The occurrence of staggers in lambs in a medium wool merino flock over three years, was investigated. Initial histopathological findings of the central nervous system were consistent with a diagnosis of degenerative thoracic myelopathy. A process of elimination suggested this was a likely genetic disorder, although further investigations may be required to confirm this diagnosis.
Cases of staggers in a flock of medium wool merino lambs in the Dubbo region were reported in October in 2014. Clinical signs first appeared 3 years prior to reporting, affecting approximately 1% of lambs. Clinical signs usually commenced at 8-9 months of age, with the youngest being 4 months old at the first onset of signs. Sheep that did not develop signs at this age never seemed to become affected.
Clinical signs involved a progressive paresis of the hind limbs, with forelimbs unaffected. The owner reports no evidence of altered mentation, tremors or blindness. The ataxia was observed as being symmetrical. All affected animals were euthanased due to eventual inability to rise, with the oldest surviving sheep being 18 months old.
The sheep were kept on mixed pasture, with no supplementary feeding. They had been kept on three different properties over the previous three years; two different properties in Goolma and then one near Dubbo. The pastures had been examined for toxic weeds, with only a very small amount if blue heliotrope on one property. There was no Solanum esuriale (wild tomato) on the properties.
The sheep had been vaccinated with 5 in 1 and Gudair®. The flock has been infected with Ovine Johne's Disease for several years.
Most rams used in the flock were home-bred, with approximately one ram per year being bought from one of two studs for several years.
A post-mortem on an affected sheep had been performed by a private practitioner nine months earlier and a brain submitted for histopathology on suspicion of polioencephalomalacia. There were no significant histopathological findings on this occasion.
A group of affected sheep were examined, all with varying levels of symmetrical hind limb paresis. The worst affected ewe had a wide-based stance and swaying of the hindquarters when walking. She also fell when attempted to run and turn, with her hind legs collapsing.
Proprioception was reduced in the hind limbs, with toe dragging and knuckling when moved. Forelimbs were normal and a cranial nerve examination was unremarkable. There was symmetrical atrophy of the hind limb musculature.
The worst affected ewe was euthanased and a post-mortem was performed. No abnormalities were detected on gross pathology.
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Histopathology showed multifocal, chronic, marked Wallerian-type degeneration of the lumbar spinal cord with digestion chambers and swollen axons. Thoracic cord was not submitted.
There was also a lymphoplasmacytic hepatitis, described as multifocal, periportal and random in distribution, of chronic duration, and mild to moderate in severity, with hepatocellukar necrosis. There was also a lymphoplasmacytic, multifocal, chronic, mild myocarditis. The significance of these lesions was not determined.
The histological features in the spinal cord were considered to be consistent with those reported in Merino lambs as degenerative thoracic myelopathy or Cooma ataxia (Harper et al., 1991).
"Staggers" in sheep can have a wide variety of causes, including a variety of plant and chemical toxicities, micronutrient deficiencies, electrolyte imbalances, bacterial and viral infections, space occupying lesions and probable neurogenetic disorders (Windsor et al., 2011). It is a term that covers a wide variety of clinical presentations, which can include ataxia, paresis, loss of proprioception, falling, tremors and convulsions.
A system for categorising the clinical signs associated with staggers into 5 different groups in order to aid diagnosis in Australia has been proposed (Bourke 1995). The clinical signs in this case could be placed in the category of 'Limb paresis with knuckling syndromes', indicating both paresis and decreased proprioception. The differential diagnoses in this category include a number of toxic plants including Romulea rosea (onion grass), Stachys arvensis (stagger weed), Trachyandra divaricata (branched onion weed), Tribulus micrococcus (yellow vine), Stypandra glauca (nodding blue lily) and Ipomoea spp (weir vine, convolvulus, morning glory) and also Anatox ingestion produced by blue-green algae. Also included are botulism and listerial myelitis, vitamin A deficiency and the enzootic ataxia form of copper deficiency. Chemical toxicities with ivermectin and the organophosphate anthelmintic, haloxon, have also been known to cause these signs. The suspected genetic disorders of ovine segmental axonopathy, neuroaxonal dystrophy and degenerative thoracic myelopathy also fall within this category and were high on the differential list in this case (Windsor et al. 2011).
