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This article was published in 1967
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INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.

Suspected Sodium Fluoroacetate Poisoning in Sheep and Cattle

J. W. PLANT, B.V.Sc., Veterinary Inspector, Gundagai

Introduction

Sodium fluoroacetate (1080) is now used extensively as a poison for rabbits. The common method of use is to mix it with carrot and spread this as trails. These trails are usually covered after the rabbits have had access, and mortalities seen in sheep have been associated with the residue of poisoned carrots in the trail.

At the dose rate commonly used, and using the Minimum Lethal Dose expressed by Meldrum and Bignell (1957), a 70 lb. sheep would have to eat 2 oz. of poisoned carrots, and a 700 lb. cow 1.5 lb. of poisoned carrots, to cause death. This is presuming that the Minimum Lethal Dose for sheep and cattle is the same. No figures were given for the Median Lethal Dose for sheep or cattle by the above authors, but figures given for other animals would suggest that they are much lower than the Minimum Lethal Dose.

Two cases were seen in the Gundagai district in 1965, long after the stock had had access to the poisoned carrot, and these cases were associated with the stress of driving the stock. The two cases discussed below showed a marked similarity to Georgina River Poisoning which has been reported by Bell et al. (1955), Barnes (1958) and also by Whittem and Murray (1960). It is known that the toxic principle in the Gidyea tree, the cause of Georgina River Poisoning, is the fluoroacetate ion. The two cases described below are thought to be due to ingestion of small amounts of sodium fluoroacetate over a period of time.

Details of Mortalities

Property 1

This property was in the Batlow area and was first visited on March 24, 1965, following a reported mortality of two breeding cows in a herd of 40 cows with some calves at foot.

The cattle were running on dry improved pasture with some bracken fern and some rock fern. There were a lot of weeds present in the gullies and some St. John's Wort.

The paddock was poisoned with "1080" on February 10, 1965, along a trail with some broadcasting. The weather was very hot and dry, and no carrot was seen by the owner three weeks later, at which time the cattle were put into the paddock (approximately March 3, 1965). No deaths had occurred in the cattle before they were put into the paddock, and none occurred while they were in the paddock.

The cattle were moved out of the paddock on March 20, 1965, and three cows were left behind, refusing to travel, with two of the cows going down. These two cows both went down suddenly, and were left alone. One cow was trembling and shaking and lay on her side: she was observed only for two to three minutes and left where she lay. The cow died in this spot and was found two days later. The second cow went down in sternal decubitus, and was also seen to be trembling. She was found dead, approximately half a mile away, two days later. The third cow appeared normal when inspected two days later.

The first cow to go down was examined 24 hours after death and very little post-mortem decomposition was seen. The only lesions found were slight enteritis, localised in a small part of the jejunum, and excess blood-stained pericardial fluid. The heart was not examined closely for any evidence of lesions in the myocardium. No carrot could be found in the rumen. No specimens were taken from this cow.

No deaths occurred in the cattle that were moved out of the paddock and the cow left behind was not moved until March 31, 1965, when she was moved quietly up to the cattle yards, which were approximately one mile away. She was put into a crush and was hit with a stick, by the owner, to force her into a truck. She went down, and died within five minutes. Symptoms described by the owner in this case were:

She went down on her knees first and started to tremble.
She then went over on her side and there was some struggling with kicking of the legs.
Breathing was very irregular.
The eye-ball rolled right back in the socket.

This cow was examined approximately four hours after death.

Findings were:

No evidence of any muscle haemorrhages.
Slight abdominal distension with some froth coming from the nostrils.
The jugular vein and the subcutaneous vessels were all distended and under marked pressure.
The liver appeared normal, the kidneys were slightly congested.
The intestines were normal, except for some four to six feet of ileum which were inflamed and haemorrhagic with some briar seeds present. The ileum distal to this was contracted and there was some slight enteritis with creamy contents suggestive of that seen with enterotoxaemia.
The heart was contracted with some petechial haemorrhages on the epicardium. Excess straw-coloured pericardial fluid was present.
The lungs were congested.
The brain showed some congestion.

Specimens were submitted for examination which proved negative for enterotoxaemia, HCN and nitrate. Sections of brain, liver and kidney showed no significant findings, but sections of heart muscle showed a few small foci of fibrous tissue replacement in one section.

No losses occurred in the other cattle on the property after this mortality.

