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Nairobi Sheep Disease: Introduction |  |
| Nairobi sheep disease is a tickborne viral disease of sheep and goats characterized by fever and hemorrhagic gastroenteritis, abortion, and high mortality. It has been reported in Kenya, Uganda, Tanzania, Somalia, Ethiopia, Botswana, Mozambique, and Republic of Congo. Although humans are susceptible, human infections are rare. It is a reportable disease in the USA and is on List B of the OIE. |
| Etiology and Transmission: |
| The causal nairovirus, family Bunyaviridae, 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 humans in India; and is serologically related to Dugbe virus, another tickborne infection in cattle, and to Crimean-Congo hemorrhagic fever virus (
Crimean-congo Hemorrhagic Fever: Introduction). It is transmitted transovarially and trans-stadially by the brown ear tick,
Rhipicephalus
appendiculatus
, in which it can survive for up to 800 days. 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. |
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| Clinical Findings: |
| A prodromal fever lasting 1-3 days follows an incubation period of 4-5 days. Sometimes, the fever is diphasic. Illness is manifest by depression; anorexia; mucopurulent, blood-stained, nasal discharge; and fetid dysentery that causes painful straining. Pregnant animals frequently abort. Death may occur in the early febrile viremic phase or follow ~2 days after remission of the fever. 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 disease in goats is usually less severe, although 80% mortality has been reported. |
Lesions:
| The main lesions are enlarged and edematous lymph nodes and hemorrhages in the GI (particularly the abomasum), respiratory, and female genital tracts; 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 kidney. Conjunctivitis with dried crusts around the nostrils
is often noted. Common histopathologic lesions are hyperplasia of lymphoid tissues, myocardial degeneration, nephrosis, and necrosis of the gallbladder. |
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| Diagnosis: |
| 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. Mouse inoculation
and cell cultures can be used for primary isolation of virus. Agar gel immunodiffusion, complement fixation, and ELISA can be valuable for detection of antigen in the infected tissues or tissue culture. Antibodies in infected or recovered animals can be detected by immunodiffusion, complement fixation, indirect fluorescent antibody tests, hemagglutination, and ELISA. |
| Differential diagnoses should include rinderpest, peste des petits ruminants, Rift Valley fever, heartwater, and salmonellosis. |
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| Treatment and Control: |
| 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. |
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