Booth, J. M. (1966c). Vet. Rec., 78:186.

Jordan, H. A., Smith, G. S., Neumann, A. L., Zimmerman, J. E. and Breniman, G. W. (1963). J. Anim. Sci., 22:738.

Seawright, D. (1966). Vet. Rec., 78:320.

Spratling, F. R., Bridge, P. S., Bernett, K. C., Abrams, J. J., Palaner, A. C. and Sharman, I. M. (1965). Vet. Rec., 77:1532

Urolithiasis

Cornelius, C. E, Moulton, J. E. and McGowan, B. (1959) Am. J. Vet. Res., 20:863.

Crookshank, H. R. (1963). Feedstuffs, 35 (44):28. Quoted by Weaver (1966).

Hoar, D. W., Emerick, R. J. and Embry, L. B. (1970). J. Anim. Sci., 31:118.

Hoar, D. W., Emerick, R. J. and Embry, L. B. (1969). J. Anim. Sci., 29:647.

King, J. O. L. (1966). Vet. Rec., 78:902.

Lamberth, J. L. (1969). Aust. Vet. J., 45:223.

Udell, R. H. (1962). Am. J. Vet. Res., 23:1241.

Vesudevan, B. and Dutt, B. (1969). Ceylon Vet. J., 17:26.

Weaver, A. D. (1966). Vet. Rec., 78:824.

Abomasal Displacement

Svendsen, P. (1969). Nord. Vet. Med. 21 Suppl. 1 - abstr. Vet. Bulletin. 40:No. 3031.

Svendsen, F. E. and Stevens, C. E. (1969). Fedn. Proc., 28:324.

Whitlock, R. H. (1969). J. Am. Vet. Med. Ass., 154:1203.


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