Phalaris aquatica with its numerous cultivars is a much-valued perennial grass species widely used in improved pastures across south-eastern Australia. However in certain circumstances, it does have the potential to become a toxic pasture plant, producing a variety of unrelated syndromes which manifest either as neurological or cardiac disturbances, presumably involving different toxins. The poisonous potential of Phalaris aquatica is dynamic and is a function of interacting plant, animal, environmental and management factors. Currently it is generally accepted that there are three distinct syndromes: chronic phalaris staggers, cardiac sudden death and ‘PE (polioencephalomalacia)-like’ sudden death, although recent evidence suggests that PE is not involved in the latter syndrome and a urea cycle disorder has been proposed.
This neurological syndrome results from the repeated or protracted ingestion of methylated tryptamine alkaloids present in P.aquatica. The compound accumulates in the CNS to directly interact with serotonergenic receptors in the motor and sensory nerve nuclei of the brain and spinal cord. This causes a functional rather than structural nervous derangement, which is demonstrated by the clinical signs being precipitated with disturbance of the flock. Animals are paretic, ataxic, have a generalised muscle tremor including head nodding and jaw champing. They display incoordination and proprioceptive deficits with frequent falling over. Some lack the ability to rise and may appear hyperaesthetic and struggle when approached. Knee-walking is frequently seen and the animals may ‘bunny hop’.
Cardiorespiratory signs can be seen with the nervous forms of intoxication, probably due to the increased effort and strain on the cardiovascular system due to the nervous incoordination, rather than any direct effect of the toxin on myocardial function The affected animals remain conscious throughout, however if recumbent for a prolonged period, may become comatose and develop cerebral convulsions. Death or recovery can occur over the ensuing weeks or months, depending on the chronicity of ingestion and the severity of clinical signs. Clinical signs can develop as soon as 1-3 weeks following the introduction to the pasture especially with the older, high tryptamine cultivars. However, with the new, low tryptamine varieties such as Sirolan, much longer periods of grazing (3-4 months) may be needed to induce staggers (Bourke et al 2003) plus a delay in development of clinical signs can occur even after being removed from the incriminating pasture, with cases developing up to 3-4 months later.
Gross pathology may reveal a green-grey discolouration of the lateral geniculate body in the brain and brainstem, with this discolouration also sometimes seen in the renal medulla. Characteristic histopathological lesions include intracytoplasmic brown pigment granules in the nerve cell bodies of the brain sections, being most concentrated in the lateral geniculate body. Wallerian degeneration may also be seen associated with the white matter (axons) of the brain and spinal cord. These lesions can usually only be detected in cases greater than several weeks duration (Bourke et al 1988).
There is no effective treatment, but animals should be immediately moved to phalaris-free pastures. Protection against this form of intoxication via intraruminal Cobalt bullets has proven protective as ruminants are able to detoxify the toxin when intraruminal Cobalt (Co) levels are high enough to match the toxic challenge. It is advised that two bullets are given to prevent a calcium carbonate coating building up around the bullet, which would decrease effective absorption of Co. Intraruminal grinders are also available for this purpose. Two bullets should be given every three years. Alternatively, top dressing the pasture with Co or individually drenching each sheep so a minimum of 28mg per head per week is given will allow potentially toxic pasture to be grazed with no adverse consequences (Blood et al 2000).
The cardiac from of sudden death form on phalaris pastures involves a sudden onset of a cardiorespiratory disorder without neurological signs. The toxin responsible is unknown, although it is considered that ruminants are able to detoxify this toxin provided it is not ingested too rapidly or in excess (Bourke et al 1988). To produce the signs seen, the toxin must act either on the cardiorespiratory centres in the medulla oblongata or on the vagal nerve endings as they innervate the heart. Toxic levels of cyanide (20mg or greater/100g of hydrocyanic acid) have been measured in phalaris plants from toxic pastures (Bourke & Carrigan 1992), thus a cyanogenic poison has been investigated.
Nitrate compounds have also been postulated as the causative agent as it has been documented that phalaris pastures can attain nitrate nitrogen concentrations >2920μg/g, with the potentially toxic concentration for sheep only 1000μg/g (Bourke & Carrigan 1988). It has also been noted that the incidence of this form of phalaris sudden death may be associated with seasonal increases of N-methyltryamine in P.aquatica (Bourke et al 2003).
Outbreaks can occur as soon as 24 hours following introduction to the pasture, however in some reports sheep had been grazing the toxic pastures for 2 weeks before outbreaks occurred. The clinical course of the disease ranges from minutes to hours; clinical signs being induced by flock disturbance or when the animals are forced to exert themselves. Cardiac disturbances include ventricular fibrillation and cardiac arrest, followed by syncope. The animals suffer from respiratory distress, their mucous membranes becoming cyanotic. Most affected sheep die, however some may spontaneously recover. As mentioned, no nervous signs are seen with this form of phalaris poisoning, nor are there any obvious gross or histopathological lesions. The prevalence is usually about 1%, being much lower than seen with cases of PE-like sudden death (Bourke & Carrigan 1992).
