Diseases caused by Akabane and related Simbu-group viruses

T D ST GEORGE AND P D KIRKLAND

GENERAL INTRODUCTION: BUNYAVIRIDAE

Introduction

Viruses in the Simbu group of the family Bunyaviridae cause congenital defects, principally arthrogryposis (AG) and hydranencephaly (HE), and abortion in cattle, sheep and goats. Throughout a broad area of the Old World, antibodies to Akabane and related arboviruses are found in cattle, sheep and wild and other domestic animals, yet disease caused by such viruses has only come to notice in recent years. These viruses produce clinically inapparent infections in non-pregnant animals. In pregnant cattle, sheep and goats, however, if the viruses reach the foetus at a critical stage of development, marked teratology, particularly of the central nervous system, may result. The physical effects are usually only apparent some months later with the birth of affected calves and lambs.

The name ‘Akabane disease’ has been used,²⁵ but it is not apt as Akabane virus is only one member of the Simbu group, several of which may produce similar defects. 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 1975.²⁵ The pioneering work in defining the complex causation of these foetal abnormalities led to the association of Japanese place names with the AG/HE syndrome, e.g. Akabane and Aino. Chuzan virus,⁴⁹ now renamed Kasba virus, produces a different form of brain abnormality. The studies in Japan and Australia, which in 1974 confirmed the link between infection with Akabane virus and AG/HE, have been reviewed.^{25, 47} Disease caused by Simbu-group viruses in Africa is poorly defined, though characteristic disease has been observed in cattle in KwaZulu-Natal, South Africa, and in sheep in Zimbabwe.⁵³

Although the association of Akabane and related viruses with epidemic AG/HE is comparatively recent (1974), the syndrome was recognized much earlier. There are reliable records of its occurrence in Australia in the early 1930s,²¹ when it was attributed to plant poisoning, in Japan in 1949,²⁵ and in Israel in 1969/70.³⁸

Other viruses of the Simbu group which have been associated with natural disease are Aino⁷ and Tinaroo, although clinical cases in the field due to Aino are not common and are rare with Tinaroo.³¹ Peaton virus has produced AG/HE in experimentally infected chick embryos and in sheep, but disease in naturally infected cattle or sheep has never been observed.⁴⁷ In recent years Cache Valley virus, which belongs to a separate serogroup within the family Bunyaviridae, has produced AG/HE in sheep in Texas.¹³ The list of viruses involved in this syndrome will probably grow.

Aetiology

Viruses within the Simbu group, one of the 36 antigenic clusters within the family Bunyaviridae, have spherical, enveloped virions, 90 to 100 nm in diameter. They have segmented single-stranded RNA and are readily inactivated by chloroform, ether and trypsin. Akabane virus degrades moderately quickly at 37 °C,²⁵ remains viable in blood samples kept at 4 °C for several months, and can be stored indefinitely at −100 °C or lower. For more information on the properties of the viruses which belong to the Bunyaviridae, see 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. The American continent (except for the presence of Cache Valley virus in Texas), Papua-New Guinea and the island countries of the Pacific are free of infection.⁵⁹ However, the distribution of Akabane virus within each country is affected by the distribution, seasonal activity and abundance of the insect vectors.

Figure 94.1 Marked arthrogryposis in a stillborn lamb following transplacental infection with Akabane virus (By courtesy of Dr W.J. Hartley)

Figure 94.2 Marked hydranencephaly in a calf. Note the almost complete absence of the cerebral hemispheres while the midbrain and cerebellum are still relatively well developed (By courtesy of Dr W.J. Hartley)

The isolation of Akabane virus from mosquitoes⁴⁶ and the biting midge, Culicoides brevitarsis, ¹¹ 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.⁴⁴ In one instance isolations of Akabane virus were made from C. brevitarsis collected near sentinel cattle at about the time that the cattle became viraemic with Akabane virus.⁶⁰ Transovarial transmission was not demonstrated in a study involving 11 600 C. brevitarsis, indicating that transovarial transmission is not a frequent event if it occurs at all.² The effects of local climate on the relative densities of a Culicoides spp. and on the transmission of Akabane virus have been described by Murray.⁴⁵

The majority of Simbu-group virus isolations in Africa were made in the course of arbovirus surveys and little is known of their veterinary significance. Akabane virus has been isolated from mosquitoes in Kenya⁴²