CASE NOTES

Neurological Inherited Disorders of Ruminants

Leah Manning Johnson (EMAI), Katie Eager (EMAI), Brendon O'Rourke (EMAI), Pedro Pinczowski (EMAI), Zoe Spiers (EMAI), Mark Krockenberger (The University of Sydney), Peter Windsor (The University of Sydney) & Imke Tammen (The University of Sydney)

Posted Flock and Herd August 2025

INTRODUCTION

Inherited diseases in livestock can have important animal welfare, production and economic impacts. A number of inherited neurologic disorders have been recognised for decades in Australia, while newly emerging diseases are continuing to be seen. With the increasing availability and affordability of whole genome sequencing analysis, associated causative variants are being identified for a number of these conditions, allowing development of tests for diagnostic investigation and informed breeding management.

Diagnosis of suspected inherited disorders in livestock requires a thorough history, clinical examination and diagnostic investigation, to exclude non-genetic differential diagnoses and characterise the phenotype of the disorder. There can be considerable overlap in clinical presentation between inherited neurologic disorders, as well as differential diagnoses of trauma, metabolic disease, toxicities (plant, heavy metal, chemical, other), parasitic, bacterial and viral diseases. Once an inherited disorder is considered likely, further diagnostic investigation depends on whether the disorder has previously been recognised in the breed, if a causative variant has been identified, and the availability of a commercial diagnostic test. If the disorder does not have an identified causative variant, additional sampling of both affected and related animals can assist in further in-depth genetic investigation.

A search of the Online Mendelian Inheritance in Animals database (OMIA)¹ was conducted to identify confirmed or possible inherited naturally occurring neurologic disorders in ruminants. The following are broad categories of some of the known inherited neurologic disorders in ruminants based on clinical presentation, with a focus on disorders recognised in livestock in Australia. This is not an exhaustive review of all suspected inherited neurologic conditions, and consultation of OMIA and discussion with EMAI laboratory staff or reporting to the Anstee Hub for Inherited Diseases in Animals (AHIDA) is recommended if you are investigating a suspected inherited condition.

Congenital disorders with macroscopic malformations of brain and/or spinal cord

Depending on the condition, presentation is often either abortion/stillbirth, or born alive but the animals often die or are euthanised. A number of congenital disorders have been identified in specific breeds and may present with clinical signs and/or gross post-mortem changes to suggest a possible genetic condition and prompt genetic testing where available. For example, in Australia, arthrogryposis multiplex (curly calf syndrome) in Angus cattle [OMIA:002135-9913], neuropathic hydrocephalus in Angus [OMIA:000487-9913] and complex vertebral malformation in Holstein-Friesian cattle [OMIA:001340-9913]². Cerebellar hypoplasia has been identified in several breeds, such as Shorthorn cattle [OMIA:000179-9913], and in some cases can occur alongside lissencephaly, for example, the recently identified lissencephaly and cerebellar hypoplasia in Dorset-cross lambs from a flock in NSW³, and Spanish Churra sheep with variants in the RELN gene [OMIA:001867-9940]⁴. However, many congenital malformations are sporadically reported and have not been proven to be genetic in origin in ruminants. For some similar conditions in other species including humans, more extensive genetic investigations have been done and associated variants have sometimes been identified. In utero infectious diseases and toxicities should be excluded depending on presentation.

Congenital neurologic disorders without primary malformations of brain/spinal cord

There are several examples of inherited neurological conditions in ruminants in Australia in which clinical signs are present at, or soon after, birth and which lack macroscopic malformations of the brain/spinal cord:

Inherited congenital myoclonus (ICM) in Poll Hereford cattle and crosses is caused by a variant in the glycine receptor alpha gene [GLRA1] (OMIA:000689-9913). Affected calves are unable to stand from birth, have stimulus induced myoclonic spasms, have lesions in the coxofemoral joints and can have hip fractures secondary to hindlimb adduction². Histologically, there are no significant changes.
Maple Syrup Urine Disease (MSUD) in Poll Hereford, Hereford and Shorthorn calves is caused by variants in the branched chain keto acid dehydrogenase E1 alpha polypeptide gene [BCKDHA] (OMIA:000627-9913)^2,5. Affected calves develop progressive signs of wide-based stance, lowered head, lateral recumbency, opisthotonus, urine with a maple syrup like odour, and death within days of birth. Histologically, within the brain there is severe white matter vacuolation/oedema².
Citrullinaemia [OMIA:000194-9913] was identified in Holstein-Friesian calves, with a causal variant in the arginosuccinate synthase 1 gene [ASS1] leading to depression, wandering, head pressing, blindness and teeth grinding in neonatal calves².

