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This paper describes three cases of what is probably a new form of storage disorder. The affected animals were English Springer Spaniels and they had developed progressive neurological signs when 2–3 years old. They had gross enlargement of the vagi and of the spinal nerves supplying the brachial plexus. By light microscopy in these nerves there were massive amounts of endoneurial loose fibrous tissue with dispersion of nerve fibres and many foamy phagocyte-like cells. In the central nervous system there was very severe cytoplasmic vacuolation of most neurones and neuroglia, perivascular phagocyte-like cells, loss of myclin, loss of Purkinje cells, numerous spheroids, hypertrophic astrocytes and fibrous astrocytosis. There was also foamy cytoplasmic vacuolation of renal convoluted tubules and pancreatic exocrine parenchyma and numerous foamy phagocyte-like cells in lymph node and lung. On ultrastructural examination membrane bound vacuoles wee present in the cytoplasm of affected neurones and phagocyte-like cells. Most of the vacuoles were empty, some contained amorphous materials and some, in neurones, contained stacks of curved or straight lamellae. It is suggested that the stored material could be an oligosaccharide.

7 cases of a focal necrotizing encephalitis associated with a severe vasculitis are described in cattle. It is suggested that these lesions may have resulted from a hypersensitivity effect due to the presence of tuberculosis elsewhere in the body.

Ten Devon cattle from a single property were affected with blindness from 14 months of age. Severe retinal degeneration progressing to atrophy was associated with widespread intracellular accumulation of pigment in the retinal ganglion cells, central nervous system and major organs. The pigment was consistent with ceroid-lipofuscin granules on histological, histochemical and ultrastructural examination. Although a familial relationship existed between affected individuals, a pattern of inheritance could not be established by examination of available breeding records. The disease is compared to similar disorders reported in man and other species.

This paper describes a neurovisceral cytoplasmic storage disease together with neuroaxonal dystrophy and dysmyelinogenesis in two of three new born goats affected with an arthrogryposis-like syndrome. The entity is compared with other conditions in which no substance can be demonstrated in cytoplasmic vacuoles.

The ceroid-lipofuscinoses comprise a group of inherited storage diseases of human beings and animals that are characterised by progressive neurodegenerative disease and the accumulation within cells of a fluorescent lipopigment. A distinct syndrome occurs in Cocker spaniel dogs in which there is a generalised accumulation of a lipofuscin-like pigment, with such a heavy accumulation in smooth muscle that the intestine and other organs have a brown discolouration. Such discolouration is not observed in other forms of ceroid-lipofuscinosis. Dogs are clinically affected in adulthood and show progressive hind limb paresis, into-ordination, and deficient postural reactions and proprioception. Spinal reflexes may be exaggerated. Behavioural or temperament changes, seizures or blindness may occur.

Thirteen of the 15 cases of polioencephalomalacia reported in this article are considered to be idiopathic. These cases are compared with two cases of polioencephalomalacia following from cyanide poisoning and all are discussed in relation to similar entities occurring in dogs and in other species.

This paper describes nine cases of a parenchymatous peripheral neuropathy in dogs, characterized clinically by posterior ataxia and paralysis, and pathologically by widespread myelin and axon destruction in ventral spinal and peripheral nerves, together with disappearance of ventral horn neurones. It is discussed in relation to nutritional and other peripheral neuropathies seen in man and animals.

This paper describes two cases of a progressive incoordination in Jack Russell terriers. Histologically the entity was characterised by widespread Wallerian-type degeneration of the brain and cord, together with focal symmetrical demyelination of the dorsolateral and ventromedial columns of the cord. One dog also showed severe ballooning of myelin sheaths in the dorsal and ventral spinal nerves and oedema and fibrosis of the sciatic nerve. Both dogs also showed degenerative changes of the central auditory pathways.

This paper describes the neural and extra-neural lesions seen in cattle, sheep and a horse associated with the ingestion of species ofSwainsona. The neural lesions consist of widespread watery cytoplasmic vacuolation of large neurones together with many spheroids (neuroaxonal dystrophy) and abnormal amounts of a lipofuscin-like pigment. Similar foamy vacuolation involves the choroid plexus, the exocrine panreatic parenchyma, the renal convoluted tubules and other viscera. The lymph nodes contain foamy macrophages in medullary sinusoids and/or much intracellular lipofuscin-like pigment.

An echocardiographical and clinical pathological investigation of the rapid loss of weight by a yearling thoroughbred fflly revealed an atrial septal defect, a ventricular septal defect and hyperfibrinogenaemia. A post mortem examination confirmed the cardiac abnormalities and revealed a severe thoracic aortitis. It is proposed that the idiopathic thoracic aortitis contributed to the horse's compromised cardiovascular homoeostasis.

In the pathological collection of native fauna diseases held at the Taronga Zoo, Sydney, there are materials from about 300 wild, free range brush-tail possums from the Sydney area. Thirty-five of these have neurologic lesions.

Selenium is an essential micronutrient, although ingestion in excess in pigs can cause disease conditions including neurological dysfunction and chronic skin and hoof lesions. Controlled feeding trials in growing swine, using the same Se content in feed sources, resulted in higher concentrations (p < 0.05) of Se in blood and organs of pigs fed seleno-DL-methionine compared with those receiving Astragalus bisulcatus or sodium selenate. Clinical signs of Se toxicity including neurological signs of paralysis were more severe and occurred sooner in the A. bisulcatus group than in the sodium selenate or seleno-DL-methionine groups. All five pigs fed A. bisulcatus developed neurological signs of paralysis, and in four the signs occurred within 5 days of the start of treatment. Four of five pigs fed sodium selenate also developed paralysis, but this occurred 4 to 21 days after treatment began. The fifth pig in the group developed signs of chronic selenosis. Two of five pigs fed seleno-DL-methionine developed paralysis on 9 and 24 days, respectively, and the remaining three developed chronic selenosis. Selenium fed to pigs in three forms [plant (A. bisulcatus), sodium selenate, or seleno-DL-methionine] resulted in neurological dysfunction and lesions of symmetrical poliomyelomalacia. These were most severe in the A. bisulcatus group, which also had polioencephalo-malacia. Although seleno-DL-methionine caused the greater increase in tissue and blood Se concentrations, this did not correlate with severity of pathological changes, since animals fed A. bisulcatus developed more severe and disseminated lesions.