Ephemeral fever remains a viral disease of considerable importance to many countries including Australia. The virus has been only partly characterised and still awaits final classification. Although BEF virus was first thought to contain 6 structural proteins there is increasing evidence to suggest that it contains the 5 proteins characteristic of the Rhabdoviridae. Although BEF is thought to be arthropod borne, the vector has yet to be identified but it is clear from the distribution of BEF that more than one vector is capable of transmitting the disease. Despite rigorous investigation of the clinical signs and the pathology of ephemeral fever, little progress has been made on the pathogenesis of the disease. This has been partly due to the difficulty of propagating BEF virus in vitro and the inability to define the site of replication. However, there is mounting evidence to suggest that BEF is immunopathologic in nature and that the clinical expression of the disease is influenced by the release of one or more mediators of inflammation. The disease is characterised by a number of haematological and biochemical changes and early and prolonged treatment with phenylbutazone is capable of reversing a number of these changes. The intravenous administration of calcium can now be considered a justifiable addition to the treatment regimen together with prolonged phenylbutazone therapy. The vaccines currently available are prepared from either live attenuated or killed virus and may be less than reliable. There appears to be a need for a reliable, inexpensive, cold-chain independent alternative vaccine.