CASE NOTES

An interesting neuropathy in Suffolk rams

Bruce Watt, Central Tablelands Local Land Services, Bathurst, Anne Jordan, Elizabeth Macarthur Agricultural Institute, Menangle and Peter Windsor, Professor Emeritus, Sydney School of Veterinary Science

Posted Flock & Herd May 2023

INTRODUCTION

Spinal neuropathies are commonly reported in sheep in Australia. Most of the reasonably well characterised entities have been reported in Merinos (Harper et al. 1986, Harper et al. 1991a, Harper et al. 1991b, Windsor PA 2006 and Windsor et al. 2011) but elsewhere a systemic neuroaxonal dystrophy has been reported in Suffolk sheep (Cordy et al. 1967).

In this case, two young Suffolk rams developed progressive hindquarter weakness in sequential years. The first author considered that the progressive development, clinical signs and 1% prevalence in two sequential years best fitted a neurogenetic disease such as ovine segmental axonopathy (OSA), although the possible impingement of a vaccination-induced granuloma on the cervical cord was also considered as the rams had been vaccinated with Gudair®. Although the clinical signs also bore some resemblance to chronic phalaris staggers, the affected ram did not have tremors and phalaris was a minor pasture component.

In the second case (the first was not examined) microscopic degenerative changes observed in the white matter were considered sufficient to account for neurological signs seen clinically. Changes of Wallerian degeneration (WD) were like those reported in OSA, although the lesion of swollen axons (spheroid formation) was a less prominent feature in the current case than reported in OSA. Other diseases with significant WD include Stachys arvensis intoxication (although stagger weed was not found on this property) and Humpy back. Degenerative myelopathy (Cooma ataxia) can cause similar lesions in merino sheep; however, it is reported as occurring mainly in the thoracic cord (Harper et al. 1991a). An inherited aetiology seems most likely but focal trauma or vertebral instability could cause similar changes.

HISTORY

In late autumn 2019 a Central Tablelands seedstock producer noticed one of 102, August-September 2018 White Suffolk rams with a staggering gait. The owner saw the same problem in a young ram the previous year. That ram was euthanased. In both cases the young rams developed the problem at 8-9 months of age and deteriorated until euthanased at 13-15 months of age.

All lambs including the rams were vaccinated with Gudair® at lamb marking. The pastures on the property are predominantly cocksfoot (Dactylus glomerata var Porto), perennial ryegrass (Lolium perenne var Victorian), tall fescue (Festuca arundinacea), white clover (Trifolium repens) and subterranean clover (Trifolium subterraneum). The pastures are approximately 10% phalaris (Phalaris aquatica). No cases of phalaris staggers have been seen on the property over the previous 30 years.

The owner reported that he has seen no further cases as of October 2022.

CLINICAL FINDINGS

A well grown one year old White Suffolk ram in fat score 2.5 was examined on 23 October 2019. When moved the ram developed a swaying gait in the hindlegs (see video 1). When the ram was made to run,it occasionally dropped to a crouch and on other occasions the hindquarters swayed either side of the midline. The ram then bunny hopped or took long steps to regain its posture. The ram could be induced to fall hindquarters first if forced to move. The ram had no evidence of tremors and no cranial nerve deficits were observed. The ram had a soft 3 cm lump below, and lateral to, the left ear presumably from the Gudair® vaccination. The ram was able to place both front and hind feet normally. Patella reflexes could not be determined as the ram held both hind legs stiff when restrained on its side.Grossly there was no evidence of a Gudair® granuloma on the dorsal midline.

Video 1. Ram movement showing swaying gait

NECROPSY FINDINGS

No gross abnormalities were detected. The brain and a section of the neck from the atlanto-occipital joint to approximately the seventh cervical vertebrae were submitted to EMAI for gross and histological examination. On transection, there was no gross evidence of abscessation, spinal cord compression or other gross abnormalities.

HISTOPATHOLOGY

Morphological diagnosis: Brainstem, cerebellum, spinal cord (White matter): Wallerian-type degeneration,severe, multifocal to focally extensive, subacute with spheroids and digestion chambers.

DISCUSSION

This case has occurred sporadically in a non-Merino breed. This entity may have genetic factors involved in disease expression, as was suspected in the European report (Condy et al. 1967) although intoxications, vaccination sequelae and deficiencies can also cause sporadic cases.

The lesions of ovine segmental axonopathy (Murrurundi disease) and neuroaxonal dystrophy (NAD; Gundagai ataxia), entities described in the Australian Merino sheep population, are generally quite distinctive as they are characterised by a recognisable distribution and appearance of the spheroidal axonal swellings. One of us (PAW) recommends specifically checking the trigeminal radices for OSA and gracile and cuneate nuclei for NAD. The spheroids are mostly foamy in OSA compared with denser more eosinophilic swellings in NAD, reflecting that OSA spheroids are due to organelle accumulation at Nodes of Ranvier along axons, whereas NAD is associated with filamentous aggregates in dorsal brain stem nuclei (on EM).

The description of Wallerian-type degeneration in this case (WD) is non-specific and simply means there has been disturbance of neuroaxonal function that has caused loss of myelin (so-called myelin ellipsoids). This occurs in OSA and NAD and may well be the source of the clinical deficits, although the presence of spheroids can be important signposts that suggest that the underlying problem likely relates to axonal transport mechanisms. WD is the lesion observed in Cooma ataxia although, as mentioned previously, has mainly a thoracic distribution. The WD lesion is also often found in the suspected intoxications described above and several others.

Defining a single case is often the first step towards accumulating a case series that can potentially have important implications for ovine breeding and flock management programs, with a possibility that the entity might offer unique insights into neuro-pathogenesis.

REFERENCES

Harper, P.A.W., Duncan, D.N., Plant, J.W. and Smeal, M.G. (1986). Cerebellar abiotrophy and segmental axonopathy: two syndromes of progressive ataxia of Merino sheep. Aust. Vet. J. 63: 18-21
Harper, P.A.W., Hartley, W.J., Plant, J.P. and Timmins, K.G. (1991). Progressive ataxia associated with degenerative myelopathy in merino sheep. Aust. Vet. J. 68: 357-358
Harper, P.A.W. and Morton, A.G. (1991). Neurological disease associated with neuroaxonal dystrophy in merino sheep.Aust. Vet. J. 68: 152-153
Windsor, P.A. (2006). Ultrastructural findings in ovine segmental axonopathy of Merino sheep. Aust. Vet. J.M. 84: 169-171
Windsor, P.A., Kessell, A. and Finnie, J. (2011). Review of neurological diseases of ruminant livestock in Australia. Editor invited paper VI. Post-natal bovine, and ovine and caprine neurogenetic disorders. Aust. Vet. J. 89: 432-438
Condy D.R., Richards W.P.C. and Bradford G.E. (1967). Systemic neuroaxonal dystrophy in Suffolk sheep. Acta Neuropathologica, 8, 133-140. Abstract accessed only.