The first evidence of an unusual problem was a phone call from a worried ratepayer, Wednesday, November 7, 1990, in the late afternoon, informing me that a number of his cows were taking fits.
On arrival at the set of yards in which the cattle were held all previous ideas regarding exaggeration were quickly dispelled as I saw more than one fully mature stud cow perform an almost complete somersault.
The owner had a small Hereford stud and 40 of his top stud cows were in the yard. All cattle were affected in one way or another, ranging from severe violent convulsions to standing still with fine muscle tremor. Ultimately not one of these cows survived.
It was apparent by this time that the problem was paddock and pasture related and was probably a toxin of unknown origin.
The recent environmental history, prior to spring 1990, was unusual in that there were three wet winters between dry summers, the winter of 1990 being very wet.
This rare seasonal pattern resulted in the winter dominance of blown grass (Agrostis avenacea) which is normally a minor species restricted to the bottom of swamps and table drains.
A generalised neurological dysfunction characterised by a wide based stance, disturbed equilibrium, ataxia. In some cattle these symptoms progressively increased before the onset of convulsions. The slightest stimulus could result in the most severe convulsions.
Animals at rest did not necessarily seek shade. On close examination many animals displayed a fine skeletal muscle fasciculation.
Cerebral convulsions were spectacular involving opisthotonos, extension of thoracic limbs and flexion of the shoulder resulting in a goose stepping gait. The forelimbs would collapse resulting in the beast falling heavily onto its brisket, shoulder or head. If the balance was sufficient they would complete a somersault and land heavily on their back.
Many would continue to convulse on the ground and display various degrees of opisthotonos, tetanic spasm, paddling, head weaving, fasciculation of skeletal muscles, salivation and frothing of the mouth, jaw champing, various involuntary eye movements, snorting, retraction of lips and rapid laboured respiration.
Profuse sweating was obvious and rectal temperature was raised (>40°C). Violent convulsions resulted in much bruising and traumatic damage particularly to eyes and eye sockets, briskets, shoulders and pelvis.
The duration of the convulsions was highly variable with the beast returning to near normality between events. The severity and frequency of convulsions was not a good indicator of the prognosis for the individual animal. Many died without showing any signs of convulsing.
Most gross PM signs were secondary as a result of the violent activities of the affected cattle. They were variable non-specific, and not present in all individuals. The most consistent were lacerations, oedema and bruising of the sub cutis and musculature of the brisket, pelvis, shoulder and head.
ther variable symptoms were petechial haemorrhages, oedema and congestion of abdominal mucosa.
Later cases were showing fatty and friable livers, icterus and haemorrhage of epicardial and endocardial surfaces.
The initial samples submitted to the Armidale Veterinary Laboratory were unremarkable. There were mild liver and brain changes only.
Increased levels of aspartate transaminase, creatinine kinase and gamma-glutamyl transferase were consistent with the presence of liver muscle and central nervous dysfunction and reflected the generalized nature of the intoxication.
Further submissions were made over the next week but did not provide any relevant information.
The search was targeted at a toxin of either bacterial or fungal origin. The active toxin in ARGT is a tunicaminyluracil-based toxin produced by bacteria (Rathayibacter toxicus) but fungi also produce similar toxins. There was no shortage of rotting vegetation and fungi. Samples of rotting vegetation were examined by Dr Chris Bourke without success.
A growth was noted growing on the Coolah grass (Panicum sp) in many areas. Samples were sent to University of New England botany department for identification. These were identified as acrostomata typical of Nigrocornus scleroticum. Feeding trials conducted by Dr. Allan Seawright could not reproduce toxic symptoms in mice.
It was not long before the research effort was across four states and involved a number of institutions such as State Departments of Agriculture, Universities and CSIRO.
Dr. Wayne Bryden of University of Sydney was able to reproduce the symptoms in a feeding trial using material from the Bogan river area. This concentrated the research effort on blown grass (Agrostis avenacea).
Dr. Allan McKay of the Waite Institute in South Australia requested samples of blown grass for investigation. Dr McKay identified the bacterial galls as Rathayibacter toxicus and the toxin was identified by Dr. John Edgar of CSIRO at Melbourne.
This effort has established that flood plains staggers (FPS), Stuarts range syndrome (SRS) and annual rye grass toxicity (ARGT) are identical toxicological syndromes with different host grasses and nematode vectors.
There is no practical treatment. By the time the clinical signs appear it is too late.
The only control option in extensive conditions would be to move the herd/flock to a known safe paddock.
The success of this really depends upon the circumstances at the time. In the 1991 case the distribution of blown grass was defined in the Bourke area which allowed the movement of affected herds and flocks to known safe areas.
The Moree situation was different in that the distribution of blown grass was much more widespread and not all of it was affected by the toxic galls.
The presence of the galls is not always obvious in extensive conditions. I advised the owners to move cattle out of the affected paddocks. This was an unfortunate and unpopular move as the cattle dropped in greater numbers when disturbed. The ‘clean’ paddocks were not safe as cattle began to die in them also, this combined with the fact that there was a shortage of feed on these properties, made any further suggestions difficult.
Eventually by trial and error we did eventually succeed in finding safe paddocks but only after more losses. The shifted cattle will continue to die for up to eight days after they are removed from a known toxic paddock so we had to wait that long before we knew if a paddock was safe or not.
Early January 1991, the deaths stopped with the advent of sufficient rain to rot the seed heads to the point that cattle could not pick them up. The period of toxicity in the Bourke area was much longer as they did not get the January rain.