In 1942 Ian MacDonald, a Veterinary Pathologist of the Institute of Medical and Veterinary Science Adelaide, reported a ‘staggers’ syndrome in sheep and cattle associated with grazing on Phalaris aquatica (formerly P. tuberosa).
This report discussed classical Phalaris Staggers as we now know it and in very similar circumstances, that is when stock, especially sheep, grazed pastures that consisted almost entirely of Phalaris during the early stages of growth following the first rains after a dry summer.
He reported that if stock were noticed at an early stage and quickly moved to a fresh pasture containing no phalaris, their nervous condition soon improved and complete recovery occurred in a few weeks. If, however, when symptoms were not noted until the disease was well established then animals were more severely affected, recovery was very slow and deaths were frequent.
It was also noted that many properties had developed pastures with phalaris dominance and never noted any problems.
There were no reports of the more acute syndromes recognised more recently.
In 1948 Le Souef (of Department of Agriculture NZ) reported classical Phalaris Staggers in sheep on the South Island of New Zealand in very similar circumstances i.e. induced in a Phalaris pasture freshly growing after autumn rains following a dry summer. In this instance 20 ex 100 were affected in May. These animals did well if left undisturbed, but still displayed staggers when moved when examined in August.
The disease was reported in the New England by Bill Southcott in 1956. He reported on a property south-west of Armidale, on which Phalaris was planted in 1947 and grazed in 1948 and 1949 without problems. In 1950 Phalaris had become dominant and Phalaris Staggers was noted in Merino weaners.
This is the first report of Phalaris Staggers in the New England I can find, despite the fact it has been grown here since M & F J White ‘Saumarez’ Armidale planted it in 1908.
Staggers occurred in similar circumstances, ie dry autumn followed by May rains and staggers appeared about a month later. The pasture was 41% fresh Phalaris 3% Sub Clover and 56% frost damaged dry Couch Grass (Cynodon dactylon) which was not eaten by sheep in the presence of fresh green Phalaris. Experiments were carried out on sheep on this plot in 1950-1953.
The death rate/recovery rate was as follows:
|Year||Affected||Recovered||Died||Did not recover|
A general conclusion was that those animals that recovered were least affected. In this case animals were maintained on the Phalaris plots constantly so recovery would not be directly related to exposure.
G Green Armidale Rural Lands Protection Animal Health Ranger was at Chiswick Pastoral Research Station from 1968 to 1997 and reports that following good autumn rains in the years 1982 and 1984 following dry summers Phalaris Staggers occurred and although he removed most affected ones to a hospital paddock with no Phalaris, many died and very few recovered.
According to CA Bourke there is good experimental evidence to suggest that Phalaris incoordination syndrome is caused by the ingestion of methyl tryptamines and the beta-carbolines known to occur in the plant. He suggests the methyl tryptamines are clinically very active, but probably less persistent in their effects than the beta-carbolines. Beta-carbolines, although present in relatively small amounts may play a significant role because of their apparently cumulative and persistent neurological actively.
It is generally reported that young plants are more toxic and Staggers commonly occurs when stock have excess to lush new growth. Bourke has suggested that the amount of toxin in higher in new growth. This typically occurs after long dry summers followed by good autumn rains. The alkaloid content may be higher with high soil nitrate or in shady or cloudy conditions.
The fact that it occurs on some properties when many other neighbouring properties have similar pastoral conditions suggests other external factors such as soil type may play a part in initiating the condition. Bourke has suggested that occurs in soil conditions if low cobalt and or high manganese levels and that limestone, sandstone and granite associated soils pose the greatest risk and basalt soils the least. This may explain why in New England the condition is relatively rare as for the most part Phalaris is planted on basalt soils. Bourke also suggests there is a temperature effect with available cobalt being lower in cold conditions.
Recent outbreaks of the ‘sudden death syndromes’ reported in Victoria were due to the cultivar Holdfast. However, Bourke has reviewed cases across Australia and found the cultivars are Sirolan, Holdfast, Sirosa, Australian and Sirroco, all cause problems at some time.
The clinical signs appear only when animals are disturbed. Initially there is hyperexcitability and generalised muscle tremor, including nodding or turning of the head. On moving the limbs movements are stiff and the hocks are not bent, causing dragging of the hind feet. Incoordination and swaying of the hindquarters follow. There is a variation in the clinical signs displayed by affected animals. Some cases walk on their knees, others bound or hop, others knuckle at the fetlocks. In more severe cases animals collapse into lateral recumbency which is accompanied by paddling movements of the legs and irregular involuntary movements of the eyeballs. There is rapid respiration and irregular tachycardia. Sheep will usually recover if left undisturbed and walk away apparently unaffected. The condition of individual sheep and may worsen especially if left on pasture and animals become recumbent and suffer convulsive episodes until death.
