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At least 19 recordsLinked to original sources
PubMed1978

A survey of Nairobi sheep disease antibody in sheep and goats, wild ruminants and rodents within Kenya.

The distribution of antibody to Nairobi sheep disease in sheep and goats in Kenya was found to coincide closely with that of the tick, Rhipicephalus appendiculatus. The proportions of a population in an enzootic area with antibody was similar in the different age groups. No antibody to the virus was found in rodent sera and while some low titres were found in some wild ruminant sera, these were considered to be most likely cross reactions with antibody to related viruses.

Animal Population Groups↗
PubMed1997

Nairobi sheep disease.

Nairobi sheep disease is probably the most pathogenic virus known for sheep and goats. It is transmitted by an Ixodid tick, both trans-stadially and transovarially and causes an acute gastroenteritis. In totally susceptible populations, mortality rates of over 90% regularly occur. The infection also causes abortion. The disease is known to occur in East Africa, Somalia and Rwanda. It may exist in the south east of Ethiopia. No evidence for its existence has been found in those parts of Africa where the principle vector tick, Rhipicephalus appendiculatus has a seasonal breeding cycle. Thus countries like Zambia, Zimbabwe and Botswana appear to be free from the disease.

Africa, Eastern↗
PubMed1978

Nairobi sheep disease in Kenya. The isolation of virus from sheep and goats, ticks and possible maintenance hosts.

Nairobi sheep disease was seen principally upon movement of susceptible animals into the enzootic areas. This occurred most frequently for marketing purposes near the main centres of population. Other outbreaks followed local breakdowns in tick control measures. The disease did not occur in epizootic form during the period under consideration. Nairobi sheep disease was isolated from pools of Rhipicephalus appendiculatus but not from many pools of other tick species. No virus was isolated from the blood or tissues of a range of wild ruminants and rodents.

Animals↗
PubMed2002

Nairobi sheep disease virus, an important tick-borne pathogen of sheep and goats in Africa, is also present in Asia.

Nairobi sheep disease (NSD) virus is the prototype of the tick-borne NSD serogroup, genus Nairovirus, family Bunyaviridae. It is highly pathogenic for sheep and goats, causes disease in humans, and is widespread throughout East Africa. Ganjam virus has caused disease in goats and humans in India. Due to their occurrence on different continents and association with different ticks, these viruses were considered distinct despite serologic cross-reactivity. Their S RNA genome segments and encoded nucleocapsid proteins were found to be 1590 nucleotides and 482 amino acids in length and differed by only 10 and 3% at nucleotide and amino acid levels, respectively. Genetic and serologic data demonstrate that Ganjam virus is an Asian variant of NSD virus. These viruses were phylogenetically more closely related to Hazara virus than Dugbe virus.

Africa↗
PubMed1983

Physical and biological properties of Nairobi sheep disease virus.

Thermal and pH stability of Nairobi sheep disease (NSD) virus were studied. The 180th mouse brain passage lost infectivity at a higher rate than "wild" virus at 4 degrees C. At 37 degrees C and neutral pH, "wild" virus again was more stable than cell culture and mouse brain attenuated strains with half-life periods of 104, 87 and 51 min, respectively. At 0 degrees C the cell culture attenuated virus was most stable at pH 7.4 with an estimated half-life of 164 h. The density of the virus in sucrose gradients came to 1.195 g cm -3. Metabolic growth inhibition studies using a halogenated nucleoside, and staining of RNase and DNase-treated infected cell cultures with acridine orange, indicated that NSD virus has a single stranded RNA genome. The growth of the cell culture adapted virus was assayed in monolayers of BHK21/13 cells at low multiplicity of infection. Cell-associated virus (CAV) was first detected at 6 h post-inoculation (PI). The titre increased rapidly until CPE appeared at 48 h and declined after 72 h PI. Cell-free virus (CFV) was first detected at 10 h PI. The titre of CFV increased up to 72 h, but on average was two log units less than the CAV titre.

Animals↗
PubMed1996

Ultrastructural studies on the replication and morphogenesis of Nairobi sheep disease virus, a Nairovirus.

The Nairovirus Nairobi sheep disease virus (NSDV) affects sheep and goats causing severe hemorrhagic gastroenteritis and high mortality. Replication and morphogenesis of NSDV was determined by electron microscopic examination of ultra-thin sections of 143B and BHK-21 cells at varying times after infection. By 4 h post-infection (p.i.) of 143B cells, virions budding from the luminal side of the bilayer membrane of smooth membrane vesicles were observed. Morphologically mature virus particles were electron-dense, spherical and of uniform size (100 nm diameter) and accumulated in smooth membrane vesicles associated with the Golgi complex. In BHK-21 clone 13 cells, mature virus particles in smooth membrane vesicles were present by 8 h p.i. The morphogenesis of NSDV was restricted to the smooth membrane vesicles of Golgi complex, and budding of virus from other sites was not detected. Extracellular virus particles were observed by 10 h p.i., before expression of cytopathic effects. The cytopathic effects were observed at 24 h p.i. in 143B cells and at 36 h p.i. in BHK-21 cells. The morphology and morphogenesis of NSDV in BHK-21 cells and in 143B cells resembles that of other members of the family Bunyaviridae.

