The clinical, parasitological and haematological parameters of tick-borne fever (TBF) in sheep were assayed. Infections were characterised by incubation periods of one to four days followed by fevers which lasted from four to 12 days. The prepatent periods ranged from two to seven days and. the visible parasitaemias persisted for six to ten days. Other clinical signs were minimal. Haematological changes, however, were dramatic; an initial leucocytosis was followed by a profound leucopaenia attributable first to a fall in lymphocyte and eosinophil numbers and later to a neutropaenia. The nature of the TBF-induced lymphocytopaenia was investigated and found to be associated with a significant decrease in the number of peripheral B-lymphocytes and with a small reduction in the number of T-lymphocytes. Evidence of immunosuppression was sought and found by measuring the primary and secondary antibody responses of TBF-infected sheep to a commercial clostridial vaccine. Injections of the vaccine elicited primary and secondary serum antibody responses in both TBFinfected and normal sheep but the antibody titres in the infected sheep were observed to be significantly lower than the titres in the normal sheep. In contrast to the suppressed humoral immune responses the cell-mediated response as measured by a delayed skin hypersensitivity reaction to dinitrochlorobenzene was unimpaired in the TBF-infected sheep. The effect of TBF on phagocytosis by neutrophils was examined. The phagocytosis of staphylococci was considerably reduced during the TBF parasitaemia; this reduction was attributed to the limited phagocytic activity of the parasitised neutrophils Tick-borne fever affected the nasal carriage of Pasteurella haemolytica in sheep; the rate of isolation of the organism from swabs of the nasal secretions increased during the reaction to Cytoecetes phagocytophila infection. The attempt to produce pyaemia in lambs by superimposing TBF on an already existing naturally acquired staphylococcal infection was unsuccessful. On the other hand, concurrent infections of sheep with C_. phagocytophila and parainfluenza-3 virus produced respiratory distress and deaths. The exacerbation of the respiratory disease in the animals with dual infections was associated with a suppressed antiviral antibody response. It is postulated that the observed potentiation of concurrent infections stems from the combined effect of the neutrophilic malfunction and immunosuppression induced by C. phagocytophila.