INTRODUCTION
The drought in the Moree area over the last 4 years has been characterised by a much greater than normal incidence of plant poisoning causing loss of livestock.
Most cases have been the usual grazing of fallow containing Yellow Vine (Tribulus terrestris) and Pigweed (Partulaca spp.).
The large numbers of half-starved travelling stock using the fallowed paddocks as relief have been a cause of some large losses, particularly of sheep.
The following case history is an example of the type of losses incurred by graziers endeavouring to save their starving stock.
The prime call on this case was to a private practitioner on 22nd June, 1980. The practitioner conducted an autopsy but as the losses had been high and the cattle were still dying at a rapid rate a call was made to the Armidale Regional Veterinary Laboratory for assistance.
A Veterinarian from the Armidale R.V.L. picked me up on the following morning and with the private practitioner we proceeded to the scene of the disaster.
CASE REPORT
The cattle affected were a mob of 460, 10 mth. old store condition Hereford and Shorthorn steers of which 48 had died by the time we had arrived and quite a number appeared very sick.
A recent history of the movement of these cattle was as follows:-
The cattle had spent a month in a failed sorghum crop on a nearby property and, according to the Manager, did extremely well on it. From there the mob was moved to another property nearby to a similar crop which was substantially eaten out after 2 weeks so for the next fortnight the cattle were shepherded during the day on the adjoining travelling stock reserve and locked up in the crop paddock at night. Finally, the cattle were taken out onto the travelling stock reserve to return to their home property, this trip took 3 days to complete.
The first losses were noted on Wednesday, 18th June, 1980, with 3 deaths followed by a further loss of 2 hd. on Thursday, 19th June, while the cattle were on their way back to their home paddock via the travelling stock reserve. No deaths were recorded on Friday, 20th, but this was followed by 18 deaths on Saturday, 25 on Sunday, 20 on Monday and 16 on the Tuesday, after which no further losses occurred, although a large number of cattle were showing clinical signs.
Affected cattle were depressed and lethargic when approached, would become excited and aggressive usually charging and stumbling at anyone approaching, when they deteriorated the ataxia became more obvious and they frothed at the mouth. The cattle would stagger about on their feed until finally when they went down they would last only a few minutes in lateral recumbency. Death occurred within hours of the first clinical signs.
The post-mortem signs of note were a generalised jaundice with a very pale yellowish liver and kidneys, marked epicardial haemorrhage and scattered haemorrhages in the omentum and intestine. The rumen contents were noted as grass, shrubs, prickly pear, belah and wilga leaves. The wilga leaves were later found to be the Myoporum deserti leaves.
Histopathology of note was marked centrilobular and mid-zonal necrosis with varying degrees of bile duct proliferation.
The post-mortem and histopathology indicated an acute hepatotoxin and considering the mouldy state of the sorghum grazed 3-4 days previous to the first deaths, a tentative diagnosis of aflatoxacosis was made.
A sample of the sorghum remnants were sent to Yarongpilly Animal Research Institute in Brisbane for identification of fungal growth and possible presence of aflatoxins. The results indicated a number of harmless fungi but no known toxic fungi especially Aspergillus flavus.
The stomach contents were forwarded to the herbarium for identification and it was this that provided the information required for the final diagnosis. The report identified a large amount of Myoporum deserti leaves in the rumen contents. These leaves had previously been mistaken for Wilga leaves at the time of the post-mortem.
With this information to go on, the Regional Veterinary Laboratory sent some liver sections to Queensland University where the lesions were identified as being pathogmonic of M. deserti poisoning.
With this information, a final diagnosis of Myoporum deserti intoxication was given.
Myoporum deserti
Much branched erect shrub 1-4m high, the branches thin, greyish-brown and usually beset with small warty swellings. Leaves alternate thick, narrowly oblanceolate or lanceolate, 205 cm long, 3.6mm wide, narrowed into a short stalk. Flowers white bell shaped about 8 mm long, with 5 rounded lobes, borne singly or in groups of 2-4 on slender drooping stalks, 5-10 mm long in the leaf axils. Fruit a more or less globular yellow drupe, about 6 mm in diameter. Flowering winter/ spring.
Distribution
Found in all mainland states mainly in inland regions, growing in a majority of soils mainly sandy loams, loams and clay loams such as poplar, box, brigalow or gidyea communities. There is quite a concentration on the travelling stock reserves between Morse and Goondiwindi and throughout the northern Warialda Pastures Protection District.
Poisonous Principle
A combination of eleven furanoid sisquiterpenes which do not occur in toxic amounts in all races of M. deserti. Of the nine (9) races identified, five (5) races are toxic, two (2) are apparently non-toxic and a further two (2) have not been tested for toxicity.
Almost all recorded field cases of poisoning have been in sheep and cattle on travelling stock routes. Animals grazing in the paddock eat the plant readily and apparently without ill affect. No definite correlation has been established between the appearance of the plants and their toxicity or otherwise.
In cases of poisoning there is generally delayed action and animals often remain unaffected until 2-3 days after eating it. A drink of water often hastens the onset of symptoms.
No therapeutic treatment is known to be effective so advice to avoid the general area with hungry stack, if possible, is the only practical advice to give.
Ref:
Poisonous Plants of Australia, 2nd Ed. Selwyn L. Everist.