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This article was published in 1939
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By D. J. WALKER. B.V.Sc.

Stock Inspector, Narrabri Pastures Protection District.

At the end of November and beginning of December, 1938, mortality occurred in two mobs of travelling sheep on the stock route near Millie, sixteen miles west of Bellata.

The first was in a mob of 1800 wethers in strong store condition and of mixed ages which had travelled for the preceding sixteen miles at least, on a fairly well watered route carrying a fair body of dry, much weather-beaten herbage, composed largely of Lambs Tongue (Chenopodium atriplicinum), and Medicago and Trifolium species, and over which distance the sheep had not had access to green feed other than a little Mimosa (Acacia sp.), and Oxalis corniculata, which has only been found growing thickly in one other place here and was again on heavy black ground which was a low ridge.

The sheep came on to the area where the feed was growing in profusion and was green and fresh. The dinner camp was made on the plant and by night there were many sick and a number dead. Mortality continued for three days after first coming on to the area, and when they left it 48 hours after arriving the loss was 170, and during this time they had travelled about six miles.

A second mob, 2700 Merino ewes, came on to the plant at midday at the same place and then travelled over half a mile of the plant to the dinner camp. Some became affected on the camp, and within a short time after moving, between 40 and 50 were down. They travelled for about a mile and a half over the plant at right angles to the route taken by the first mob but still on the Oxalis, with a very small amount of Yellow Vine (Tribulus sp.) in addition but no Acacia sp. This mob as well as the other were affected before watering, and each had travelled about a mile from the last water before coming to the green feed.

Early next morning, about 18 hours after first eating the plant, between 170 and 180 were scattered dead along a mile and a half of stock route. The following morning, 40 hours after first eating it, there were 240 dead and a further ten or so died within the next two days.


Earliest symptoms were not observed personally, but were stated to be a slight trembling and a trembling, staggering gait. When down, they were on their briskets with their necks outstretched along the ground. They were depressed. Dead sheep lay in the same position as live sick sheep. Though the posture was similar to sheep affected with hypocalcaemia, they did not show the same tendency to have the hind legs stretched out behind them. No scouring or evidence of it was observed. Quite a large number assumed other varied postures, such as on their sides with the legs outstretched, and on their briskets with the head to the side. In the second mob, about thirty per cent. were in the position associated with hypocalcaemia.

No tetanic spasms or inability to use hind or forelegs only was seen, such as are recorded by Bull (1) in cases of chronic poisoning by Oxalis cernua, and in his cases the sheep were also bright.

Post Mortem Findings.

The liver was considered to be slightly greasy (histologically the change was found to be cloudy swelling and early congestion) and the gall bladder was distended.

Before opening the intestines and abomasum, it was seen that they were congested. On opening, the congestion was found to be comparatively slight, and a piece of mucous membrane two inches long and half an inch wide was shed in one sheep. Near the pylorus the congestion was more marked. The congestion of the small intestine was still more marked than in the abomasum but was not thought sufficient of itself to cause serious ill-effect. The mesenteric lymphatic glands were considerably enlarged and oedematous. The rumen was full of what appeared to be Oxalis sp., the ingesta in the ileum was thicker in consistency than usual, and the faeces were hard and dry.

The serous surfaces of the heart, thoracic and abdominal cavities were apparently normal. The lungs were quite normal and the heart rather flaccid.


Glenffeld Research Station's report on specimens forwarded was most interesting. No organisms were detected in any of the pipettes from spleen, liver, kidney, blood, pancreas, or mesenteric lymphatic glands.

Estimation of calcium and magnesium in blood serum showed 2.7 mgm. per 100 ml. for magnesium, which is approximately normal, whilst calcium was 7.3 mgm. per 101 ml., which is about 25% below normal. It is interesting to compare these figures with those recorded in Grass Staggers of sheep by Blumer, Madden and Walker (2), in which there is a hypocalcaemia and a hypermagnesaemia which is possibly of a compensatory nature.

Unfortunately, the estimations may not give a true indication of the amount of diffusible calcium, and some appreciable quantity of the insoluble oxalate is probably included in the figure for calcium.

The kidneys, which had been macroscopically normal, were pathologically significant. To quote verbatim from the official report: In the case of the kidney, very interesting changes were observable in the cortical zone. Some of the glomeruli were contracted, whilst the epithelium of the convoluted tubules was necrotic, and in several places had desquamated. Collection of crystals were apparent throughout the whole of the conical zone and in close proximity to the convoluted tubules. The presence of these crystals was associated with deposition of fibroplastic tissue suggesting that they were definitely exerting an irritant effect. No crystals were discernible in the straight tubules. Although it has not been established diagnostically, it will be seen that these crystals were very probably calcium oxalate formed as a result of a reaction of the oxalic acid formed from the plant and the calcium in the blood serum.


