Diseases caused by Akabane and related Simbu-group viruses

Preferred citation: Anipedia, www.anipedia.org: JAW Coetzer and P Oberem (Directors) In: Infectious Diseases of Livestock, JAW Coetzer, GR Thomson,
NJ Maclachlan and M-L Penrith (Editors). PD Kirkland and TD St George, Diseases caused by Akabane and related Simbu-group viruses, 2018.

Diseases caused by Akabane and related Simbu-group viruses

Previous authors: T D ST GEORGE AND P D KIRKLAND

Current authors:
P D KIRKLAND - Senior Principal Researcher Scientist, Manager Virology Laboratory, BVSc, PhD, FAMS, Elizabeth Macarthur Agriculture Institute, Woodbrigde Road, Menangle, New South Wales, 2568, Australia
T D ST GEORGE - Retired from Commonwealth Scientific & Industrial Research Organisation, DVM, MVSc, BVSc, Virus Consultants International, 44/260 Cliveden Avenue, Corinda, Queensland, 4075, Australia

Introduction

Many viruses in the Simbu-group of the genus Orthobunyavirus family Peribunyaviridae, order Bunyavirales1 have not been identified as pathogens but those that are pathogenic usually cause congenital defects after infection of a susceptible pregnant small stock and  cattle. The defects  are principally arthrogryposis (AG) and hydranencephaly (HE) and can be associated with abortion in cattle, sheep and goats.  These viruses usually produce clinically inapparent infections in non-pregnant animals. However, in pregnant cattle, sheep and goats, if the viruses reach the foetus at a critical stage of development, marked teratology, particularly of the central nervous system, may result. The defects are usually only apparent some months later with the birth of affected calves and lambs. Some Simbu-group viruses also occasionally cause post-natal encephalitis in a range of mammalian species. Antibodies to Akabane and related arboviruses are found in cattle, sheep, goats and wild and other domestic animals in Africa, Middle East and the Asian-Pacific region.  In 2011 Schmallenberg virus, a previously unrecognised Simbu virus, has emerged and spread throughout most of Europe.30

The name ‘Akabane disease’ has been used,35 but it is not apt as Akabane virus is only one member of the Simbu-group, several of which may produce similar defects, including the recently recognised Schmallenberg virus. Akabane virus is nevertheless by far the best studied and probably most pathogenic member of the group.

The relationship between Akabane virus and congenital AG/HE was first recognized in Japan between 1972 and 1975.35 The studies in Japan and Australia, which in 1974 confirmed the link between infection with Akabane virus and AG/HE, have been reviewed.35, 63 Disease caused by Simbu-group viruses in Africa is poorly defined, though AG/HE has been observed in cattle in KwaZulu-Natal, South Africa, and in sheep in Zimbabwe.69

Although the association of Akabane and related viruses with epidemics of AG/HE is comparatively recent (1974), the syndrome was recognized much earlier. There are reliable records of its occurrence in Australia in the early 1930s29 when it was attributed to plant poisoning, in Japan in 194935 and in Israel in 1969/70.50

Other viruses of the Simbu-group which have been associated with similar disease are Aino,12 Peaton, Schmallenberg,6 Shamonda31 Shuni81 and Tinaroo, although clinical cases in the field due to Aino are not common and are rare with Peaton52 and Tinaroo.43 Schmallenberg virus has been responsible for an extensive outbreak of congenital defects in cattle, sheep and goats following its emergence in fully susceptible livestock populations in western Europe in 2011.6, 17 Shuni virus has been associated with encephalitis in horses and a range of wildlife species in South Africa81 and congenital defects in ruminants in Israel.22 Cache Valley virus, which belongs to a separate serogroup within the family Peribunyaviridae, is widely distributed in North America and has been reported to produce AG/HE in sheep in Texas.19

Aetiology

Viruses within the Simbu-group, one of the 36 antigenic clusters within the family Peribunyaviridae, have spherical, enveloped virions, 90 to 100 nm in diameter. They have tripartite segmented single-stranded RNA and are readily inactivated by chloroform, ether and trypsin. Akabane virus degrades moderately quickly at 37 °C,35 remains viable in blood samples kept at 4 °C for several months, and can be stored indefinitely at −70 °C or lower. For more information on the properties of the viruses which belong to the Peribunyaviridae, see General Introduction: Bunyaviridae and Rift Valley fever.

Epidemiology

Most of Africa, Asia (excluding Russia), and Australia may be regarded as endemic for Akabane virus and, in all probability, many of its antigenic relatives. Schmallenberg virus is the only Simbu virus that has been identified in Europe and England. The American continent (except for the presence of Cache Valley virus of the Bunyamwera serogroup), Papua-New Guinea and the island countries of the Pacific are believed to be free of infection with Simbu-group bunyaviruses.74 However, the distribution of Akabane and related viruses within each country is affected by the distribution, seasonal activity and abundance of  insect vectors.

The isolation of Akabane virus from mosquitoes62 and the biting midge, Culicoides brevitarsis,18 preceded its incrimination as a cause of disease in sheep or cattle and was a necessary step in unravelling the aetiology. Despite the association between Akabane virus and biting arthropods, the virus has not yet been transmitted experimentally to any vertebrate by any species of insect. The virus has, however, been shown to multiply in experimentally infected C. brevitarsis and to reach the salivary glands in 10 days.59

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