The clinical course varies from days to weeks to months in duration. The onset of staggers may follow weeks of grazing or several months of grazing, or it may be delayed until weeks or months after animals have ceased grazing Phalaris dominant pastures. Recovery or death can occur over the ensuing weeks or months and some remain permanently affected.
In cattle, the signs may be restricted to stiffness of the hocks and dragging of the hind toes, but severe cases similar to the common syndrome in sheep also occur. Additional and more common signs observed in cattle include an extraordinary incoordination of the tongue and lips in prehension so that the hungry animal, trying desperately to ear, can only prehend a few stalks of grass at a time. The jaw movements are quite strong, but the tongue stabs and darts and lacks the sinuous curling movements normally present. There may also be an inability to put the muzzle to the ground so that prehension can only be affected from a raised manger or hayrack. Affected cattle are often hyperexcitable and difficult to handle and may crash through fences and gates when handed.
No gross lesions. There is characteristic green/grey pigmentation of tissues in the renal medulla, brainstem and mid-brain. This is thought to be merely indicative of the groups on neurones affected by the Phalaris alkaloids rather than being the cause of the clinical signs. The dysfunction that generates the nervous signs affected livestock is probably biochemical rather than anatomical.
Animal tests — nothing pathognomic.
Plant material — tests for causative tryptamines are not generally available.
Move off Phalaris pasture slowly and with care and hope for the best.
It is suggested that Cobalt administration will prevent the ‘staggers’ syndrome but not other forms of Phalaris Poisoning. Cobalt has to be given orally (ie parental administration is not effective) at a dose rate equivalent of 28mg/week at intervals of not less than a week. Additional Cobalt can be given by spreading it on pasture mixed with fertiliser. I can find no records of it having been carried out in New England, except Southcott who trialled it in the 1950’s with some suggestion that it prevented staggers.
The concept of breeding for Phalaris Cultivars with low contents of tryptamines is made unfavourable by the fact that such selection favours a significant increase in toxic Beta- carbolines and the ‘low alkaloid’ cultivars are potentially poisonous as older varieties.
The association between the ‘staggers’ and the plants should suggest the diagnosis. The appearance of these signs only on exercise is significance. Diagnostic confirmation tests require demonstration of causative tryptamines in feed materials.
Differential diagnosis list for incoordination:
McDonald, I W (1942). A ‘Staggers’ Syndrome in Sheep and Cattle Associated with Grazing on Phalaris tuberosa. AVJ 18:132-189.
Le Souef, H D (1948). Poisoning of Sheep by Phalaris tuberosa. AVJ 24:12-13.
Southcott, W H (1956). Observations on Phalaris Staggers in Sheep. AVJ 32:225-228.
Watson, R W, McDonald, W J A, Bourke, C A (2000) Phalaris Pastures. Agfact 5.1. NSQ Agriculture.
Green, G (2005) pers com.
Bourke, C A (1992). Toxins in Pasture Plants — Phalaris Toxicity Proc.Aust.Soc.Anim.Prod. 19: 399-402.
Bourke, C A, Carrigan M J and Dixon R J (1990). The Pathogenesis of the nervous syndrome of Phalaris aquatica toxity in sheep. AVJ 67: 336-358.
Bourke, C A, Rendell, D and Colegate S M (2003). Clinical Observations and Differentiation of the Peracute Phalaris aquatica Poisoning Syndrome in Sheep known as ‘Polioencephalomalacia — like sudden death’. AVJ 81:698-700.
Bourke C A, (1998). Factors affecting the incidence of PE ‘sudden death’ form of Phalaris aquatica poisoning in sheep. In Proceedings of the Ninth Australian Agronomy Conference. Australian Society of Agronomy, Wagga Wagga pp326-329.
Bourke C A (1994). The clinico-toxicological Differentiation of Phalaris spp Toxicity Syndromes in Ruminants. In Plant Associated Toxins CAB International pp523-528.
Radostits, O M, Gay, C C, Blood D C and Hinchcliff K W (2000). Veterinary Medicine, Ninth Edition, L B Saunders pp1651-1653.