I initially saw the affected ewes in mid August 2001. They were of mixed ages, three to five years old and had been run in different paddocks on good feed. Some had been on a failed rye corn crop and others had been on a mixture of native and improved pasture. All of the ewes had access to sheep pellets at some stage during late pregnancy/ early lactation. They all had lambs at foot, the majority had twins (this flock tends to have a very high fecundity). The ewes were shorn the previous October and were backlined at shearing. They had not been jetted since the summer. The owner had seen one ewe the past year with similar clinical signs, but it had died. The owners advised that all of the ewes had different sires.
Ten out of 400 ewes (2.5%) were affected to varying degrees. On the initial examination (on a relatively cool day of 14 - 15°C) two of the ewes had temperatures of 40°C. The other ewes had normal temperatures. They exhibited symptoms of forelimb paresis and proprioceptive deficits with intermittent knuckling over in the fetlocks. Muscle wasting was evident particularly over the shoulder. Hyperextension of the forelimbs was present during placement and lifting. Their general mental behaviour was not affected, appetite appeared normal and neck pain could not be elicited.
When I revisited them on 13th September, they were also displaying hind limb paresis with bunny-hopping when forced to run. They appeared to have shown a general improvement, even though the hind limb paresis had occurred since the previous visit. There was a tendency for the worst affected sheep to arch the back and carry the fore and hind limbs well under the body. Muscle wasting was still present, but it seemed to have improved somewhat. A video was taken of the ewes and sent to Chris Bourke for his assessment. (Chris provided an assessment of the clinical signs displayed, with comments providing possibilities to investigate further on the property. He commented that the signs were suggestive of either a primary myopathy, restricted to the shoulders and hips or to a spinal cord dysfunction in the region of the upper thoracic vertebral bodies, or both). The clinical signs gradually diminished and the majority of the ewes returned to normal after three to four months. Two ewes were affected in the following year, although I didn’t see these ewes.
Apart from the obvious muscle wasting over the shoulders, there was very little associated gross pathology in the one ewe autopsied. There was no gross evidence of subluxation of thoracic vertebral bodies.
Samples submitted for histopathology included brain, skeletal muscle and spinal cord (T1-2, T4, T5, T6, T9-10 and lumbar). Findings were limited to the spinal cord, where there was ‘occasional symmetrical axonal swelling at the dorsoventral funiculi, sometimes associated with demyelination throughout the spinal cord’.
Any treatment or control options
Affected ewes were shedded and treated with antibiotic, however it seems very unlikely that the antibiotic treatment would have brought about any improvement.
A follow-up paddock walk with an Agronomist from NSW Ag failed to find any plants of interest. The owner thought that onion grass may have occurred on the property, but not in significant amounts.
Romulosis occurs due to a fungus grown on the weed onion grass (Romulea rosea). Clinical signs vary from knuckling over of the fetlock joints to staggering, walking on the knees and sternal and lateral recumbency due to the associated muscle weakness, paresis and paralysis (A.A. Seawright, Chemical and Plant Poisons, 2nd Ed.) Affected animals are generally bright and retain a good appetite. Gross pathology is generally unremarkable, or there may be mild swelling of the liver and kidneys. The most significant lab findings are microscopic changes found in the spinal nerve roots, especially the ventral roots and in peripheral nerves. Most commonly, there is myelin degeneration and axonal swelling. (Ibid.)
According to Chris Bourke’s classification system for locomotor disorders of sheep in Australia (Bourke, C.A., Aust Vet J 1995; 72:228-234), the syndrome observed would be classified under Group 2 syndromes, (i.e. Limb Paresis with Knuckling Syndromes), and sub-grouped under Complex Entities. (pers. comm. Chris Bourke).