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This article was published in 1963
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INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.
Some Nervous Diseases of Ruminants
W. J. HARTLEY, M.R.C.V.S. Senior Lecturer in Preventive Veterinary Medicine, Faculty of Veterinary Science, The University of Sydney
It is obviously impossible at this meeting even to attempt to discuss all the nervous disease conditions affecting ruminants. It is my intention therefore to briefly refer to several disease conditions which are characterised by special lesions in the Central Nervous System or supporting tissues, and with which some of you may not be familiar.
The following disease conditions will be discussed:
Ataxia and posterior paralysis in sheep.
Phalaris tuberosa staggers in sheep.
Focal symmetrical encephalomalacia in sheep.
Polioencephalomalacia in sheep and cattle.
Pseudolipidosis and neuronopathy in cattle.
Hydranencephaly and arthrogryposis in cattle.
Some of these conditions have not, to my knowledge, been reported in this country, but it is highly probable that all occur.
ATAXIA AND POSTERIOR PARALYSIS IN SHEEP:
Excluding congenital developmental abnormalities of the C.N.S., posterior incoordination, often leading to posterior flaccid paralysis is usually a sign of impaired conductivity of the spinal cord. The more important causes are (a) "Spinal Abscess" and (b) Enzootic Ataxia.
(a) The term "Spinal Abscess" is given to the condition in which one, or more, extradurally situated abscesses occur in the tissues adjacent to the spinal cord, and which impinge upon and cause constriction of the spinal cord. The original site of the abscess is not always obvious but in some cases the vertebral body alone is involved and in others the intervertebral articulations. In some cases the infection spreads in the meninges causing a suppurative meningitis and myelitis.
Most cases of 'spinal abscess' occur in lambs less than two months of age and it is presumed that, in the majority of these the infection gains access through the unhealed navels at or shortly after, birth. However, isolated cases are seen in adults. The organisms mainly concerned are Fusiformis spp., Staphylococcus aureus and Pasteurella hemolytica.
(b) Enzootic Ataxia (copper deficiency). It is thought that, with the replacement of copper drenches by the newer anthelmintics. more cases of enzootic ataxia or "sway back" are likely to be seen in Australia.
This condition may be present at birth or it may appear, in otherwise healthy lambs, at 1 to 3 months of age. In the congenital form, lambs are usually born inco-ordinated or paralysed, and on autopsy there is usually extensive cavitation of the white matter of the cerebral cortex.
The delayed form is characterised by a gradually progressive posterior inco-ordination with eventual posterior flaccid paralysis. There are no macroscopic lesions but microscopically there is a symmetrical demyelination of the dorso lateral and ventral columns in the lumbar spinal cord together with degeneration of some ventral horn neurones.
An additional feature of copper deficiency, which may also cause posterior paralysis, is spontaneous fracture of osteoporotic vertebrae.
PHALARIS TUBEROSA STAGGERS IN SHEEP:
Phalaris tuberosa staggers have been known as a distinct clinical entity in sheep in Australia for many years. Although Phalaris is widely used in improved pastures the incidence of outbreaks of Phalaris staggers is apparently very low. However, when the condition does occur both the morbidity and mortality may be very high.
The cause of the entity is not known, but it is presumed that under certain, as yet undefined, growth conditions, the plant contains a neurotoxin. The condition is not due to a cobalt deficiency although cobalt can apparently prevent it.
Phalaris tuberosa staggers usually occur only when the plant dominates the pasture and the toxicity is considered to be greatest when the plants are young and rapidly growing. Clinical signs appear 2 to 3 weeks after sheep are put onto pasture showing new growth, usually in the Autumn and early Winter.
The clinical signs seen in sheep affected with Phalaris staggers are probably familiar to most of you. The signs, which a exacerbated on driving or disturbance, include hyper-excitability, tremors, head nodding, stiff stilted gait, incoordination, buckling at the knees, prostration and epileptiform convulsions. At a property near Canberra sudden deaths in otherwise healthy sheep have been seen in sheep grazing Phalaris. Badly affected sheep seldom recover even if taken off the offending pasture. Less severely affected sheep apparently make a full recovery.
