Summary An investigation of 78 cases of typical Australian Stringhalt from 52 properties in Victoria was carried out from 1985 to 1987. Horses were either examined in the field (n = 52), referred to the Veterinary Clinical Centre (n = 13) or clinical details were obtained verbally (n = 13). In addition 10 cases of false or atypical stringhalt were examined. Detailed soil and pasture analysis was carried out on 14 properties where Australian Stringhalt had occurred. Information was also obtained on epidemiology of the condition from a survey of practitioners. Fifty of the 52 cases examined in the field occurred in horses that were dependent upon poor quality unimproved dry pasture. In all but a few cases, there was no pasture improvement or fertiliser application, leading to the development of weed‐dominated pastures, particularly by flatweed, Hypochaeris radicata. The range of clinical signs exhibited by horses with Australian Stringhalt was described and a grading system proposed to classify horses according to severity of signs. Laryngeal abnormalities were present in 10 of 11 cases examined endoscopically and these horses exhibited increased electromyographic (EMG) activity in the long digital extensor muscle at rest and during hindlimb flexion. To a large extent, the EMG changes disappeared and digital extensor muscle atrophy improved in two horses that were monitored to recovery. Deep peroneal nerve conduction studies in four horses with Australian Stringhalt showed a substantial reduction in nerve conduction velocity and when stimulated at 50 Hz were unable to sustain activation of the long digital extensor muscle. EMG and evoked responses appeared to be sensitive indicators of the state of the disease. Spontaneous recovery over a period ranging from a few days to over 18 months occurred in 78 per cent (45 out of 58) of field cases available for follow up, although eight horses were destroyed on humane grounds or for pathological investigation.

Summary Nine horses with clinical signs of Australian Stringhalt were killed and tissues collected for a detailed pathological study. Lesions were limited to peripheral nerves and muscles. The most severely affected nerves were the superficial and deep peroneal, distal tibial, plantar digital, volar and recurrent laryngeal nerve with changes characterised by a selective loss of large diameter myelinated fibres with various degrees of demyelination, fibrosis, Schwann cell proliferation and onion‐bulb formation. A routine evaluation of the brain and spinal cord by light microscopy failed to reveal any consistent abnormalities. Morphometric analysis of deep peroneal and recurrent laryngeal nerves confirmed the reduced number of large diameter myelinated axons. Teased fibre preparations of these nerves did not show any abnormalities in internodal distance. The most severe muscle lesions were in the long and lateral digital extensors, cranial tibial, dorsal cricoarytenoid, gracilis and lateral deep digital flexor with extensive atrophy of fibres and diffuse fibrosis. Histochemical evaluation of the long digital extensor from 3 affected horses showed an abnormally wide distribution in fibre size and a reduction in type II fibres compared with controls. These lesions are consistent with a distal axonopathy leading to neurogenic muscle atrophy. The distribution of neuromuscular lesions in Australian Stringhalt may be explained by the susceptibility of longer, larger myelinated nerve fibres to injury, but the cause for this distal axonopathy remains unknown.

Of 467 cat serums tested for antibody to feline immunodeficiency virus (FIV) 120 (26%) were positive. The average age of positive cats was 7.5 years (range 1 to 16 years), and 67% were male. Of 110 serums collected in 1980, 27 (24.5%) were positive. A wide variety of clinical signs including oral cavity disease, anorexia, weight loss, lethargy, depression, fever, respiratory and urinary tract disease, conjunctivitis, abscesses, anaemia and lymphadenopathy were observed in the cats with serum antibody. There was often a history of chronic disease or recurrence of particular or various clinical signs in these cats. FIV was isolated from 4 of 8 FIV antibody positive cats by cocultivation of patient lymphocytes with donor lymphocytes in the presence of interleukin 2.

A 7-year-old male, black Labrador Retriever dog had a shifting leg lameness and reduced exercise tolerance for 2 to 3 days. Because of marked splenomegaly a splenectomy was done. The spleen was turgid with round edges and weighed about 4.5 kilograms. Tissue was mottled blue-grey and the cut surface bulged. Lymphoid follicles were not obvious.Ten days after surgery the dog was weak, anorectic and anaemic. The dog was killed and necropsied 3 hours later. The carcass was obese, mucous membranes were blanched, and the blood was watery.The liver was enlarged, mottled brown-red and firm, with sharp notched edges. On section, there were pale tracts about portal triads and darker centrilobular areas. Firm raised irregularly-shaped pink-yellow plaques, 1 to 3 centimeters in diameter, were on the anti-mesenteric serosal surface of the ileum and large intestine. The lesions extended through the serosa into the tunica muscularis and mucosa. Mesenteric, bronchial and peripheral lymph nodes were enlarged, firm, tan-yellow and had no corticomedullary differentiation.The renal capsules adhered to the surfaces of the kidneys, leaving focal pits and depressions when removed. The medulla was congested and pale linear streaks extended through the cortex into the medulla. Glomeruli were prominent. The lungs were congested. The left ventricle of the heart was dilated and the left atrioventricular valves were thickened. Bone marrow was grey-tan.Formalin fixed parts of liver, intestine and mesentery were processed for electron microscopy. With light microscopy there was massive infiltration of most body tissues, especially spleen, bone marrow, lymph nodes, palatine tonsils ( fig. l), Peyer's patches and liver, by macrophages with ovoid large open nuclei, a prominent single nucleolus and copious, finely granular to foamy, grey, cytoplasm. The cytoplasm contained many acid-fast bacilli.Macrophages and bacilli were found free in the efferent lymphatics and sinuses of the tonsils, in subpleural and perivascular lymphatics of the lung, under the endothelium of vessels, within sinusoids and in subcapsular, periacinar ( fig. 2), and periportal areas of the liver. They were found occasionally along capillaries in the adrenal and in subcapsular accumulations in the kidneys. The plaques along the intestine contained masses of bacilliladen macrophages extending from the serosa through the tunica muscularis, submucosa and lamina propria. Many plasma cells were in the lamina propria. Peyer's patches of the ileum and lymphoid follicles of the large intestine were most severely affected.Perivascular cuffing by mononuclear cells and lymphocytes was evident throughout the brain, the leptomeninges and spinal cord. A few glial nodules were randomly distributed throughout the cerebrum, usually associated with blood vessels. Only a few acid-fast bacilli were found free or within mononuclear cells in brain and cord. Electron microscopy showed many bacilli, from 1.1 to 1.3 X 0.2 to 0.5 micrometers, within cytoplasmic vacuoles in macrophages ( fig. 3 ) .Mycob...

The clinical, pathological and epidemiological factors were investigated in 12 horses presenting with severe neurological signs. Although the cases involved differing central (n = 1), spinal cord (n = 4) and peripheral nerve (n = 7) deficits in a number of instances, there were similar pathological findings. The possibility of a unifying aetiological factor, such as a toxicosis, is discussed because of the pathological similarities and as the cases appeared during an unusually long dry period.