On 18th April, 1950, the writer was called to investigate a mortality occurring in sheep on a soldier settler's farm near Quirindi, in the Tamworth District. The area of the holding is approximately 600 acres, about half of which consists of creek flats and the remainder gently undulating country. The farm was being used for fat lamb raising in conjunction with wheat growing; and had at the time, although not fully improved, a carrying capacity of about one ewe to the acre.
The flock was in very good condition and consisted of 530 crossbred sheep, of which 470 were two and four-tooth ewes, mated early in March, to Dorset Horn rams, and 60 lambs about seven to eight months old. There were also two rams still running with the flock. The ewes were October shorn and had been dipped about four weeks prior to the commencement of the mortality. The lambs were dipped at the same time, straight off shears.
On 12th April the owner noticed the first signs of sickness. Three ewes were affected and these died later in the day. The sheep then were moved to another paddock some two miles away; on an adjoining property. On 15th four ewes were found dead. From then on over the next two weeks the mortality rate was very high. On 16th about 20 more died and there were several sick. On the 17th, thirty died and a large number were sick. On the day the investigation commenced a further thirty died and several were sick. The mortality rate continued at a high level, and when the next visit was made to the property, on 21st, 160 sheep in all had died. Between that date and 27th a further 55 were lost. The last death occurred on 10th May; and altogether 250 sheep had died over a period of 28 days. The mortality was confined to the ewes; neither the lambs nor the rams being affected.
Mention should be made at this stage of the seasonal conditions prevailing prior to and during the mortality. Over January and up to the middle of February, 1950, about six inches of rain were registered, and pastures were good. A dry period followed and no worthwhile rain was received until 5th April, when three inches were registered in two days; causing flooding on the lower part of the property. Towards the latter end of March pastures had deteriorated, but Oxalis corniculata—Yellow Wood Sorrel was the dominating plant in the pasture of Paddock A, where the flock was running. Following this rain seasonal conditions were excellent and many other plant species appeared.
Paddock A, where the sheep had been running until 5th April, consisted of approximately 200 acres of fallowed land with a creek frontage. When flooding occurred in this paddock the flock had to be moved to higher ground (Paddock B) and there it stayed until the first deaths occurred. It was considered early in the mortality that weed poisoning was responsible. In Paddock A, Yellow Wood Sorrel was very prevalent, but it was only a secondary plant in Paddock B. This plant was incriminated as causing some type of oxalic poisoning, and as the losses were occurring in the ewes only, the condition was thought to be associated with pregnancy. However, the absence of mineral imbalance and failure to respond to calcium and magnesium therapy, together with the negative post-mortem and early laboratory findings, tended to disprove this theory. Nevertheless, subsequent histological examinations clearly indicated that the deaths were due to uraemia; most probably brought about by the ingestion of the suspected plant.
The first sign noticed was that affected sheep walked with a stiff, proppy and unsteady action. Later they became cast and remained on their sides, unable to rise; with legs rigidly extended. Using reasonable force the hind legs could not be flexed and the forelegs only with difficulty. The head was retroflexed, and when the animal was picked up the body was as rigid as a board. The general appearance was not dissimilar to that seen in the last stages of tetanus. The animals responded to external stimuli, and additional rigidity was caused by noise or tapping of the body or legs. There was some degree of trismus and the jaws could be opened only slightly. There did not appear to be any evidence of blindness. Movement of the membrana nictitans was slow. Frothing at the mouth and a discharge from the nose was observed. Respiration was rapid, 130-140 per minute, and stertorous—could be heard some distance away. Temperature varied from 102°F. to 104°F. The pulse rate was shallow and difficult to count, averaging 80-100 per minute. Defaecation appeared to be normal. Sickness early in the mortality lasted about two to three days; later the symptoms were not so pronounced and often affected sheep lived for several days before death supervened. According to the owner no affected animals recovered.
