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This article was published in 1964
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INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.

Some Observations on the Pathology of Swainsona Poisoning in Sheep, and Possible Lines of Further Investigation

JOAN C. KATER, B.V.Sc., Veterinary Research Officer, Glenfield.

The clinical signs of Swainsona poisoning, or "pea struck", in sheep which have been described by Hurst (1942) and Diplock (1962), indicate central nervous system involvement. However, there is no apparent record of central nervous system lesions in animals suffering from Swainsona poisoning, other than a brief reference to "peripheral neuritis" by Hurst (1942). A number of affected sheep have been examined from time to time at the Veterinary Research Station, Glenfield, but in no case, prior to 1963, were lesions observed.

Through the continued interest of field officers, specimens have been received from 22 sheep from 11 properties in the Mudgee, Scone, Tamworth, Warialda-Inverell and Moree P.P. Board districts during 1963-64.

Macroscopically no consistent or significant abnormalities were noticed in these sheep. In a small number of the brains there was a suggestion of orange pigmentation in the internal capsule and ventral corpora quadrigemina and pons.

Microscopically in every case there were lesions in the central nervous system. These were of two types which were distributed in approximately equal number.

Type 1

Varying numbers of eosinophilic, more or less spherical accumulations of material, were seen lying free in the brain stem and cord, particularly in the internal capsule, cerebellar peduncles and medulla. These bodies, known as spheroids, are thought to be swollen and degenerating axons, but special nerve fibre stains are required to confirm this. These "axonal swellings", while not specific to Swainsona poisoning, are not known to occur in such profusion or with the same topographical preferences in any other disease of the central nervous system in sheep. Similar axonal lesions are described in infantile neuroaxonal dystrophy, a chronic degenerative disease of the central nervous system in man. Cowen & Olmstead (1963), in which a metabolic defect in the axon, possibly genetically determined, is suggested as being involved in the pathogenesis.

Type 2

There were varying degrees of swelling and fine vacuolation of neurones, the most commonly and severely affected being the large neurones in the hind brain stem and cord and the Purkinje cells of the cerebellum. In some cases neurones, both large and small, throughout the brain were affected. This neuronal swelling was always associated with mild to severe axonal swelling as described for type 1, and, where Purkinje cells were affected, swellings occurred also on their dendrites. These neuronal changes have been described as "pseudolipidosis type" lesions, as they are indistinguishable from a condition in Aberdeen Angus calves described by Whittem & Walker (1957). Special stains in the latter case demonstrated that the vacuoles in the swollen neurones were not occupied by lipid, in contradistinction to the human infantile lipoid dystrophies. Special stains have yet to be done on the sheep brains, but the lesions described probably represent the result of a deranged metabolism within the affected cells.

Lesions similar to type 2 have been seen in sheep in New Zealand (Hartley & Kater 1962, Manktelow (pers. comm.) 1962, but the aetiology was not explained in either case.

Lesions in organs other than the central nervous system have been confined to the presence of "spheroids" in the pars nervosa of some of the pituitaries examined, and the presence of pigmented macrophages in liver and lymph node sinusoids. Associated with the "pseudolipidosis" type lesion, there was commonly cloudy swelling of the liver cells, severe swelling and vacuolation of the cortical tubule epithelial cells in the kidney, and packing of lymph node sinusoids with vacuolated macrophages.

In two brains where there was severe axonal swelling, extracellular brown pigment was seen in association with these lesions.

On five of the eleven properties, where more than one affected sheep was examined, both type 1 and type 2 lesions were seen in separate sheep. In all cases where Swainsona poisoning was suspected, one or both types of lesion were seen, and the evidence so far indicates that the lesions are a result of Swainsona ingestion.

The type of lesion present does not appear to bear any relation to the severity or duration of clinical signs. It can be postulated that, as axonal degeneration is common to both types of lesion, it is the initial lesion, and is followed in some cases by neuronal changes, but this may be clarified by further investigation.

Liver copper levels were determined in sheep from 7 of the properties under investigation, and all were within the normal range.

Swainsona plants from seven properties were identified. Six were Swainsona galegifolia and one, from the Moree district, was Swainsona greyana.

Discussions with property owners and Veterinary Inspectors have brought out the following points:

(1) On some heavily infested properties where Swainsona-free areas are not available, and recommended control measures have failed or are impracticable, sheep and cattle grazing may be rendered uneconomic.

(2) Young sheep appear to be more susceptible, or to take to the pea more readily than older sheep.

(3) Sheep brought onto Swainsona infested properties are particularly susceptible, or more readily become addicted to the pea, if they have previously been on lucerne.

(4) Early Spring rains after a mild Winter tend to bring Swainsona on before other grass or herbage, stock thus being encouraged to take to it before other green feed becomes available.

Possible lines of further investigation would be:

(1) To establish the role of Swainsona in the production of the Central Nervous System lesions, by carrying out feeding trials, preferably on an affected property.

(2) To study the pathogenesis of the Central Nervous System lesions by identifying a number of sheep when they first show clinical signs, and slaughtering these at varying intervals from the onset of signs.

(3) To do field trials on affected properties to test the value of various possible prophylactics.

(4) To test Swainsona extracts prepared by Dr. Riggs at Armidale, for toxicity in a suitable laboratory animal, in an effort to identify the toxic principle.

(5) To ascertain the magnitude of the field problem, by encouraging owners to report suspected cases and collecting available information.

References:

Cowen, D., and Olmstead, E. V. (1963) — J. Neuropath & Exper. Neurol., XXII: 175
Diplock, P. T. (1962), The Veterinary Inspector.
Hartley, W. J. and Kater, Joan C. (1962) — N.Z. vet. J., 10 : 128