Because of the similarity in symptoms in Grass Staggers of sheep, it was thought that intravenous administrations of calcium gluconate was worth trying. Three sheep were given 30m1. of a ten per cent. suspension of this salt. (It was carried dry and mixed in a cup with water when required). One of these showed no improvement, but the other two became brighter but were still unable to walk. A much better response might reasonably have been expected if the condition had been an uncomplicated hypocalcaemia.

In the second mob, ten were given calcium gluconate injections intravenously and showed improvement as in the previous mob. About a dozen were drenched with a pint of milky suspension of slaked lime in water, and died fairly rapidly. About 15 others were drenched with a pint of limewater; according to the owner, the majority of these recovered. These 15 were not so severely affected as the others. Some, not treated, also recovered, but according to the owner, limewater was beneficial.


Bull (1), in cases of chromic oxalic acid poisoning due to Oxalis cernua, found an average content of 10.16 mgm. per 100m1. He arrives at the conclusion that the cases in which tetany is present are due to an alkalosis from the reaction of sodium and potassium oxalates with the calcium salts of the serum. The ionised calcium salts, removed in this way from the blood as a diffusible component, are replaced from the calcium reserves, and the continuation of this reaction leads to the accumulation of the soluble alkaline salts of sodium and potassium. Damage to the kidney has probably in most cases been sufficiently extensive to interfere with the normal function of correcting the mineral balance by excreting the excess. Consequently, it is considered that the poisoning is due not to the acid property of oxalic acid, if it should happen to be present in any quantity in this form, but to the oxalate radicle.

Rek (3) found in oxalate poisoning in pigs that the addition of calcitun hydroxide to the food, which was sugar-beet leaves, prevented poisoning. When poisoning had already occurred calcium therapy was of no value, but magnesium hydroxide subcutaneously or intravenously showed good therapeutic effects. Just why this should be so is not understood.

Read (4) states that the oxalate is present in Wood Sorrel (Oxalis acetosella) as potassium hydrogen oxalate, which is only slightly soluble in water. It would be most likely that in Oxalis corniculata it is present in a similar form.

Attempts at treatment were all undertaken more than twenty-four hours after the plant was ingested, and it is considered probable that early drenching with limewater would prevent most of the losses in such cases as have been described.

The short period over which loss occurred, and the still shorter period which elapsed between ingestion of the plant and the evidence of symptoms, is in marked contrast to the cases of Oxalis cernua poisoning recorded by Bull (1) in which losses began from seven to eight weeks after coming on to the pasture, sick sheep taking up to a month to succumb, though mostly were found dead.

It should be borne in mind that one lot of sheep were paddocked and the other travelling. Here no losses occurred in the paddocked sheep, probably due to the fact that the paddocked sheep had access to much larger areas in which there was some scattered green feed and a considerable amount of roughage.

In one case of sheep paddocked near the stock route where losses occurred, T. Isbister, B.V.Sc., Stock Inspector, Pilliga, investigated and was of the opinion that the trouble was probably due to the Oxalis corniculata which was growing in the paddock. In a specimen of serum forwarded, a hypocalcaemia and a hypermagnesaemia were found.

Two days later a visit was paid to the property, when the owner stated that the sick sheep examined were the same as had been effected previously. The sick sheep examined were not thought to be suffering from Oxalis poisoning in the same form as seen in the larger mortalities.

In symptoms and post-mortem lesions they were identical with those seen in an outbreak of Salmonella infection, and this was confirmed by bacterial examination of pipettes of blood, liver, etc. The total loss was only 17 sheep out of 1700.

The grounds for assuming the toxicity of Oxalis corniculata are:

1. The plant was eaten under circumstances almost amounting to a feeding test.

2. Kidney lesions were found to be very similar to those encountered in poisoning due to Oxalis cernua.

3. Symptoms were what might have reasonably been expected, the toxic principle being assumed to be an oxalate in this and other species.

4. Two other species of Oxalis are recognised as being poisonous, namely, Oxalis acetosella and Oxalis cernua.


The history, symptoms and lesions on sheep assumed to be suffering from acute poisoning by Oxalis corniculata are outlined.

Attempts at treatment are outlined, and although no definite results were obtained, it is considered that early drenching with calcium hydroxide would be of considerable value.

The mineral balance in discussed, in agreement with Bull (1), who found that an algalosis exists, and it is considered that death is due to this.

The reasons for considering the plant to be toxic are set out.


I have to thankfully acknowledge the permission of Mr. C. C. Blumer. B.V.Sc., District Vet. Officer, North, and Mr. W. L. Hindmarsh, B.V.Sc., M.R.C.V.S., D.V.H., the Director of Veterinary Research, Glenfield, for permission to use information contained in official reports in the preparation of this paper.


  1. Bull, L. B. (1929), Aust. Vet. J.—5 : No. 2, p. 60-69
  2. Blumer, C. C., Madden F. J. and Walker D. J. (1939)—Aust. Vet, J., Vol. XV., No. 1, p. 24-27
  3. Rek. L. (1934), Zverolek Obz. 27. Abstracted in Veterinary Bulletin
  4. Read. J. (1930), "Textbook of Organic Chemistry." G. Bell & Sons Ltd., London


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