Of consideration in the clinical history was that approximately only 1% of lambs were affected, affected animals first displayed clinical signs at the same age, and these signs occurred despite the sheep being placed on three different properties. The likelihood of the same toxic plant being ingested in a single age group on three different properties is considered to be very low, as is a bacterial or viral infection occurring in the same single age group in three consecutive years. Further, the histological findings consistent with a previously described putative hereditary neuropathy, is suggestive that these lambs were also affected by this same suspected genetic disorder. Unfortunately, the relatively low prevalence of these suspected genetic merino neuropathies has meant that research funding to examine their suspected genetic basis has not been available. This means that the diagnosis is largely based on the flock and animal history, clinical signs, consistent histological lesions, and exclusion of other differential diagnoses that could be responsible for the clinicopathological findings.
The lack of systemic illness and slow progression of signs are not consistent with botulism, listerial myelitis or anatox ingestion. There was no history of drenching with ivermectin or organophosphates.
The blood copper levels taken from four affected sheep were well within normal limits, as were calcium levels. Vitamin A deficiency is very unlikely given that they were grazing on pasture and there were no cases of blindness noted, which is often seen with Vitamin A deficiency (Bourke 1995).
Stypandra glauca also causes blindness and thus was excluded from the differential diagnoses (McKenzie 2012). Stachys arvensis toxicity has been reported as involving laboured breathing and trembling or shivering muscles, pyrexia and tachycardia which drastically worsens when moved (McKenzie 2012). This does not fit the clinical picture seen in this case, as the sheep appeared to be systemically normal, with only hind limb strength and proprioception affected.
Romulea rosea and Tribulus micrococcus both need to dominate the pasture in order for nervous effects to occur, which was not the case on any of the properties (McKenzie 2012). Trachyandra divaricata is restricted to coastal areas (McKenzie 2012). In cases of Ipomoea spp ingestion, it would be expected to see altered mentation, hyperexcitability and manic behavior, which was not noted in this case (McKenzie 2012).
After excluding other causes of staggers with decreased hind limb proprioception, the previously described, suspected neurogenetic disorders listed above were considered. These disorders are known to occur at a steady, low incidence and are found in flocks that are from related blood lines and are geographically close together.
Ovine segmental axonopathy occurs in older fine wool merinos, aged between 1 and 5 years (Windsor et al. 2011). Though the clinical signs and rate of incidence (0.1-1%) were consistent with those found in this case, the age of affected animals and histopathology findings were not.
Neuroaxonal dystrophy and degenerative thoracic myelopathy are both possible causes of the clinical signs seen in this case and histopathology is required to differentiate between the two. Neuroaxonal dystrophy is known to occur in medium wool merino sheep aged between 4 and 7 months old, with an incidence of 1% annually (Windsor et al. 2011). Degenerative thoracic myelopathy is reported as affecting lambs 5 months and older with an incidence of 0.5-2% annually (Harper et al. 1991).
The characteristic histopathological lesions seen in neuroaxonal dystrophy of multifocal axonal swellings in the grey matter of the brainstem and midbrain, particularly in the cuneate and gracile nuclei were not noted in this case (Windsor et al. 2011).
The Wallerian-type degeneration of the lumbar spinal cord seen in this case was consistent with degenerative thoracic myelopathy, though thoracic spinal cord was not collected, which would have provided the best information for this case (Harper et al. 1991). The plan for the future is to collect brains and spinal cords from more affected sheep as disease occurs, in order to assess all regions of the spinal cord and establish a series to determine if the histopatholgical findings are consistent.
After a process of elimination, a likely diagnosis of a neurogenetic disorder was determined in this case. Further examination of affected individuals is required to establish a series to determine if this is as a result of degenerative thoracic myelopathy, or if it is a different entity entirely.
I would like to thank Peter Windsor for his advice regarding ovine neurogenetic disorders, as well as his assistance in reviewing this paper. I would also like to thank Andrew Thompson and Patrick Staples for their contribution of their pathology expertise.