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Bruce Watt and Mandi Carr, Tablelands Livestock Health and Pest Authority and Zoe Spiers and Kaiser Dawood, State Veterinary Diagnostic Laboratory, Menangle

Posted Flock & Herd March 2011


Studies conducted in the mid 1980's on progressive ataxia in Merino sheep, involving at least 36 farms in the Yass district, identified two distinct clinical and pathological syndromes (Harper et al 1986). It was concluded that the signs of cerebellar ataxia in one cohort were attributeable to cerebellar abiotrophy (CA) and the other cohort displayed hindlimb ataxia and paresis associated with lesions of segmental axonopathy (SA). Of the farms on which a diagnosis was made, 7 were affected by CA, 4 were affected by SA and both diseases occurred on 3 farms.

A range of conditions produce symptoms of spinal or cerebellar dysfunction in sheep and need to be considered in the differential diagnosis. These include neurogenetic syndromes, plant and chemical toxicities and infectious agents. The important exotic diseases rabies and scrapie can also both cause impaired locomotion in sheep.



The owner of a finewool Merino flock near Peelwood (central tablelands of NSW) noticed a two year old Merino ewe in a mob of 320 that over the previous six months has become progressively weaker with a swaying gait and therefore was unable to keep up with the mob. The owner reported that he had seen 5 similar cases over the last two years with clinical signs generally developing at 18 months to 2 years of age.

This mob was part of a flock of Merinos that ran on pastures dominated by native grasses including weeping grass (Microleana sp) and red grass (Bothriochloa sp) but also included naturalised plants such as clover species and some phalaris (Phalaris aquatica). The sheep had been vaccinated with Gudair beside the base of the ear at lamb marking. They had also been treated with long acting selenium and had been vaccinated against clostridial diseases.


The ewe was bright, alert and responsive and in body condition score 2.5. It walked with a swaying gait in the hind quarters. When pushed or made to turn quickly the ewe collapsed in the hind legs. When standing, the hind feet were frequently positioned asymmentrically towards one side of the body rather than being positioned symmetrically below the pelivs. The general appearance was of hindquarter weakness.

Patellar reflexes appeared exaggerated but the ewe was otherwise clinically unremarkable.

Post-mortem and pathology findings

Following euthanasia and an autopsy, samples were submitted to comply with TSE surveillance guidelines. No abnormalities were detected at autopsy. Histologically, there was marked vacuolation in the white matter of the CNS; particularly, the cerebellar peduncels, obex and spinal cord. Gliosis; and specifically reactive astrocytes were found in the most affected area. Digestion chamber, Wallerian degeneration, and spheroids were found in the thoracic spinal cord.

Image of sheep with abnormal gait
Image of sheep sitting
Images 1 and 2: The affected ewe walked with a swaying gait and readily collapsed
in the hindquarters if pushed.
Image of sheep with abnormal stance
Image 3: When standing, the ewe often swayed laterally, leaving the hind legs positioned to the side.



On the 9th July 2010 a merino sheep producer near Lyndhurst, SW of Bathurst, reported a four-year-old wether with neurological signs. The wether had progressively deteriorated over the previous 12 months but had now reached the stage where the stumbling, ataxia and falling over was marked especially during mustering. The wether remained with the mob despite the neurological deficits.


The wether was in good body condition. Clinical signs included a wide base stance, head tremor, nystagmus, lack of balance, hypermetria, hyper-reflexion and in-coordination. A video of the affected wether demonstrating these symptoms is attached to this website.

Post-mortem and pathology findings

The animal was humanely euthanased and a necropsy performed. TSE procedures were followed. There were no obvious gross necropsy findings but the histopathology performed on the brain revealed a decreased number of Purkinje cells with an accumulation of glial cells at the junction between the granular and molecular layers, extending minimally into both. There was mild axonal degeneration (spheroids) within the white matter tracts of the brain stem. Cerebellar abiotrophy was diagnosed. TSE tests were negative.


Many of the diverse range of neurological diseases of sheep in Australia are referred to as 'staggers' syndromes. Several of these are neurogenetic syndromes. In Australian Merinos, these include segmental axonopathy, cerebellar abiotrophy, thalamic-cerebellar neuropathy, neuroaxonal dystrophy, degenerative thoracic myelopathy, neuro visceral ceroid lipofuscinosis and Alexander's disease (Windsor, 2006; review in press in AVJ 2011).

Harper et al (1986) observed a form of axonal dystrophy, described as segmental axonopathy in 1 to 4 year old sheep from the Yass district. The sheep had clinical signs indicative of spinal cord pathology. The condition was characterised by 'spheroids' or widespread segmental axonal ballooning in the white matter of the brain and spinal cord. Lesions resembled the same condition that Hartley and Loomis (1981) described previously as Murrurundi disease. Segmental axonopathy has also recently been described in Merino sheep in New Zealand (Jolly et al, 2006).