During several visits paid to the property numerous post-mortem examinations were held. In addition, two autopsies were made on sheep forwarded on different occasions to Glenfield Veterinary Research Station. None of the post-mortems revealed any marked abnormalties. In animals destroyed, it was noticed that the blood was dark and clotted quickly. The contents of the rumen were dry as the animals had not drunk for some time. Mucous membrane of the small intestine appeared to be slightly congested. The abdominal blood vessels were distended. The first portion of the large intestine contained a clear, slimy mucus. The kidneys and liver appeared to be slightly congested. Brain and spinal cord did not reveal any gross abnormality, and there was not an excessive quantity of cerebro-spinal fluid present. All ewes examined were in lamb; about one to two months. In one post-mortem held by the writer and one at Glenfield the foeti showed multiple subcutaneous petechial haemorrhages.
Early in the mortality it was thought that mineral imbalance might be the condition affecting these sheep and the owner was requested to give injections of calcium borogluconate. About twenty sheep were treated; each receiving 90 mls. of a 25% solution, with some receiving 180 mls. Two of these sheep were given, in addition, 45 mls. of a 20% magnesium sulphate solution. Although it was thought that a slight improvement followed in some, this was not maintained and they all ultimately died. To confirm these results and eliminate the possibility of mineral imbalance, the writer administered intravenously calcium and magnesium to seven sheep. Little, if any, improvement in the condition resulted and the sheep subsequently died. Similar treatment was tried at Glenfield on the sheep submitted, with no response.
Hypoglycaemia also was considered as a possible cause, but intraperitoneal injections of 20% glucose–90 mls. to one animal and 180 mls. to another—were administered with no beneficial effect.
Botanical examinations of rumen contents from three sheep did not reveal any known poisonous species. Oxalis corniculara was not identified in the contents due to the fact that the flock had been removed from Paddock A, where the plant was prevalent, to Paddock B, where only occasional plants occurred. Also, eleven days had elapsed after moving the sheep before the first rumen contents were secured for examination.
On 1st May, Mr. K. Mair, Senior Botanist of the Department of Agriculture, inspected the property and made a comprehensive plant survey. This was carried out 19 days after the mortality commenced, and 25 days after substantial rain had changed the pastoral outlook. The list of species identified is far too lengthy to mention here. but his comments about "Yellow Wood Sorrel" should be quoted. "Oxalis corniculata was prevalent on the river flats (this is Paddock A), but occasional only on the high ground (this is Paddock B). It occurred in all stages of growth. Mr. Harding had considered this species potentially troublesome, and had a specimen in his office when I arrived there, and confirmed his identification of the plant. There is so little of it where the sheep are grazing now that it was not possible to observe whether it was being eaten to any extent."
At Glenfield Veterinary Research Station a very comprehensive and detailed examination was made of an extensive range of specimens submitted. These examinations were more or less duplicated by the Director of Veterinary Research, on material obtained at the Station from live sheep forwarded for examination. The ingesta was tested for strychnine, HCN, nitrate and nitrite with negative results. Bowel contents and smears did not indicate that the mortality was due to Entero-toxaemia. Bacteriological examination of material from lung, heart, liver, spleen, kidney, cerebrum, cerebellum and foetal heart did not reveal any organisms of significance. Transmission experiments in sheep, guinea pigs and rabbits with material from various sites of the nervous tissue and abdominal organs, failed to set up the condition. The bacteriological examinations and transmission experiments proved conclusively that, the condition was not due to a bacterial or virus infection, and that the condition was not related in any way to any form of infection.
Serum Analysis.—Analysis of serum samples submitted by the writer from six sheep showed a range of calcium levels from 8.7 mgm % to 10.6 mgm % and of magnesium from 2.1 mgm % to 3.5 mgm %. A sample secured at Glenfield, from a sheep submitted, revealed a calcium level of 9.8 mgm % and magnesium of 1.7 mgm %. These levels are for total blood calcium and magnesium and, being within the normal range, appeared to discount any suggestion of mineral imbalance. However, it is probable that the amount of diffusible calcium in the blood was below normal values in these cases, but the estimation of calcium in this form was not then possible at Glenfield. Unfortunately, at the time estimation of blood urea could not be made at Glenfield. These probably would have shown high values; as is expected in poisoning by Oxalis corniculara.
