Nairobi sheep disease (NSD) is a tickborne viral disease of sheep and goats characterized by fever, hemorrhagic gastroenteritis, abortion, and high mortality. It is possibly the most pathogenic virus of small ruminants. Most other species do not appear susceptible; however, a few clinical cases have been reported in blue duikers (Cephalophus monticola). The African field rat (Arvicanthus abyssinicus nubilans) is a potential reservoir host. Reports of endemic NSD are mainly clustered in eastern and central Africa from Ethiopia to Democratic Republic of the Congo; however, serologic evidence suggests that this or a similar virus might also occur elsewhere in Africa (eg, Botswana and Mozambique). A variant known as Ganjam virus, once thought to be a separate virus, circulates in parts of Asia including India, Sri Lanka, and China.
Etiology and Transmission of Nairobi Sheep Disease
Nairobi sheep disease virus (NSDV) is classified in the genus Orthonairovirus, family Nairoviridae. It is a member of a group of serologically and genetically related bunyaviruses such as Dugbe virus, Hazara virus, and Crimean-Congo hemorrhagic fever virus Crimean-Congo Hemorrhagic Fever .
The principal vector for NSDV in Africa is the brown ear tick (Rhipicephalus appendiculatus) in which the virus can survive up to 800 days. Transovarial and transstadial transmission occurs via this vector. The unfed adult ticks can transmit the virus for >2 years after infection. Haemaphysalis intermedia is the principal tick vector in Asia; however, Ganjam virus also occurs in other members of Haemaphysalis Haemaphysalis spp Few of the currently recognized 167 species of Haemaphysalis parasitize livestock, but those that do are economically important in Eurasia, Africa, Australia, and New Zealand. Some haemaphysaline... read more , which could be important in specific geographic areas. Additional ticks, including Rhipicephalus spp Rhipicephalus spp Approximately 60 of the 84 described rhipicephalid species are found in sub-Saharan Africa. The other rhipicephalid species have their origins in Eurasia and northern Africa, with R sanguineus... read more and Amblyomma variegatum ticks Amblyomma spp More than half of the approximately 135 known Amblyomma species are endemic to the New World. Amblyomma ticks are large, three-host parasites. They have eyes and long, robust mouthparts... read more in Africa, also may be involved in transmission of these viruses. Nairobi sheep disease virus is shed in urine and feces; however, the disease is not transmitted via contact between animals.
Clinical cases tend to occur when naive animals are moved into endemic areas or when climatic conditions, such as heavy and prolonged rainfall, allow the tick population to increase or expand into nearby areas.
Clinical Findings of Nairobi Sheep Disease
The incubation period of Nairobi sheep disease is usually 2–6 days. Clinical signs begin with a steep rise in body temperature (41°–42°C [105.8°–107.6°F]), which persists for 1–7 days. Leukopenia and viremia usually coincide with the febrile phase. Common clinical signs include depression, anorexia, mucopurulent to hemorrhagic nasal discharge, occasional conjunctivitis, and fetid dysentery that causes painful straining. Diarrhea usually occurs 1–3 days after the onset of fever and worsens as the illness progresses. Pregnant animals frequently abort. Death tends to occur 2–7 days after the initial clinical signs, with some animals succumbing before the characteristic clinical signs appear; however, some sick animals survive up to 11 days. Death in the later stages of the illness is usually associated with dehydration and debilitation from diarrhea. The prognosis is poor in animals with severe clinical signs.
Breed-related differences in susceptibility have been reported in the field, although not necessarily substantiated by studies in experimentally infected sheep. In Africa, the mortality rate in the field is as high as 70%–90% for indigenous breeds of sheep; however, it is 30% for exotic and cross-breeds. Conversely, Ganjam virus causes higher mortality in exotic than indigenous breeds in India. The clinical signs in goats are similar to those in sheep but usually less severe, although mortality up to 80% has been reported. The presence of colostral immunity not only protects lambs and kids from exposure early in life but also allows development of active immunity, enabling survival in tick-infested areas.1 References Nairobi sheep disease is a serious tickborne viral disease of small ruminants in Africa. It is characterized by peracute deaths and acute illness with severe hemorrhagic gastroenteritis. Ganjam... read more
White WR. Nairobi sheep disease. In: Foreign animal diseases. 7th ed. Richmond, VA:United States Animal Health Association; 2008. p. 335-41.