In affected sheep, at autopsy, there is a greenish brown discolouration of the liver and a greenish grey pigmentation of the medulla of the kidneys. In the brain there is a focal symmetrical greenish grey pigmentation of the mid and posterior brain stem. In the cord there is a similar pigmentation of the dorsal root ganglia. Histologically the pigmentation in the brain is confined to the neurones many of which show degenerative changes.
FOCAL SYMMETRICAL ENCEPHALOMALACIA:
The term focal symmetrical encephalomalacia is given to a specific neurological entity characterised by focal symmetrical softenings in the brain, and it almost certainly caused by the delayed effects of Clostridium perfringens Type D toxin.
The condition has been seen in New South Wales and is probably widespread in Australia. It has a sporadic incidence in lambs usually in association with outbreaks of enterotoxaemia.
F.S.E. can occur in any age of sheep but is more common in lambs between one and four months of age. Clinically it is characterised by a wide variety of neurological signs including dejection, head pressing, blindness, aimless walking, circling and epileptiform convulsions. Affected animals survive for up to 5 days.
On post-mortem examination there are, in the brain, large bilateral symmetrical focal areas of non inflammatory necrosis, often containing haemorrhage, in the anterior and mid brain stem and in the cerebellar peduncles.
POLIOENCEPHALOMALACIA IN SHEEP AND CATTLE:
This condition has been seen in cattle and sheep in New Zealand the U.S.A. and in Great Britain and almost certainly occurs in Australia. The aetiology is unknown.
The disease is seen in two forms; the severe form with a low morbidity and a high mortality, the mild form with a relatively high morbidity and low mortality. There are no predisposing factors associated with the severe form, but the chronic form in sheep almost always follows some managemental interference such as shearing or crutching.
The severe form is characterised by a wide variety of neurological signs. The animal is usually found prostrate with opisthotonus, nystagmus, absence of eye preservation reflex and with intermittent convulsions. Less severely affected sheep are able to stand, are dejected, some adopt a dog-sitting, star gazing attitude and some walk aimlessly or in circles.
The mild form is characterised by dejection with blindness and eventual recovery in many affected sheep in from 4-6 weeks.
Pathologically, in the acute form the cerebral cortex is very friable and on slicing the brain there are extensive bilateral areas of yellowish grey discolouration of the dorsal and lateral cerebro-cortical grey matter. In the mild cases there are often no gross lesions except for a focal line of cleavage between cerebro-cortical grey and white matter. Histologically there is, in the severe form, extensive cerebro-cortical necrosis and, in the mild cases, laminar cortical necrosis.
PSEUDOLIPIDOSIS AND NEURONOPATHY IN CATTLE:
This entity occurs only in the Angus breed and it has been seen on several properties in New South Wales since 1950. Although only the Angus breed is affected, the present evidence in this country and in New Zealand, where it also occurs, suggests that it is not inherited. The cause of this condition is not known but would appear to be the result of an inborn error of metabolism. A similar condition has been seen also in sheep in New Zealand.
It is seen in calves from a few weeks of age up to about 15 months and it progresses over a period of a few weeks to several months. The neurological signs include muscle tremor and ataxia, particularly on excitement, aggressiveness and a stilted gait with a tendency to topple over. There is loss of condition and often eventual paralysis.
On autopsy there is often moderate dilation of the lateral ventricles. Microscopically there is a liquid-like degeneration of the Purkinje cells of the cerebellum and of the large neurones in the posterior brain stem.
HYDRANENCEPHALY AND ARTHROGRYPOSIS:
These two congenital developmental abnormalities occur together, often in outbreak form, on some properties in some seasons. The condition was commonly encountered in New South Wales in 1955, but only sporadic cases were seen until 1962 when many further outbreaks occurred. All breeds of cattle have been affected, including crossbreds. Both hydranencephaly (replacement of the cerebral hemispheres by a fluid-filled cavity) and arthrogryposis (permanent joint contracture) can occur together in the same animal or they can occur separately.
Calves affected with arthrogryposis frequently cause dystocia and have to be removed manually. In addition to the joint fixation there is neurogenic muscular atrophy and absence of ventral horn neurones in the spinal cord.
Calves affected with hydranencephaly alone are born alive, are able to walk about, although somewhat uncoordinatedly, and are totally blind.
The cause of this condition is not known. It would appear probable that these animals are subjected to some infection, intoxication, or deficiency in early pregnancy and this interferes with anatomical development of the foetal C.N.S.