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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↗
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↗
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↗
PubMed1977

White muscle disease of sheep and associated tissue selenium levels in Western Australia.

White Muscle Disease of sheep occurs in Western Australia as distinct syndromes in lambs and weaner sheep. Mean liver selenium concentrations of lambs and weaners with WMD and unaffected by WMD were 0.19 and 0.46 ppm, and 0.20 and 0.41 ppm (dry weight) respectively. There was considerable overlap between levels suggesting that selenium status was not the only factor involved in the development of WMD.

Animals↗
PubMed1977

Histological and histochemical studies of fetal skin follicles in Border disease of sheep.

The structure of the epidermis and dermis, and the distribution of reticulin, glycogen, lipid and sulphydryl groups in the skin have been examined in control and Border disease affected sheep fetuses at 95 and 115 days' gestation. In Border disease, there was a temporary retardation of development of the epidermis and skin follicles at 95 days. There was no difference in the structure of the dermis between control and experimental fetuses at either age. No evidence was found to suggest that the keratogenous process was abnormal in Border disease, but the sulphydryl zone of the primary fibres of affected fetuses was situated nearer the skin surface than in control fetuses. This may have been a consequence of the larger size of primary follices in Border disease. Glycogen present in the undifferentiated epidermis of both groups at 95 days' gestation was absent from the stratified squamous epithelium of the 115 days's fetuses. Glycogen and lipid droplets were present in the outer root sheath of primary follicles of all fetuses examined, but their significance is unknown.

Animals↗
PubMed1978

The cerebrospinal fluid in visna, a slow viral disease of sheep.

The temporal development of the CSF abnormalities was examined in visna, a chronic neurological disease caused by a persistent viral infection of sheep. Two types of changes were observed. During the first 30 to 40 days there was an intense mononuclear pleocytosis associated with high protein and proportionately elevated IgG. Later, there was a persistent slight pleocytosis associated with mildly elevated protein which had an increased proportion of IgG and antivisna antibody. These later cellular and protein changes are similar to those found in a number of chronic neurological diseases of man.

Animals↗