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Sudden death caused by phalaris in some ewes

J Rogers, DVO, PIRSA, Bremer Rd, Murray Bridge, SA and Dr Effie Lee, Veterinary Pathologist, Gribbles, SA

Posted Flock & Herd May 2019


This producer has a small farm in the Mt Pleasant area that he visits most days, as he does not live on the property. One Saturday morning in late November he visited to find 15 Dohne ewes dead and one moribund. Local vets were unavailable to assist in a timely manner.

The initial suspicion was a poisoning event when the moribund sheep and two others were examined. On brain histopathology, there was very mild neuronal pigmentation; however the grey-white matter interface has multifocal acute astrocytic reaction with swollen astrocytes characteristic of exogenous ammonia intoxication probably associated with phalaris sudden death (or peracute polioencephalomalacia (PE)-like sudden death) toxicity. The pasture available was of good quality - a mix of rye grass, clover, cocksfoot and phalaris, with no obvious poisonous weeds, and other sheep and cattle grazing nearby appeared unaffected. The remaining sheep in the paddock were moved to an adjacent paddock and no further deaths occurred.

Image of dead sheep in paddock
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Image of dead sheep in paddock
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The owner is a careful and particular manager and is well educated in sheep production. This mob of 230, 5 or 6 year old Dohne ewes in score 3+ condition were shorn and drenched about 2 weeks previously. On Saturday 24th November 15 ewes were found dead in a paddock, 1 more was moribund, while the balance of the flock still in the paddock was grazing happily. The ewes appeared to have died overnight or early in the morning, and 4 or 5 had been attacked by foxes. The owner has not experienced mortalities like this in the past. On close examination of the pasture it appeared that clumps of phalaris had been selectively grazed in preference to other species. The weather has been cool with some light rain in the past week and so it is likely that young phalaris shoots had been available.


A moribund ewe was euthanased and autopsied, together with two others that appeared to have died within 4-6 hours. All had full rumens and were in good body condition, with a slight reddening of the abomasal mucosa seen as the only notable post-mortem change.

Blood tests showed very high urea, AST and CK levels in particular, and ocular fluids were negative for nitrate / nitrite levels. Brain histopathology of acute astrocytic reaction characterized by swollen astrocytes with an enlarged, pale, vesicular nucleus in the grey-white matter interface established the diagnosis:

Brain and cranial cervical cord (Sheep 1-3): Acute astrocytic reaction consistent with phalaris sudden death toxicity. Small intestine (Sheep 1): Enteritis, eosinophilic, multifocal, minimal to moderate; with protozoan parasites.

Sodium 143 mmol/L (139 - 152)
Potassium 3.4 mmol/L (3.9 - 5.4)
Na/K 42.1
Chloride 90 mmol/L (95 - 103)
Bicarb. 33 mmol/L (18 - 28)
Anion Gap 23 mmol/L
Urea 31.0 mmol/L (2.8 - 7.2)
Creat. 154 umol/L (70 - 97)
Calcium 1.25 mmol/L (2.40 - 3.20)
Phosphate 3.10 mmol/L (1.61 - 2.35)
Magnesium 0.9 mmol/L (0.5 - 1.5)
B-OH Butyr. 1.2 mmol/L (< 0.9)
Protein 55 g/L (60 - 82)
Albumin 30 g/L (25 - 40)
Globulin 25 g/L (30 - 42)
T. Bil. 3 umol/L (< 9)
Alk Phos 147 U/L (84 - 220)
GGT 52 U/L (30 - 66)
AST 2147 U/L (53 - 153)
GLDH 37 U/L (< 20)
CK 156545 U/L (69 - 182)
Chol. 1.4 mmol/L (1.3 - 2.0)


Phalaris toxicity is well documented, but rarely seen in this area of the Adelaide Hills. It typically occurs in cooler, mild weather in autumn to early summer when fast growing shoots are available and both sudden death and a "staggers" syndrome can be seen. The toxic principles are dimethylatryptamine and phenylethylamine (alkaloids) that act on cardiac muscle and brain tissue1. Sudden death is from either acute cardiac sudden death syndrome or peracute PE-like sudden death, while the incoordination syndrome ("staggers") occurs after prolonged exposure, when sheep are disturbed and driven. The acute cardiac sudden death syndrome is associated with heart failure with neither neurological signs nor histopathology. Peracute PE-like sudden death however is considered a result of hyperammonaemia from toxin interference with the urea cycle3.


Government veterinary services provide an important role in assisting diagnosis and disease surveillance activities particularly where situations are complex, remote or private veterinary services are stretched or diminishing. This producer contacted me having been to a workshop some years ago that PIRSA presented, reaffirming the fact that producers will contact the people they know first for advice.

Although phalaris poisoning (acute death or staggers) cannot be treated in affected animals, fortunately removal from the source does aid recovery. In high risk situations administering cobalt prior to exposure does seem to have a protective effect. This can be done orally at weekly intervals (28mg / week) or in fertiliser applications1 but in this situation, simply waiting until phalaris pastures are more mature before grazing with sheep should be sufficient.


  1. Veterinary Medicine a textbook of the diseases of cattle, sheep, pigs, goats and horses. Radostits OM, Gay, CC; Blood, DC; Hinchcliff KW. 9th edition. WB Saunders 2000
  2. Phalaris Poisoning Syndromes. Associate Professor Peter Windsor, Farm Animal Health, University of Sydney. Posted Flock & Herd September 2016 www.flockandherd.net.au
  3. Bourke CA, Colegate SM, Rendell D, Bunker EC & Kuhn RP (2005). Peracute ammonia toxicity: A consideration in the pathogenesis of Phalaris aquatica 'Polioencephalomalacia-like sudden death' poisoning in sheep and cattle. Australian Veterinary Journal 83:168-171


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