On external examination of the carcass, the most striking features are soiling of the hindquarters with feces (or a mixture of blood and feces) and, especially in animals with prolonged scouring, dehydration. Also common are conjunctivitis and dried crusts around the nostrils as a result of nasal discharge.
Postmortem examination findings include enlarged and edematous lymph nodes, mild splenomegaly, and hemorrhages in the GI tract (particularly the abomasum), respiratory tract, female genital tracts, and gallbladder, spleen, and heart. Petechial and ecchymotic hemorrhages in the mucosa of the cecum and colon frequently appear as longitudinal striations and are sometimes the only lesion evident. Subserosal hemorrhages may occur in the cecum, colon, gallbladder, and kidneys. Conjunctivitis with dried crusts around the nostrils is often noted. Animals that die during the initial viremic stage may have few lesions other than lymphadenitis and petechial and ecchymotic haemorrhages on the serosa of the GI tract, spleen, and other internal organs.
Common histopathologic lesions are hyperplasia of lymphoid tissues, myocardial degeneration, nephrosis, and coagulative necrosis of the gallbladder.
Diagnosis of Nairobi Sheep Disease
History of exposure to ticks
Confirmation of diagnosis (antemortem) by virus isolation, detection of viral antigens or nucleic acids, and serologic testing
The occurrence of a disease in sheep or goats with high mortality accompanied by a tick infestation is suggestive of NSD, especially if it follows movements into endemic areas or changes in tick populations. Confirmation of suggestive clinical signs and lesions requires detection of virus or viral antigens, nucleic acids, and antibodies. The preferred specimens are plasma from febrile animals, mesenteric lymph nodes and spleen for direct virus detection, and serum to detect antibodies. Little or no virus can be isolated from plasma after the fever ends; however, nucleic acids may be found by RT-PCR assay. Personal protective equipment should be used when conducting postmortem examination and handling the agent in the laboratory.
Certain baby hamster kidney cell lines (eg, BHK21 clone 13 cells and BSR cells) and lamb or hamster kidney cell cultures are the most sensitive cells for primary virus isolation. Nairobi sheep disease virus can be identified in cell cultures with fluorescent antibody tests. It may also be recovered in sheep or suckling mice. Agar gel immunodiffusion (AGID) is particularly useful for detecting viral antigens in infected tissues at laboratories that do not have culture facilities or at field investigation laboratories. Complement fixation and ELISA have also been used to identify viral antigens. Use of RNA probes targeting the S and L segments of Dugbe virus has potential as a rapid diagnostic tool for NSD.
Indirect fluorescent antibody tests are recommended for detecting antibodies in infected or recovered animals. Immunodiffusion, hemagglutination, ELISA, and complement fixation may also be used; however, the marked anticomplementary activity in many sheep sera can complicate interpretation of the latter test. Cross-reactions with other nairoviruses, especially Dugbe virus, can be an issue in serologic tests.
Treatment and Control of Nairobi Sheep Disease
No specific antiviral agent is available for treatment of Nairobi sheep disease. Supportive treatment, including good shelter and the provision of quality feed, may improve survival. Unaffected animals in the flock may be treated with acaricides (eg, pyrethroids in a grease, cypermethrin pour-on products, or various dip preparations).
In endemic areas, clinical cases are infrequent unless susceptible animals are introduced. Such animals should be vaccinated, as should those exposed when the range of the tick vector extends. Two types of experimental vaccines have been developed—a modified-live virus vaccine attenuated in mouse brain and an inactivated oil adjuvant vaccine. A single dose of the modified-live virus vaccine produces rapid immunity; however, revaccination is necessary to maintain full protection. Two doses of the inactivated vaccine are required to elicit good protection. Neither of these vaccines is produced commercially.
Acaricides may be used short-term in areas bordering enzootic areas as a barrier to range expansion of the tick vector. Long-term tick control for prevention of NSD is not feasible.
Zoonotic Risk of Nairobi Sheep Disease
Infections in humans are uncommon; however, accidental infections have occurred in laboratory workers, resulting in a flu-like illness with fever and nonspecific clinical signs such as joint aches, nausea, and general malaise. One naturally transmitted Ganjam virus infection was reported in a European boy who developed a febrile illness in India.
Nairobi sheep disease is a systemic viral illness of small ruminants with a high case fatality rate in naive animals.
Outbreaks have been associated with movement of naive animals into endemic areas or expansion of the tick vector's range during favorable climatic events.
There is no specific treatment or commercial vaccine; however, experimental vaccines may be available in some areas.