The differential diagnosis of SA includes a range of diseases of the spinal cord that cause hind limb paresis and then general weakness. Vertebral abscessation and pyogranulomas intruding on the cervical cord (most commonly subsequent to misdirected Gudair vaccination) are occasionally encountered as causes of hind limb weakness in sheep in NSW (Windsor and Eppleston, 2006). Vertebral abscesses usually occur in young sheep subsequent to bacteraemia via either skin wounds or the umbilicus although an ascending infection from tail docking is also possible. Cervicothoracic vertebral subluxation has been reported in Corriedales near Albury and in other breeds overseas. The condition caused sudden onset tetraplegia in sheep from 9 months to 3 years of age and was apparently preceded by a myopathy of the neck muscles in lambs (Hartley, 1994). Chronic consumption of the common, introduced summer weed Tribulus terrestris (cathead or caltrops) can lead to irreversible nervous system damage in sheep. While this disorder is characterised by 'profound hind limb paresis,' it is uniquely unilateral (Bourke, 1995). Intoxication from the ingestion of Stypandra spp (blind grasses) causes 'an incoordination of the gait, particularly in the hind limbs, which is accentuated by exercise' (Seawright, 1982). However, affected animals also appear blind and die within five days of continued exposure. While Stypandra glauca is widespread in NSW, it is the Western Australian species ( S. imbricata and S. grandiflora) that are known to be toxic (Seawright, 1982).

Several other plants toxins are reported to cause a combination of limb paresis and knuckling. 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). Gorrie (1962) described a 'progressive flaccid paralysis' in sheep on onion grass (Romulea rosea). Abortions and extreme infertility occurred in association with paralysis on some affected properties. Stachys arvensis is widespread in NSW and has been reported to cause a rapid onset high flock prevalence pelvic limb paresis and a proprioceptive deficit in sheep (Philbey et al 2001). Tribulus micrococcus is a native plant that grows on inland clay and loam soils north of Wagga (PlantNET, 2011). Trachyandra divaricata is an introduced weed that grows on coastal sand dunes from Stockton to Wollongong (PlantNET, 2011) so is unlikely to be a significant threat to commercial sheep producers.

Organophosphates, widely used in the sheep industry for decades can potentially cause a delayed neurotoxicity. Seawright (1982)noted that 'the earliest observed effects are disturbances in proprioception, leading to ataxia, and this may be followed in severe cases by peripheral motor neuropathy and posterior paralysis especially with enforced exercise.' In practice, however the currently and previously registered products containing organophosphates are not reported as having caused neurotoxicity (Craig Stevenson and Neil Cooper pers comm.).

While infectious myelitis is unusual in Australia, Seaman et al (1990) reported an outbreak of listerial myelitis post dipping. Neospora caninum has also been described as a rare cause of a fatal non-suppurative myelitis (and meningoencephalitis) in sheep from southwest NSW (Bishop, et al 2010). In this case, clinical signs were mainly referable to the central nervous system although affected sheep also displayed ataxia. In the mild or paralytic form of rabies, animals develop a weak swaying gait. However, rabies in sheep is also accompanied by behavioural changes including sexual excitement, aggression and vigorous wool pulling. Scrapie can also cause locomotor disorders but clinical signs usually include intense pruritis, muscle tremours and emaciation (Radostits et al, 2007).

Cerebellar abiotrophy, also referred to as cerebellar cortical abiotrophy, is a neurological condition affecting Purkinje cells causing them to die off. Without Purkinje cells, the animal loses its sense of space and distance, making balance and coordination difficult. Purkinje cells do not regenerate, so once atrophied, their useful life is lost permanently. The exact cause is no known but a genetic link is likely. Daft lamb disease appears to be an inherited cerebellar atrophy while the lambs from ewes fed pea vine silage also suffer from cerebellar disease. Cerebellar atrophy abiotrophy is known to occur in Arabian horses and inherited cerebellar degeneration occurs in Gordon setters (Harper et al, 1986).


Peter Windsor has contributed to veterinary science across a wide field. One of these fields is a study of neurological and genetic diseases of sheep and cattle where his contribution has been substantial, sustained and impressive. We would like to acknowledge this. We would also like to express our appreciation for the helpful comments Peter made in the preparation of this paper.


  1. Bishop S, King J, Windsor P, Reichel M, Ellis J and Slapeta J. (2010) The first report of ovine cerebral neosporsis and evaluation of Neospora caninum prevalence in sheep in New South Wales. Vet. Parasitol
  2. Bourke CA. (1984) Staggers in sheep associated with the ingestion of Tribulus terrestris. Aust Vet J. 61: 360-363
  3. Gorrie, CJR. (1962) Ovine abortion in Victoria. Aust Vet J, 38:138-14221
  4. Harper PA, Duncan DW, Plant JW, Smeal MG. (1986) Cerebellar abiotrophy and segmental axonopathy: two syndromes of progressive ataxia of Merino sheep. Aust Vet J 63:18-21
  5. Jolly RD, Johnstone AC, Williams SD, Zhang K, Jordan TW (2006) Segmental axonopathy of Merino sheep in New Zealand. NZ Vet J 54:210-7
  6. Philbey AW, Hawker AM and Evers JV. (2001) A neurological locomotor disorder in sheep grazing Stachys arvensis. Aust Vet J., 79: 427-430
  7. Radostits OM, Gay CC, Hinchcliff KW and Constable PD. (2007). Veterinary Medicine, 10th Edition, p 1389
  8. Seaman JT, Carrigan MJ, Cockram, FA and Carter GI. (1990) An outbreak of listerial myelitis in sheep. Aust Vet J 67:142-3
  9. Windsor PA. (2006) Ultrastructural findings in ovine segmental axonopathy of Merino sheep. Aust Vet J. 84:5, pp169-172
  10. Windsor P.A., Eppleston J. (2006). Lesions in sheep following administration of a vaccine of a Freund's complete adjuvant nature used in the control of ovine paratuberculosis. N.Z. Vet. J. 54(5): 237-241


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