Epidemiology and control of bovine ephemeral fever

Abstract

Bovine ephemeral fever (or 3-day sickness) is an acute febrile illness of cattle and water buffaloes. Caused by an arthropod-borne rhabdovirus, bovine ephemeral fever virus (BEFV), the disease occurs seasonally over a vast expanse of the globe encompassing much of Africa, the Middle East, Asia and Australia. Although mortality rates are typically low, infection prevalence and morbidity rates during outbreaks are often very high, causing serious economic impacts through loss of milk production, poor cattle condition at sale and loss of traction power at harvest. There are also significant impacts on trade to regions in which the disease does not occur, including the Americas and most of Europe. In recent years, unusually severe outbreaks of bovine ephemeral fever have been reported from several regions in Asia and the Middle East, with mortality rates through disease or culling in excess of 10–20%. There are also concerns that, like other vector-borne diseases of livestock, the geographic distribution of bovine ephemeral fever could expand into regions that have historically been free of the disease. Here, we review current knowledge of the virus, including its molecular and antigenic structure, and the epidemiology of the disease across its entire geographic range. We also discuss the effectiveness of vaccination and other strategies to prevent or control infection.Electronic supplementary materialThe online version of this article (doi:10.1186/s13567-015-0262-4) contains supplementary material, which is available to authorized users.

Expression of the G1 epitope of bovine ephemeral fever virus G glycoprotein in eukaryotic cells

“…In addition, neutralising G protein monoclonal antibodies injected intraperitoneally conferred passive protection against intracerebral infection of suckling mice (Cybinski et al, 1990). Hence, it appears that the G protein delivered in a properly folded form and with an appropriate adjuvant is adequate to induce protective immunity (Walker & Klement, 2015). Amino acids variations have been detected in the major neutralisation sites (G1, G2, and G3) of the G protein but they did not affect on the neutralisation phenotypes of epitopes targeted by the MAbs (Trinidad et al, 2014).…”

“…Therefore, the influence of these vaccines in the field may be poor unless further booster doses are administered at the regular intervals. More researches based on advanced technologies are needed to reduce the required number of doses and extend the duration of protection (Walker & Klement, 2015). Hence, the aim of the present study was to construct a eukaryotic plasmid, expressing G1 epitope of BEFV G glycoprotein gene, for application as a possible DNA vaccine for immunisation of animal models and evaluation of its efficacy in future studies.…”

“…BEF can be spread rapidly and leads to considerable economic losses in the cattle industry (Walker & Klement, 2015). Prevention and control of BEF infection can be made through vaccination and treatment of affected cattle (Wallace & Viljoen, 2005;Aziz-Boaron et al, 2013).…”

“…It occurs in many tropical and subtropical regions around the world from the southern tip of Africa to the Nile River Delta, across the Middle East through South and southeastern Asia, into northern and eastern Australia, and throughout most of China, extending into Taiwan, the Korean Peninsula and southern Japan (Walker & Klement, 2015). Signs, which occur sud-denly and vary in severity, can include a sudden onset of fever (41-42 o C), stiffness, lameness, depression, cessation of rumination and constipation (Walker, 2005;Zheng et al, 2009).…”

“…Prevention and control of BEF infection can be made through vaccination and treatment of affected cattle (Wallace & Viljoen, 2005;Aziz-Boaron et al, 2013). Several researches have been directed towards the development of an efficient vaccine for BEF including live attenuated, inactivated, subunit G protein-based, and recombinant vaccines (Walker & Klement, 2015). The BEFV G glycoprotein is the target of virus neutralising antibodies (Cybinski et al, 1992;Uren et al, 1994).…”