Nairobi sheep disease

F G DAVIES AND C TERPSTRA

GENERAL INTRODUCTION: BUNYAVIRIDAE

Introduction

Nairobi sheep disease (NSD) is a tick-transmitted viral disease of small ruminants, mainly of sheep, for they are usually more numerous in the areas where the tick vectors, which are principally of the genus Rhipicephalus, are found. Goats are kept in the drier semi-arid zones. The disease is characterized by fever, debility and prostration, a haemorrhagic gastroenteritis, abortion and a high mortality. Nairobi sheep disease virus (NSDV) of the family Bunyaviridae is one of the most pathogenic viruses for small ruminants in East Africa.^{2, 5, 6, 18}

Nairobi sheep disease was first recognized by Montgomery in Kenya in 1917¹⁸ in sheep and goats after they had been moved from the dry semi-arid areas of the northern and southern parts of Kenya to the vicinity of Nairobi. It occurs in Kenya, Uganda, Tanzania and Ruanda,² and has also been described from Northern Somalia and the haud (highland, Acacia-bushed grasslands), which is the contiguous ecozone of Region V of Ethiopia.^{6, 22, 24} Some NSD-positive sera have been found in sheep in Botswana and the Mozambique coastal plain, extending into South Africa’s northern KwaZulu-Natal Province.^{15, 28} The results of further studies have, however, suggested that the latter may have been cross-reactions with other Nairoviruses in the test systems used (mouse virus serum neutralization tests) and not be specific for NSD. In addition, many sheep and goat sera from Zambia and Botswana were subsequently tested and a few very low titre positives found, which also suggest crossreactions with other nairoviruses, and not specific responses to NSD infections.⁷ The clinical disease has not yet been diagnosed in these countries of southern Africa.

The identical or closely related Ganjam virus has been isolated from several species of Haemaphysalis ticks (intermedia and wellingtonii) in many Indian states and in Sri Lanka.

Aetiology

Nairobi sheep disease virus (NSDV) is classified in the family Bunyaviridae, genus Nairovirus^{22, 25}(see Rift Valley fever). It is sensitive to lipid solvents and detergents and is rapidly inactivated at high and low pH values. Even in the range of optimal stability (pH 7,4 to 8,0) in the presence of 2 per cent serum, the virus is rapidly inactivated with a half-life of 6,8 days at 0 °C and 1,5 hours at 37 °C.²⁵

Nairobi sheep disease virus is antigenically identical, or very closely related to Ganjam virus and more distantly related to Dugbe virus, which is responsible for a tick-transmitted infection of cattle in Nigeria.⁸There is no reported evidence for any immunological diversity between strains isolated from different geographical areas.

The virus replicates in vitro in primary or secondary cell cultures derived from sheep or goat testes and kidneys, in continuous cell lines of BHK, PS and Vero cells, and in cell lines prepared from Rhipicephalus appendiculatus ticks.^{1, 14, 20} Infected cells usually develop cytopathic effects, which become more obvious after one to two passages. Staining with haemotoxylin and eosin reveals typical eosinophilic intracytoplasmic inclusion bodies.¹ These are ring- or spindle-shaped, polar or bipolar inclusions, which can also be observed by immuno- fluorescence. They contain large clusters of polyribosomes, which are revealed by electron microscopic examination.²⁶ Electron microscopy shows that virus replication occurs in the cytoplasm by budding from the membranes of smooth surface intracellular vesicles associated with the Golgi complex. Virus particles are released by exocytosis and by cell lysis. The molecular basis for this is the retention of viral envelope glycoproteins G1 and G2 in the Golgi complex during replication. Virus particles are spherical in shape and approximately 80 to 100 nm in diameter, with a denser core and a double envelope of 5 nm thickness. They are typical of bunyavirus particles.

Nairobi sheep disease virus produces a fatal infection in infant mice when inoculated intracerebrally or intraperitoneally. Adult mice are only susceptible by the intracerebral route.²⁹ The virulence of the virus decreases rapidly after serial passage in the brains of infant mice. A statistically significant difference was observed in the duration of illness and mortality between Persian fat-tailed sheep infected with the fifth mouse brain passage of the Entebbe strain and those infected with the progeny of the fifth brain passage after re-passage through ticks.²⁶

A mouse brain attenuated strain has been propagated in embryonated hens’ eggs following chorioallantoic inoculation and modification of virulence has also followed passage in adult mouse brain.⁶

Epidemiology

Sheep and goats are the natural vertebrate hosts of NSDV. Cattle, African buffalo (Syncerus caffer), horses and pigs are refractory to infection. Although natural and even fatal infections have been reported in blue duikers (Cephalophus monticola), and viraemia and an immune response demonstrated in experimentally infected field rats (Arvicanthis abyssinicus nubilans), serological studies have not supported a suggestion that small antelopes or wild rodents are significantly involved in the maintenance cycle of NSDV.⁴ The waterbuck (Kobus ellipsiprymnus) and other wild ruminants, which are heavily infested with Rhipicephalus appendiculatus, do not have a high prevalence of NSD antibody.⁴ Antibodies have...