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Simon Choi (Veterinary student, University of Sydney), Anon, Erika Bunker (State Veterinary Laboratory) and Bruce Watt (Tablelands Livestock Health and Pest Authority, Bathurst)

This paper was first published in Skirting the Issues, the Official Newsletter
of the Australian Sheep Veterinarians, Spring 2012 edition
Posted Flock & Herd December 2012


Sheep poisoned by phalaris (Phalaris aquatica) present with several entities. The first, a sudden death syndrome occurs within 48 hrs of exposure to phalaris and can be further differentiated into 'cardiac-sudden death' and 'polioencephalomalacia-like sudden death.' The second entity is a nervous syndrome known as 'phalaris staggers' (Gallagher et al 1964, Bourke et al 1987, Bourke et al 1990, Bourke 1995, Finnie et al 2011). 'Staggers' is a term used to describe a neurological disorder characterised by an unsteady stumbling gait (Rending et al 1976). The neurological syndrome can take either a sub-acute form from which recovery is possible, or may present as a chronic, degenerative disease.

This is a report of phalaris staggers affecting only the lambs from a mob of first cross ewes and lambs that occurred on an Andesite derived soil (regarded as low risk), with deaths continuing to occur for seven months post exposure and clinical signs for eight months.


The owner of a mob of 349 mixed age Merino ewes marked 347 first cross autumn lambs on 18 June 2011 and placed the mob into phalaris dominant paddocks for five weeks (5 August 2011 to 10 September 2011). On the 10 September 2011, a lamb was seen with signs of phalaris staggers and consequently the mob was moved to a cocksfoot/clover dominant paddock the next day (11 September 2011) where they remained until weaning on the 5 October 2011. Several more lambs had developed moderate symptoms by weaning. From weaning until 13 November 2011, lambs had grazed on pasture containing red grass (Bothriochloa spp.), subterranean clover (Trifolium subterraneum), soft brome (Bromus mollis) and small amounts of phalaris and lucerne (Medicago sativa) except for 2 weeks where lambs were run on a relatively new pasture containing some phalaris. By 22 March 2012, phalaris staggers affected 58 lambs. Of the 58, 31 died and 27 clinically affected lambs were either sold or retained. The total number of deaths can be seen in Table 1. Clinical signs of progressive neurological disease continued to arise in lambs for approximately 7 months after exposure to phalaris.

Chart of cumulative lamb deaths
Table 1. Cumulative deaths in lambs since initial exposure on 5 August 2011
Chart of total lamb deaths
Table 2. Deaths from phalaris poisoning over time. Limited observations occurred between
20 September 2011 and 5 December 2011, therefore the 10 deaths reported on
5 December 2011 are a cumulative total of deaths between
20 September 2011 and 5 December 2011
In summary, after initial exposure from the 5th of August 2011:
Table of dates of lamb deaths

It can be seen that clinical cases arose for seven months after initial exposure to the phalaris dominant pasture or six months after the first case was seen.


A clinically affected 11-month-old first cross lamb was examined on 3 May 2012. The lamb was bright, alert and responsive with a body condition score of 3/5. The lamb showed proprioceptive deficits (knuckling) in both front limbs and hind limbs, which was more pronounced in the hind limbs. A short, stiff and 'proppy' hind limb gait was evident in addition to the animal displaying a wide based stance. Patellar reflexes appeared normal. The lamb had soil in its mouth and nostrils. Clinical signs were exacerbated when the animal was forced to move and when stressed it frequently collapsed, remaining in sternal recumbency. The owner (EL) noticed affected animals head shaking and trembling early in onset of disease, although this was not seen on 3 May 2012. Cranial nerve responses were normal and the lamb had normal conscious perception and mentation.

Image of lamb abnormal posture
Figure 1. an affected lamb


Following euthanasia and necropsy, the brain was submitted for histopathology. No abnormalities were detected in the necropsy examination except for a few Haemonchus in the abomasum. Histopathology of the brain revealed brainstem pigment deposits consistent with phalaris intoxication in addition to mild multifocal chronic non-suppurative meningoencephalitis. Single sarcocysts were also present, embedded without reaction in the parenchyma of the medulla and midbrain.


It is well known that intra-ruminal cobalt bullets prevent phalaris staggers (Lee et al 1957). On properties that regularly experience the problem, routine cobalt administration is appropriate. However, during the spring and summer of 2011-12, phalaris staggers was seen outside its normal distribution (Watt 2011). Phalaris staggers has not been seen previously on the property subject to this outbreak. Its occurrence was therefore difficult to predict and prevent.