Various storage disorders have been identified in ruminants in Australia, and affected animals may present with signs at, or shortly after, birth, or develop signs at a later stage in life depending on the breed and the defect. Some examples of storage diseases described in Australian ruminants include:

α-Mannosidosis [OMIA:000625-9913] in Angus, Murray Grey, Squaremeater and Galloways, a lysosomal storage disease due to two breed-specific variants in MAN2B1².
β-Mannosidosis [OMIA:000626-9913] in Salers cattle and in Anglo Nubian goats, a lysosomal storage disease due to variants in MANBA^2,6,7.
Glycogen storage disease II (Pompe's disease, acid maltase deficiency, generalised glycogenolysis) [OMIA:000419-9913] in Brahman, Shorthorn, Droughtmaster, Blanco Orejinegro cattle, with three different variants identified in GAA (all have been documented in Australia) leading to defective α-glucosidase^6,8,9.
Glycogen storage disease V (McArdle's disease) [OMIA:001139-9913] in Charolais and Red Angus with 2 causal variants in PYGM, reported overseas with unconfirmed cases in Australia⁶.
Neuronal ceroid-lipofuscinosis (NCL, Batten disease) in Devon cattle [OMIA:001482-9913] and in Merino sheep [OMIA:001443-9940] with causal variants in CLN5 and CLN6, respectively, reported in Australia (NCLs have been reported in a number of other breeds and species overseas).
Niemann-Pick Disease, type C1 [OMIA:000725-9913] in Angus and Angus cross calves in Australia with a causal variant in NPC1¹⁰.

Ataxia

Ataxia is the uncoordinated voluntary movement of head, trunk and limbs. Ataxias may be subdivided into proprioceptive, cerebellar and vestibular ataxia¹¹.

Proprioceptive ataxia

Proprioceptive ataxia occurs primarily with spinal cord disorders, occasionally with brain disorders, however with the latter there are other, often predominating, clinical signs¹¹. Other signs that may be seen, depending on the condition, include swaying, stance abnormalities, gait abnormalities and/or proprioceptive deficits¹¹. Inherited conditions involving ataxia are often progressive over time (with some exceptions, e.g. familiar episodic spinocerebellar ataxia in sheep, OMIA:001723-9940) and clinical signs are frequently exacerbated by stress, exercise and yarding. Trauma, compressive lesions, toxicities (plant, heavy metal, organophosphates, other), and some infectious diseases should be excluded.

Segmental axonopathy [OMIA:001492-9940] in fine wool Merino sheep in Australia and New Zealand with onset of clinical signs from one to five years of age. Affected animals present with progressive hindlimb ataxia with toe knuckling and dragging of hind feet, collapse, falling to the side, difficult rising and dog sitting and clinical signs are exacerbated by exercise, stress, yarding and shearing^12-14. Gross lesions are either absent or non-specific. Diagnosis is either by histopathology, with distinct histologic lesions, and/or the newly developed genetic test available through EMAI, performed preferably on Allflex TSU samples or EDTA blood (testing on other sample types possible, please contact EMAI to discuss further).
Degenerative thoracic myelopathy [OMIA:000079-9940] is a possible inherited disorder reported in Merino sheep (medium wool) in Australia. Affected sheep present with clinical signs from five months of age, including progressive hindlimb ataxia, hindlimb weakness, wide-based hindlimb stance, swaying, dog-sitting and recumbency¹⁵. On histopathology, there is axonal/Wallerian degeneration within the thoracic spinal cord of variable severity¹⁵. Submission of representative sections of the nervous system (brain and cervical, thoracic and lumbar spinal cord segments), thorough gross examination (e.g. assess for evidence of trauma, compressive lesions in spinal canal), and assessment for toxic plants, are essential in excluding differential diagnoses that may have an overlapping histologic phenotype. An underlying causative variant has not been identified so far.
Alexander disease [OMIA:001208-9940] has been suspected once in three 18 month old Merino sheep in Australia with progressive hindlimb incoordination, lagging behind, loss of hindlimb function and recumbency necessitating euthanasia¹⁶. No gross lesions were observed, but on histopathology of the brain, Rosenthal fibres (eosinophilic fibres within astrocytes) were detected within the brain and spinal cord^6,16. The underlying causative variant has not been identified so far.
Progressive ataxia of Charolais cattle [OMIA:000527-9913] is an autosomal recessive inherited disorder of dysmyelination recognised in Charolais cattle, and Charolais cross breeds, in numerous countries including Australia¹⁷. Clinical signs are usually seen from one to two years of age (can be from six months to five years), are progressive, and may include hindlimb ataxia, unsteady or uncoordinated gait, difficulty rising, recumbency and, in some cases, tremors. While there are no gross changes on post-mortem, histologically there are distinctive demyelinating plaques within specific areas of the white matter of the brain and within spinal cord white matter. A variant has been identified in the kinesin superfamily protein gene KIF1C ¹⁷.

