Nairobi sheep disease (NSD) is a tickborne viral disease of sheep and goats characterized by fever and hemorrhagic gastroenteritis, abortion, and high mortality. The disease was first identified near Nairobi, Kenya, in 1910, and NSD virus was shown to be the causative agent in 1917. The disease is endemic in Kenya, Uganda, Tanzania, Somalia, Ethiopia, Botswana, Mozambique, and Republic of Congo. Human infections are rare; however, accidental infections have been reported among laboratory workers, resulting in fever, joint aches, and general malaise. The African field rat (Arvicathus abysinicus nubilans) is a potential reservoir host. NSD is a reportable disease in the USA and is one of the OIE listed diseases.
NSD virus is classified in the genus Nairovirus, family Bunyaviridae, and is possibly the most pathogenic virus known for sheep and goats. It is identical to or closely related to Ganjam virus, a tickborne infection of sheep, goats, and people in India. Genetic and serologic data demonstrate that Ganjam virus is an Asian variant of NSD virus. Both Ganjam and NSD viruses are phylogenetically more closely related to Hazara virus than Dugbe virus. In addition, the NSD virus is serologically related to Dugbe virus, another tickborne infection in cattle, and to Crimean-Congo hemorrhagic fever virus (see Crimean-Congo Hemorrhagic Fever Crimean-Congo Hemorrhagic Fever read more ). It is transmitted transovarially and transstadially by the brown ear tick, Rhipicephalus appendiculatus, in which it can survive up to 800 days. The unfed adult ticks can transmit NSD virus for >2 yr after infection. Other Rhipicephalus spp and Amblyomma variegatum ticks also may transmit the disease. The virus is shed in urine and feces, but the disease is not spread by contact.
In natural outbreaks, disease usually occurs 5–6 days after susceptible animals move to areas infested with R appendiculatus. Clinical signs begin with a steep rise in body temperature (41°–42°C [105.8°–107.6°F) that persists for 1–7 days. Leukopenia and viremia usually coincide with the febrile phase. Diarrhea usually appears 1–3 days after the onset of fever and worsens as infection progresses. Illness is manifest by depression; anorexia; mucopurulent, blood-stained, nasal discharge; occasional conjunctivitis; and fetid dysentery that causes painful straining. Pregnant animals frequently abort. In peracute and acute cases, the time between the appearance of disease and death is usually 2–7 days but may be as long as 11 days in less acute cases. Experimental infection has shown that indigenous Persian fat-tailed and European breeds of sheep are equally susceptible; however, mortality rate in the field is as high as 70%–90% for indigenous breeds of sheep and 30% for exotic and cross-breeds. The clinical signs in goats are similar to those in sheep but less severe, although 80% mortality has been reported. The presence of colostral immunity not only protects lambs and kids from early exposure to infection but also allows development of active immunity, enabling survival in tick-infested areas.
The most striking features on external examination of the carcass are the hindquarters soiled with feces (or a mixture of blood and feces) and dehydration, especially in animals with prolonged scouring. Also common are conjunctivitis and dried crusts around the nostrils as a result of nasal discharge. Necropsy findings include enlarged and edematous lymph nodes; mild splenomegaly; and hemorrhages in the GI (particularly the abomasum), respiratory, and female genital tracts, as well as in the 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 be seen in the cecum, colon, gallbladder, and kidneys. Conjunctivitis with dried crusts around the nostrils is often noted. Common histopathologic lesions are hyperplasia of lymphoid tissues, myocardial degeneration, nephrosis, and coagulative necrosis of the gallbladder.
The occurrence of a disease in sheep or goats with high mortality accompanied by a tick infestation is suggestive, especially if it follows movements into endemic areas or changes in tick populations that have been induced by heavy and prolonged rainfall. Confirmation of suggestive signs and lesions requires detection of virus or viral antigen and antibodies. The preferred specimens are plasma from febrile animals, mesenteric lymph nodes, spleen, and serum. Personal protective equipment should be used when conducting a necropsy and handling the agent in the laboratory. Mouse inoculation and cell cultures can be used for primary isolation of virus. Sheep are the most sensitive animals for isolation, whereas a baby hamster kidney cell line and lamb or hamster kidney cell cultures are the most sensitive cells. Agar gel immunodiffusion, complement fixation, and ELISA can be valuable for detection of antigen in the infected tissues or tissue culture. New probes have been developed targeting the S and L segments of Dugbe virus and can potentially be used as a rapid diagnostic tool for NSD. Antibodies in infected or recovered animals can be detected by immunodiffusion, complement fixation, indirect fluorescent antibody tests, hemagglutination, and ELISA.
Differential diagnoses include peste des petits ruminants (see Peste des Petits Ruminants Peste des Petits Ruminants read more ), Rift Valley fever (see Rift Valley Fever Rift Valley Fever read more ), heartwater (see Heartwater Heartwater read more ), and salmonellosis (see Salmonellosis Salmonellosis read more ).
No specific antiviral agent is available for treatment. Unaffected animals in the flock may be treated with acaricides (eg, pyrethroids in a grease, cypermethrin “pour-on” products, various dip preparations). Longterm tick control is not cost-effective in endemic areas.
In endemic areas, clinical signs are not seen 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 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.