This outbreak only affected lambs either at foot or post weaning. No ewes were affected despite the same or greater exposure to phalaris. During outbreaks of phalaris staggers, it is usual that some classes of sheep are affected while others are not. Young and recently introduced sheep are most at risk. On properties subject to intermittent outbreaks in susceptible classes of livestock some form of risk assessment is worthwhile, to enable to most cost effective administration of preventative measures.

While the clinical and histopathological findings support the diagnosis of phalaris staggers, it is possible that Sarcocystis infection caused the multifocal chronic non-suppurative meningoencephalitis. Kessell et al (2011) excluded Sarcocystis from the protozoa that cause significant CNS infection in Australian ruminants. Elsewhere, Uggla and Buxton (2007) also considered that they normally do not cause clinical signs. Nonetheless, sarcocystosis has been reported to cause brain pathology and central nervous signs in sheep including hind limb weakness, ataxia, trembling, generalised paresis, anorexia, weight loss and death generally within seven days of onset of clinical signs (Buxton 1998). However, definitive diagnosis involves the presence of schizonts in the CNS endothelium in association with nonsuppurative inflammation (Fitzgerald et al 1993).

There is some evidence that clinical neurological disease caused by sarcocystosis has occurred in Australia. Dubey et al (1989) reported a case of a 3-week-old lamb with neurological signs and microscopic lesions and schizonts consistent with Sarcocystis tenalla in the brain and spinal cord. More recently two 18-month-old Poll Dorset rams from a property in NSW showing progressive neurological signs were diagnosed with sarcocystosis; they had a non-suppurative encephalitis, and while no protozoa were noted in the brain there were abundant sarcocysts in the heart muscle (Bunker, unpublished data 2012). Confirmed clinical cases are rare in Australia while there is a high prevalence of infection without clinical disease.

Phalaris is well known to cause delayed onset clinical signs. Bourke et al (1987) investigated outbreaks of phalaris staggers in the Orange district of NSW between 1981 and 1996. Affected sheep were divided into two groups; those with an acute syndrome characterised by sudden development of neurological signs with absent microscopic changes in the CNS and those with a chronic syndrome characterised by the gradual development of neurological signs with the presence of characteristic microscopic changes in the CNS. Only until several weeks after the sheep had ceased grazing phalaris did animals with chronic phalaris toxicity (staggers) develop clinical signs. A study of 180 weaned lambs grazing on phalaris found a delay of more than four months between the cessation of grazing phalaris and the first appearance of clinical signs. In some sheep, clinical signs were found to persist for up to five months after they had been removed and placed on phalaris free pasture (Bourke et al 1987).

The risk of phalaris toxicity is influenced by the pasture composition. Flocks grazing phalaris pastures that contained an appreciable proportion of lucerne had no staggers at any time and the study concluded that phalaris staggers only occurred when phalaris was consumed almost exclusively, either from choice or because of the lack of alternate grazing. The sheep in this case were placed into paddocks that were either dominated by phalaris or comprised of phalaris during its most toxic rapid growth phase.

Phalaris has been found to be most toxic during rapid growth (autumn and winter) and when placed under environmental stress. Under field conditions, studies have found that the hazard from phalaris decreases as the plant matures. However, this may be because other species dilute the phalaris or because they contain more cobalt (Lee et al 1956, Rending et al 1976, Bourke et al 1987).

Several other plant toxins have been found to cause limb paresis and knuckling in sheep. These include Romulea rosea (onion weed), Stachys arvensis (stagger weed), Trachyandra divaricata (branched onion weed) and Tribulus micrococcus (yellow vine or spineless caltrop) (Bourke, 1995). Continued ingestion of caltrop (Tribulus terrestris) has also produced neurological disorders in sheep delayed in onset by up to nine months (Bourke et al 1987).

Variations in soil cobalt status may explain some of the variability in the incidence of phalaris staggers on different farms. Studies have shown that the cobalt status of a particular soil is strongly correlated with the cobalt status of the parent rock from which it is derived (as seen in Table 3).

Table of rock types
Table 3: Cobalt status of different rock types (Bourke 1998)

Bourke (1998), in his examination of phalaris staggers on farms within a 50km radius of Orange NSW found a significant positive correlation between soil cobalt levels and outbreaks of phalaris staggers. He did not record any outbreaks of staggers on basalt derived krasnozems and euchrozems, which have high cobalt levels. This outbreak occurred on a red podsolic soil (Lawrie pers. comm.) which although Andesite derived, has from moderate to very low cobalt levels (Bourke 1998).


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