Cerebellar diseases with ataxia

Cerebellar disorders may present with cerebellar ataxia, hypermetria/dysmetria, tremors, wide hindlimb stance/gait¹¹. Inherited/suspected inherited cerebellar disorders in ruminants vary widely in age of presentation, with some present from birth, while for other disorders, clinical signs might not be seen until four years or age or later.

Cerebellar abiotrophy [OMIA:000175-9940] has been reported in several breeds of sheep, but in Australia has been seen in fine wool Merinos, with onset of disease from three to six years of age. In Merinos, clinical disease manifests as ataxia, dysmetria, fine head tremor and falling and clinical signs are progressive¹². Histologically, there is degeneration and loss of Purkinje cells within the cerebellum, with Bergmann gliosis¹². Current research at EMAI is focussed on identifying a likely causative variant.
Cerebellar abiotrophy [OMIA:000175-9913] in Angus cattle (and crossbreds) has an onset of clinical signs from birth to eight months, and affected animals present with ataxia, falling down, head tremor, wide-based stance, hypermetria, and seizure-like episodes¹⁸. Histologically, there is degeneration and loss of Purkinje cells, glial reaction and some axonal swellings of Purkinje cell axons^6,18. A causative variant has not been identified. 'Familial convulsions and ataxia' is reported overseas in Angus cattle, however clinical signs occur at a younger age in the latter⁶.
Thalamic-cerebellar neuropathy [OMIA:000723-9940] was reported in medium wool Australian Merino sheep in 1993^6,19. Clinical signs are observed from two years of age and include hindlimb paresis, hindlimb ataxia, thoracic limb hypermetria, fine mild head tremor, wide-based stance, incoordinated gait and falling^6,19. Histologically, neurons are swollen and stain pale, with adjacent axon and dendrites often also swollen, there is vacuolation of fibre tracts and some axonal degeneration¹⁹. Affected areas include thalamus, cerebellum, pons, medulla oblongata and spinal cord fibre tracts (ventral and lateral columns, all levels)¹⁹.

Vestibular diseases with ataxia

Vestibular ataxia occurs due to problems with the inner ear and/or brainstem (or flocculonodular lobe of cerebellum)¹¹. Vestibular diseases can often present with ataxia, rolling, falling, head tilt, nystagmus, wide-based stance, swaying¹¹. In a number of inherited conditions, vestibular signs may be observed alongside other CNS clinical signs (particularly if lesions involve multiple areas within the CNS).

Neuroaxonal dystrophy [OMIA:000715-9615] [OMIA:002105-9940] has been reported in Merino sheep and Merino-Border Leicester x Polled Dorset sheep in Australia, as well as other breeds overseas (e.g. Romney, Perendale, Coopworths, Suffolk, Swaledale)^20-25. In Merino sheep, clinical signs have been reported from 8 weeks and 4 months of age^24,25. Clinical signs in Merinos include progressive hindlimb ataxia, wide-based hindlimb stance, swaying, difficulty rising and recumbency²⁵, with owner reporting possible reduction in vision in the report from Victoria²⁴. In the report on cross-bred lambs from Victoria, clinical signs appeared earlier and were more severe²³. There are typically no gross findings on post-mortem. A diagnosis is made on histopathology; axonal spheroids or spheroids are seen throughout the grey matter and often in nearby neuronal cell bodies. Distribution of histologic changes is key to diagnosis, as spheroids are most numerous within the grey matter and are typically bilaterally symmetric, with predisposed sites, including some brainstem and midbrain nuclei, as well as grey matter of the spinal cord. While an inherited disorder has been postulated, a likely causative variant has only been identified in Swaledale sheep in the United Kingdom²². There has been a single case report on an 18 month old Angus cow from South Australia, with axonal spheroids changes of similar distribution to neuroaxonal dystrophy in sheep²⁶. There are numerous acquired causes of axonal spheroids, however distribution and severity of lesions, and history, can often help distinguish likely cause(s).

Convulsive disorders

Multifocal symmetrical necrotising encephalomyelopathies [OMIA:001097-9913] [OMIA:001488-9913] [OMIA:001490-9913] include three different syndromes reported in different breeds. Convulsions are reported in this disease in Angus. In Angus, signs are seen from two to six weeks, are rapidly progressive, and include ataxia, tremors, tetanic spasms, opisthotonos, bruxism, hyperaesthesia and convulsions⁶. A symmetrical necrotising encephalopathy has been reported in sibling Limousin calves in NSW in 1990 (semen from UK), and previously reported overseas in Limousin cross calves²⁷. Clinical signs were progressive from four months of age and included failure to thrive, ataxia, blindness, forelimb hypermetria, hyperaesthesia and aggression^6,27. In Simmentals, clinical signs are observed from five to 12 months of age, including poor doing, ataxia, paralysis, recumbency and aggression with rapid progression^6,28. It is thought that these conditions are autosomal recessive inherited, however causative variants have not been identified for these conditions^6,1. Histologically, these conditions have bilaterally symmetrical areas of malacia in specific areas depending on the breed, that can often be seen grossly as areas of discolouration^6,28.