Again there is no treatment and stock should be removed immediately from the paddock with as little stress as possible to avoid eliciting further mortalities. Once moved, there should be no more new cases. Intraruminal Co administration is not preventative for these cases. The incidence of cardiac sudden death syndrome does appear to be greatest during the first few months of new growth, typically autumn to early winter (Bourke & Carrigan 1992): thus it is wise avoid grazing phalaris dominant pastures during this period.
‘PE-like sudden death’ involves an acute onset of neurological signs and death that differ greatly from those of phalaris staggers. The animals display ataxia, decreased awareness, cerebral blindness, aimless walking and head pressing and often die in and episode of cerebral convulsions with opisthotonos. No disturbance is needed to precipitate the clinical signs. The greatest mortalities occur within 48 hours following the introduction to the pasture, with the highest incidence of disease seen during autumn through to late winter. The noxious pasture is only poisonous for several weeks during this season though.
As with cardiac sudden death, the toxin responsible for this condition is unknown. Suggestions include agents known to produce thiamine-deficient PE in sheep such as thiamine antagonists (thiaminases) or amine co-substrates. A pyridoxine antagonist has also been suspected. However more recently a mechanism involving hyperammonaemia due to the causative toxin interfering with the urea cycle has been proposed. This postulated pathogenesis simulates citrullinaemia seen in Holstein-Friesian calves and was initially suspected because of the identical histopathological lesions seen in sections of cerebral cortex submitted from Citrullinaemia (Harper et al, 1986) and PE-like phalaris sudden death cases. The lesion seen is diffuse spongiform change involving astrocytes and sparing neurones, the latter being affected in thiamine-deficient PE. Elevated levels of ammonia levels in aqueous humor of these cases is similar to that seen in plasma in Citrullinaemia, suggesting compromise of the urea cycle in PE-like phalaris sudden death.
There is no treatment or consistent method of preventing outbreaks of ‘PE-like’ sudden death. Investigations into prevention have included prophylactic administration of thiamine and pyridoxine. This was based on the idea that the causative toxin, as mentioned above could be some form of thiamine or pyridoxine antagonist. The study in question failed to demonstrate any protective effect of these substances, however did not completely dismiss the possibility of their use for prophylaxis. This was based on a number of reasons outlined in the paper such as the rate of action of the toxic antagonistic agent was too rapid for the dose administered of the prophylactic agent (Bourke et al 2003).
‘PE-like’ sudden death outbreaks occur more commonly when hungry stock are put on phalaris dominant pastures that have been spelled or involved in rotational grazing where an abundance of new shoots has been available. The toxic potential of phalaris pastures also seems to increase when rain has followed a period of moisture stress.
Therefore it is advised that the phalaris pastures are continuously grazed or set-stocked to keep the new growth during autumn/winter to a minimum, and that hungry sheep should not be placed on previously spelled phalaris dominant pastures, especially not following periods of moisture stress or heavy frosts. From autumn through to late winter it may be wise to test the toxic potential of a paddock by placing a group of sentinel sheep onto the paddock 48 hours before the entire flock is given free access. If no clinical cases have been seen within this time, the pasture is generally considered safe, and it is assumed that the animals can adequately adapt to the toxic challenge.
The poisonous potential of phalaris pastures is dynamic. It has been proven that the level of noxious alkaloids responsible for the chronic staggers syndrome are increased during certain periods, this being influenced by interacting plant, animal and environmental factors. As the toxins responsible for the other conditions remain unknown, there has been speculation on associations between increased incidence of outbreaks and these interacting factors. Increased alkaloid content in the foliage of P.aquatica has been measured during periods of moisture stress, frost conditions and decreased light intensity, such as overcast weather or shading. Fertile soils such as those nitrogen-enriched with leguminous plants, or fertilised with superphosphate have also been found to have higher levels of the tryptamine alkaloids.
New shoots are also more concentrated sources of the toxic alkaloid, with poisonous potential of the pasture rapidly declining after it has reached a certain height. The new cultivars such as Sirolan and Sirosa are lower alkaloid strains than older varieties such as Holdfast. Other potential risk factors include s the soil type, with limestone soils inherently low in cobalt and associated with increased incidence of phalaris staggers. Basaltic soils are high in cobalt and hence staggers is not common in areas where these soils dominate. It appears that animals have the ability to adapt to the toxic agent across the spectrum of disease syndromes. Animals that are newly introduced to phalaris and those with alterations in feed intake, as occurs in cell grazing systems, are considered at greater risk of intoxication.
Consideration of these risk factors suggests that producers should aim to avoid putting hungry stock on freshly-shooting phalaris dominant pastures, especially following periods of frosts or moisture stress. If the stock have been transported or yarded for a period of time without access to food, they should be fed before being placed on the pasture. Continuously grazing or set-stocking pastures to keep new growth at a minimum especially during the autumn and winter months may assist. Intraruminal cobalt bullets are also an effective measure to protect against Phalaris staggers, and allow potentially toxic pastures to be utilised and grazed. It is important to remember however that they serve no purpose in the prevention of the other forms of toxicosis. As the phytotoxins responsible for the acute poisonings are yet to be identified the only way to prevent the occurrence of acute intoxication is to adhere to the management strategies that have been proven to be sound over many years.
Additional information is available in more recent reviews (Finnie et al 2011; Alden et al 2014)