Urine Analysis.–Two urine samples also were examined, with the following results:—
|Sample 1||Sample 2|
|Reaction to litmus||Acid||Alkaline|
|Rothera Test||Weak Positive||-|
|Oxalate in Sediment||Approx. 0.5 mgm.||-|
|Acetone Bodies||Strongly Positive||Positive|
There was a noticeable, whitish deposit in Sample 1, which showed the acid reaction. This appeared to be mainly ammonium urate, with approximately 0.5 mgm of calcium oxalate.
The presence of the acetone bodies in the urine was not thought to have any actual significance, so far as the cause of the mortality was concerned. It was considered that they may have been the result of starvation or failure to eat for a certain period (sheep had been affected for three days when samples were secured), as circumstances such as these will result in the complete metabolism of fats.
Technical difficulties existed preventing accurate determinations of the total oxalate content in the urine. It is known that small, amounts of oxalic acid are normal constituents of urine, and although the amount of calcium oxalate recovered from the acid urine was only small, it was probably significant, in view of the difficulty that existed in obtaining an accurate estimation.
Histological.—The histological examination proved most enlightening and clearly indicated that the death of these sheep was due to uraemia. Macroscopically, from examinations in the field there were no outstanding changes in the kidney. This was contrary to the findings of Bull (1929), who investigated oxalic poisoning of sheep due to another of the Oxalis spp, known as "Soursobs"–Oxalis cernua—and found on post-mortem that the kidneys were small and white. The histological report from Glenfield proved most interesting and is quoted: "The kidneys in all cases from the Quirindi mortality revealed an extensive disseminating necrosis, which appeared to commence in the cortex in the region of the glomeruli and extended from the convoluted and straight tubules to the medulla. This led to complete kidney dysfunction, giving rise to uraemia and subsequent death."
At the same time as the Quirindi investigation was in progress, another small mortality occurred near Tamworth. Two merino ewes died out of a mob of 200. One ewe only was examined, but according to the owner other the had exhibited similar symptoms before it died two days previously. The clinical picture was exactly similar to that seen in the cases at Quirindi. These ewes were also pregnant, probably about two months. Post-mortem examination did not reveal any marked changes and the kidneys appeared normal. Serum calcium and magnesium levels were within normal range. The growth of Oxalis corniculata was very prevalent in the paddock where the flock was running.
In South Australia, Bull (ibid) reported "Poisoning of Sheep by Soursobs". The condition he describes is very similar to the mortalities reported here. The main points of similarity noted were:—
(1) Only pregnant ewes affected in the mortalities investigated by the writer and losses almost entirely restricted to this class of sheep in the condition described in South Australia.
(2) Symptoms—stiff gait, rigidity, tetanic spasm and trismus.
(3) Total blood calcium estimations were within the normal range.
(4) Histological examination of kidney showed extensive damage.
The main points of difference were found on post-mortem examinations:—
(1) The kidneys were small and white in most of the South Australian cases, but these macroscopic changes were not evident in the mortalities in the Tamworth district.
(2) The observations by Bull of effusions into the serous cavities were not seen.
(1) It is concluded that Oxalis curniculata was responsible for the death of 250 out of 470 ewes.
(2) Only pregnant ewes were affected, probably due to the fact that some metabolic disturbance associated with pregnancy renders them more susceptible. This may be bound up with the call on the calcium reserves of the body to supply the requirements of the lambs.
(3) Total blood calcium and magnesium levels were not changed.
(4) Calcium and magnesium therapy did not effect any improvement.
(5) The animals showed symptoms of tetany and marked damage to the kidneys. The damage to the kidneys was not visible macroscopically.
(6) Following the ingestion of Oxalis corniculata, deaths may result some days, or even weeks, after the plant has been eaten; while it appears that the ingestion has to be over a period for harmful effects to occur.
Grateful acknowledgement is made to Mr. A.N.A. Harris, D.V.O., Armidale, for his co-operation in the investigation of this mortality, and his permission to use information contained in official papers; as also for the assistance given by the Director of Veterinary Research and his staff in carrying out the laboratory examinations.
Bull, L.B. (1929)—Aust vet. J., 5:60.