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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.

This paper reports the first isolation of equine arteritis virus (EAV) in Australia and serological evidence of exposure to EAV in Australian horses. Twelve Standardbred stallions imported from North America were found to shed EAV in semen. One hundred and seven stallions were tested for serum antibodies to EAV and 73% of Standardbred stallions tested were seropositive as compared to 8% of Thoroughbred stallions. Serum antibody was detected in 71% of Standardbred mares, 6% of Standardbred racehorses and 1% of Thoroughbred mares and racehorses. Examination of stored serums demonstrated that EAV had been present in Australia since at least 1975.

break of equine viral arteritis (EVA) occurred on a considerable number of Thoroughbred breeding farms in Kentucky in 1984. Subsequent events have shown that this was a watershed event. That occurrence resulted in a dramatic increase in the significance with which this disease would henceforth be perceived by many horse industries worldwide. Greater awareness, surveillance, and improved diagnostic capability collectively have led to an increase in the number of reported outbreaks of EVA over the intervening years. Spread of this infection internationally can almost invariably be attributed to the movement of carrier stallions or shipment of virus-infective semen. The increase in number of confirmed outbreaks of the disease bears little relationship, however, to the known global distribution of the causal agent, equine arteritis virus (EAV). Based on the results of serosurveillance surveys and diagnostic testing, it would appear that the majority of cases of EAV infection continue to be asymptomatic. Where investigated, the virus has not been shown to be a significant cause of abortion or illness and death in young foals. Outbreaks at racetracks, sales yards, etc are very infrequent in occurrence.

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.(ABSTRACT TRUNCATED AT 250 WORDS)

Adverse reactions to intramuscular injections of procaine penicillin G are reported in 11 horses, five of which died. The clinical findings are presented and suggest central nervous involvement in most cases. Post mortem findings in one horse were consistent with anaphylaxis whereas in other cases the clinical findings, duration of treatment, speed of onset and subsequent completion of treatment supports diagnosis of an acute procaine toxicity syndrome.

Five horses with Australian stringhalt were treated with 15 mg/kg phenytoin orally for 2 weeks. During the second week of the trial, 3 of the horses were given an additional dose of 10 mg/kg phenytoin. The response to treatment was clinically assessed by grading the severity of the gait abnormality at the walk, trot, turning and backing twice daily. There was a significant (P less than 0.05) improvement in the gait abnormality when pre-treatment values were compared with the mean of the last 3 assessments before treatment stopped. When reassessed 2 weeks after treatment ceased, there remained a significant (P less than 0.05) improvement compared with pre-treatment values at the trot and on backing, but not at the walk or turning. Surface electromyographic recordings were made weekly from the long digital extensor muscle, and there was a change to a near normal recording by the end of treatment. Plasma phenytoin concentrations were monitored during the trial, and the dose rates used achieved a steady state with a mean plasma level of 37 +/- 7 mumol/l. There was wide variability between plasma concentrations in different horses, although there was no difference in absorption between administration of the phenytoin as a paste, or when it was mixed in the feed. Although mild tranquilization was seen after treatment, there were no clinical, haematological or biochemical signs of toxicity from the phenytoin therapy.