Property 2

This adjoins the first property, and here the mortality was seen in sheep. There were 700 aged Merino wethers running on similar country to the previous property. No losses were seen until the sheep were moved into a paddock which had been poisoned with "1080" a week before.

The carrot had been laid in trails and when the sheep were put into the paddock no carrot could be seen on the trail. The weather had been very hot and the carrot would have dried and shrivelled.

The first losses occurred two days after the sheep were put into the paddock. Fifty sheep were found dead and the remainder were moved out of the paddock. Another eight sheep died while they were being moved from the paddock; the sheep running out of the mob and dying suddenly in convulsions. Further losses occurred after this and were associated with movement of the mob. A further 50 sheep died over a period of eight weeks from the time they were originally placed in the poisoned paddocks. No losses were seen from March 16, 1965, to April 8, 1965, when the sheep were put back in the poisoned paddock. This was 11 weeks after the paddock had been poisoned, and no losses occurred in the first three days subsequent to April 8, 1965. However, when the owner went to move the sheep out of the paddock three sheep went down and refused to travel. When seen two days later two of the sheep were dead and the third sheep was still alive.

Further deaths occurred in the mob every time the owner moved them, the sheep dying very suddenly.

The only symptoms seen by the owner were sheep which died in convulsions, or other sheep which trembled and then died. In all cases death occurred shortly after symptoms were first seen.

In some of the later deaths the owner noticed that the sheep, were breathing very rapidly before they died. Inspection of the sheep in the mob revealed apparently normal sheep when seen from a distance. The sheep, when driven, went down within 40 yards and when examined showed a slow, irregular respiratory rate and tachycardia. The conjunctival vessels were injected. An affected sheep was taken to the shed, shorn, put in a paddock and observed when it showed a deep irregular respiration. This returned to normal after ten minutes and the manager when contacted that night stated that the sheep appeared normal.

Two sheep were examined post-mortem on the property and examination of these sheep revealed the following:

No post-mortem decomposition.
The intestines appeared normal apart from some inflammation of the caecum, and some congestion of the intestines.
The liver and kidneys appeared normal although there was evidence of previous fluke infestation.
The pleural cavity of both sheep showed excess pleural fluid with congestion of the lungs.
The heart of each sheep showed some petechial haemorrhages of the epicardium, and some inflammatory areas in the myocardium together with pale fibrous areas suggestive of scar tissue.
Other organs appeared normal.

Examination of heart muscle at Glenfield Veterinary Research Station revealed mild interstitial oedema, congestion and scattered small foci of fibre necrosis with inflammatory response.

Discussion

In both of these mortalities losses were experienced long after the stock had had access to the poisoned carrot. The clinical picture matched that of Georgina River Poisoning of cattle as described by Barnes (1958). When the mortalities were being investigated, the work done on the Gidyea had not been seen and a complete examination of the heart muscle was not carried out. However, there is every reason to believe that over a period the stock had been eating small amounts of the dehydrated carrot bait that was lying in the trail.

Whittem and Murray (1963) administered small amounts of potassium fluoroacetate daily to stock and were able to produce cardiac lesions. By giving small amounts of potassium fluoroacetate, insufficient to kill the animal immediately, they were able to produce a typical cardiac histopathology. This was seen even in animals which died after receiving only two treatments one day apart.

Heart muscle from only three cases in these mortalities were submitted for examination and in each of the three cases there were lesions in the heart muscle on histopathological examination. These lesions were similar to those reported in Georgina River Poisoning.

Summary

Two mortalities involving sheep and cattle are described. These mortalities showed symptoms very similar to those described for Georgina River Poisoning, where the symptoms and mortality are due to the action of the fluoroacetate ion on the myocardium.

These mortalities were associated with the suspected ingestion of small amounts of carrot poisoned with "1080" over a period of some weeks.

Histopathology revealed lesions resembling those which have been described following dosing of sheep with small amounts of fluoroacetate ion.

Acknowledgements

It is desired to acknowledge the assistance of the Director of Veterinary Research, Glenfield, and Miss Joan Kater in carrying out the histopathological examination of the specimens submitted.

References

Barnes, J. E. (1958) — Aust. Vet. J. 34:281

Bell, AT, Newton, L. G. Everist, S.L. and Legg, J. (1995) — Aust. Vet. J. 31:24

Meldrum, G. K. and Bignell, J. T. (1957) — Aust. Vet. J. 33:186

Whittem, J. H. and Murray, L. R. (1963) — Aust. Vet. J. 39:168