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Literature concerning cobalt, selenium, Vitamin E deficiencies and Ostertagia circumcincta infection was reviewed togther with the interrelationship of these factors to immune function in lambs. Two experiments were described. In the first, the inter-relationship between cobalt deficiency, O. circumcincta infection and immune function was examined. Sixty, nine to twelve week old Blueface Leicester cross Swaledale and Scottish Blackface lambs were assigned to three treatment groups dependent upon their maternal cobalt status thus: deficient lambs came from cobalt deficient ewes; depleted lambs came from cobalt sufficient ewes but were then fed a cobalt deficient diet; sufficient lambs also came from sufficient ewes by their status was maintained by weekly administration of a cobalt supplement. All lambs were fed a diet deficient in cobalt. The groups were then sub-divided into infected and non-infected, the latter receiving 2000 L3 O. circumcincta three times per week for 16 weeks. Cobalt deficient lambs suffered extremely high mortality rates, regardless of infection, in comparison with a much lower rate among depleted lambs and none in the sufficient group. A possible link between hepatic encephalopathy and white liver disease was found. Neither liveweight effects nor anaemia attributable to poor performance associated with helminth infection were noted. However, cobalt deficient lambs had significantly reduced liveweight and anaemia in comparison with sufficient controls although some degree of anaemia was also evident in the latter group. Anaemia was found in depleted lambs, which matched sufficient controls in liveweight in the early part of the experiment but showed liveweight impairment during the latter part presumably after exhaustion of maternally derived cobalt reserves. Deficient lambs suffered more pathogenic 0. circumcincta infection than their sufficient controls as measured by plasma pepsinogen concentrations but values found in all infected lambs were nonetheless greater than those in non-infected counterparts. Prolonged elevation of plasma pepsinogen concentration indicated a continued establishment of incoming larvae in infected groups which was confirmed by maintained circulatory eosinophilia particularly in cobalt deficient and depleted lambs. Depleted infected lambs revealed plasma pepsinogen concentrations similar to sufficient infected controls in the early part of the experiment but which rose substantially thereafter, again presumably after the exhausion of maternally derived cobalt reserves. Infected sufficient lambs had plasma pepsinogen values which were much lower than those found in depleted or deficient lambs. Similar effects were noted in worm egg count data. Total worm counts at sacrifice of four depleted and four sufficient lambs revealed significantly higher burdens in the depleted lambs. Absence of significant stunting, difference in adult:larval proportion and difference in male:female ratio in total worm counts suggested that immunity to infection was incomplete in those lambs. High mortality among cobalt deficient lambs prevented the collection of meaningful comparative data. Significantly impaired immune function as measured by ability of neutrophils to kill ingested yeast cells was noted in cobalt deficient and depleted lambs in comparison to their sufficient controls. Attempts to investigate phagocytic impairment further were inconclusive. Serological response to O. circumcincta was relatively low in all lambs in Experiment 1 and not thought to be indicative of immunity. Serological response to Clostridium tetani toxin revealed no significant difference in pre-vaccination titre in any group of lambs, thus suggesting no impairment in maternal passive transfer of those antibodies associated with cobalt deficiency.