Two calves given a mean of 16.1 g and 16.4 g ripe Castanospermum australe seeds/kg body weight daily for 13 and 16 days respectively developed haemorrhagic gastroenteritis. The first calf died. The second calf had mild myocardial degeneration and necrosis and mild nephrosis at necropsy. Two calves given a mean of 16.8 g unripe C. australe seeds/kg body weight daily for 18 days remained clinically normal and had mild gastritis at necropsy. The activity of alpha-glucosidase was reduced in the mononuclear cells of peripheral blood and in skeletal muscle. This was attributed to the presence of the indolizidine alkaloid, castanospermine, in the seeds. The toxin causing the gastroenteritis and other lesions is unknown.

Summary Stieep were experiraentalty infected with bovine leukaemia virus (BLV) by the inoculation of PBL from leukaemic sheep. Antibodies to viral structural proteins were detected at from 2 to 6 weeks after inoculation. At seroconversion, all sheep had a marked increase in the number of circulating lymphocytes, due essentially to an increase in the number of B cells. The number of circulating B cells then decreased but remained higher than pre-infection levels. A second increase in this population preceded the development of a B cell lymphoblastic leukaemia. Generalized lymphosarcoma was diagnosed at necropsy of all sheep. Variation between individual sheep in the time from infection to the development of tumours allowed two clearly delineated groups of nine sheep to be compared. A study of changes in the B cell and T cell populations during the first 16 weeks of infection suggested that the initial response to infection influences the subsequent rate of leukaemogenesis. At seroconversion the number of circulating B cells was significantly higher in group 1 (1016±l-51X10'/l)than in group2(6-47±276X10'/l). Group 1 sheep became leukaemic at 20-50 weeks after infection, whereas group 2 sheep did not do so until 70-95 weeks after infection.

The effect of levamisole treatment every 3-4 weeks, cobalt therapy, or both, on the performance of yearling cattle grazing together on known cobalt-deficient pastures on a siliceous sandy soil in south-eastern Queensland was studied between August 1978 and October 1979. In the first stage of the observations, from August to March, the responses (Pc0.05) in liveweight gain compared with the controls (C) were 18, 54 and 75 kg for levamisole (L), cobalt bullets (B), and both (LB) respectively. Thus the responses were additive with no interaction. Deaths were recorded in the control and levamisole only groups in March. Steers in the levarnisole only group were treated with cobalt in March (L + B). Liveweight gains between March and October were 9, 71,47 and 41 kg for C, L + B, B and LB groups, respectively (L + B > B, LB > C, P< 0.05). Cobalt therapy increased faecal worm egg counts in undrenched groups between November and April (P<0.05). At 30 weeks after the start of the study many animals in groups C, L and B were anaemic. Cobalt concentrations in green panic ranged from 0.015 to 0.029 �g/g dry matter and in Siratro from 0.036 to 0.048 �g/g dry matter.