Episodic disorders (Episodic ataxia, collapse or other)

There are several disorders in which clinical signs are present intermittently and it is important to distinguish between neurologic ataxia and musculoskeletal and metabolic causes of intermittent weakness or collapse.

Myotonia congenita [OMIA:000698-9940] is a myopathy rather than a neurologic disorder but is included here for awareness. Myotonia congenita has been identified in Merino sheep in NSW, Australia, as an autosomal recessive disorder associated with a missense variant in the chloride channel gene CLCN1 ²⁹, and has previously been identified in Rasa Aragenosa sheep in Spain³⁰ and in goats. Merino sheep have episodes of collapse with tetanic spasms, or episodic stiff rigid hindlimb gait, often induced by movement or startle³⁰. Sheep are typically normal between episodes, although some may lose condition over time compared to counterparts. Creatine Kinase (CK), a muscle enzyme, is typically within reference range or mildly elevated²⁹. A diagnostic test for the recently discovered Merino variant is now available through EMAI.

Postural and locomotor disorders with secondary effects on the neurologic system

Cervicothoracic vertebral subluxation [OMIA:002313-9940] has been reported in a number of sheep breeds worldwide, and in Merino sheep in Australia^31,32. Affected animals show a dropped or U-shaped neck with variable onset of neurological clinical signs such as hindlimb ataxia, and may present with variable neck rigidity or pain and inspiratory stridor. Grossly, there is subluxation or deviation at the junction of the cervical and thoracic vertebrae, leading to variable spinal cord compression^31,32. Histologically, there is degeneration within the spinal cord, and degeneration, necrosis, haemorrhage, mineralisation and/or regeneration within the cervicothoracic paravertebral musculature^31,32. This condition is postulated to be inherited based on pedigree analysis, and the genetic cause is currently being investigated at EMAI³¹.

Peripheral Neuropathies

Clinical signs will relate to which peripheral nerves are involved. While peripheral inherited neuropathies have been reported in many species, there are no current reports of confirmed inherited primary peripheral neuropathies in Australia.

Conclusion

The awareness of conditions for which diagnostic testing is available has assisted in reducing incidence of these specific diseases. A list of the genetic testing offered at EMAI can be found at www.dpi.nsw.gov.au. Neurological diseases currently under investigation are listed in Table 1. Please contact us if you are aware of additional cases for these conditions.

Reporting of any suspected or confirmed inherited diseases to the Anstee Hub for Inherited Diseases (AHIDA), an online portal for surveillance and reporting of inherited diseases in Australian animals (hosted by the Sydney School of Veterinary Science) is encouraged (ahida.sydney.edu.au). Anonymous reporting is possible, submitters who provide contact information can request to be connected to researchers who may be able to offer additional advice or collaborative research. Alternatively, contact the EMAI laboratory directly, as we are happy to discuss sample collection, diagnostic approach and testing options.

Table 1: Suspected inherited conditions with neurologic involvement currently being investigated at EMAI

Species	Breed	Condition
Sheep	Merino	Cerebellar abiotrophy: Signs from 3-6 years of age. Progressive ataxia, dysmetria, fine head tremor, falling. Histologically evidence of Purkinje cell degeneration and loss.
Sheep	Merino (other breeds worldwide)	Cervicothoracic vertebral subluxation: Dropped or U-shaped neck, hindlimb ataxia, inspiratory stridor. Grossly, subluxation or deviation of junction of cervical and thoracic vertebrae, often with haemorrhage/necrosis/mineralisation in paravertebral musculature.
Sheep	Merino	Degenerative thoracic myelopathy: Signs from 5 months of age. Progressive hindlimb ataxia and weakness, wide-based hindlimb stance, swaying, dog-sitting, recumbency. Histologically, axonal degeneration within the thoracic spinal cord (with exclusion of other non-inherited differential causes excluded).
Sheep	Merino, cross breeds (other breeds worldwide)	Neuroaxonal dystrophy: In Merino sheep, signs from 8 weeks to 4 months of age; Progressive hindlimb ataxia, wide-based hindlimb stance, difficulty rising, recumbency. Histologically, axonal spheroids with a distinct, bilaterally symmetrical distribution in predisposed areas of grey matter.

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