Animals↗
PubMed1977

The laboratory diagnosis of Nairobi sheep disease.

The laboratory methods available for the isolation and identification of Nairobi sheep disease virus have been compared. The results show that inoculation of tissue culture (BHK 21 C 13) with suspensions of infected organs or plasma followed by fluorescent antibody tests on coverslip preparations gave the quickest means of identification. This test did not depend on the production of a cytopathic effect. Primary isolation of the virus in infant mouse brain and identification either by fluorescent antibody methods or by complement fixation with antigen prepared from the mouse brain offers a slightly more sensitive isolation system and would be recommended where no tissue culture facility exists.

Animals↗
PubMed1985

A survey of sheep diseases in Canada.

A mail survey of disease occurrence in Canadian sheep flocks was conducted. The survey, which covered the period from September 1982 to August 1983, utilized flocks on the Record of Performance (ROP) sheep program and relatively complete data were available from 116 flocks. Data about lambing rates, incidence of a variety of lamb and ewe diseases and reasons for culling were obtained. At the same time a retrospective evaluation of records of diagnoses of sheep diseases recorded at diagnostic laboratories across the country was performed. Data from the years 1978 to 1982 were obtained and summarized. A lambing percentage of 153% (1.53 lambs live born per ewe lambing) was observed and an additional 0.05 lambs were stillborn. The major identified causes of mortality amongst lambs were starvation, pneumonia, scours and accidents. Pasteurella spp. were the etiological agents most commonly associated with pneumonia in lambs and Escherichia coli had the same predominant position with regards to nonparasitic scours. A large discrepancy existed between the proportional mortality rates for internal parasites and coccidiosis as determined from the farm survey data compared to diagnostic laboratory data. This suggests that clinical parasitism may not be adequately recognized at the farm level. Abortions in ewes occurred in approximately half the flocks, but generally at a low level and no severe abortion storms occurred. Pneumonia was the most commonly identified cause of mortality in ewes and although Pasteurella spp. appear to be the most important etiological agents, regional differences were apparent.(ABSTRACT TRUNCATED AT 250 WORDS)

Abortion, Veterinary↗
PubMed2002

Clinical variation in foot and mouth disease: sheep and goats.

Foot and mouth disease (FMD) in adult sheep and goats is frequently mild or unapparent, but can cause high mortality in young animals. The recent outbreak of FMD in the United Kingdom has highlighted the importance of sheep in the epidemiology of the disease, although there have been numerous examples in the past where small ruminants have been responsible for the introduction of FMD into previously disease-free countries. The difficulty in making a clinical diagnosis should encourage the development of more rapid screening tests to assist in future control programmes.

Animals↗
PubMed2003

Vaccines for lumpy skin disease, sheep pox and goat pox.

Sheep pox, goat pox and lumpy skin disease (Neethling) are diseases of sheep, goats and cattle respectively, caused by strains of poxvirus, within the genus Capripoxvirus. Strains affecting sheep and goats are not totally host-specific; some cause disease in both sheep and goats while others may cause disease in only one species. Those causing disease in cattle appear to be specific for cattle, and this is reflected in the different geographical distribution of lumpy skin disease (LSD) and sheep pox and goat pox (sheep and goat pox); LSD is confined to Africa, while sheep and goat pox are present in Africa north of the equator, and throughout West Asia and India, as far East as China and Bangladesh. Occasionally sheep and goat pox spreads from Turkey into Greece. All strains of capripoxvirus so far examined are antigenically indistinguishable, and recovery from infection with one strain provides immunity against all other strains. Because of this antigenic homology among all strains, there is the potential to use a single vaccine strain to protect cattle, sheep and goats.

Animals↗
PubMed1996

Detection of scrapie agent in the peripheral nervous system of a diseased sheep.

In an attempt to determine whether scrapie infectivity can be found in the peripheral nervous system of a scrapie-diseased sheep, mice were inoculated intracerebrally or intraperitoneally with 10-fold dilutions of homogenates of Nervus (N.) axillaris, N. ulnaris, N. medianus, N. ischiadicus, N. tibialis, N. fibularis, and N.saphenus. Mice were observed for clinical signs of scrapie for 700 days and their brains were analyzed for accumulation of pathological prion protein by immunoblot. Substantial amounts of infectivity were found in all peripheral nerves tested except N.saphenus. Infectivity at titers of approximately 10(4.5) mouse infectious units (MIU)/g were detected in N. axillaris and N. ischiadicus, of approximately 10(3.0) MIU/g in N. ulnaris, N. medianus, N. tibialis, and N.fibularis, and of 10(6) MIU/g in the cerebellum. Since muscles are traversed by the nerve tracts tested, mutton of scrapie-diseased animals should not be regarded as being free of scrapie agent.

Animals↗