The duration of immunity as measured by virological, serological and clinical responses following infection with influenza A/equine/Newmarket/79 (H3N8) was assessed in repeated challenge experiments in which ponies were infected by exposure to aerosols of infectious virus. Previous infection stimulated complete clinical protection which persisted for at least 32 weeks as demonstrated by the absence of febrile responses and coughing in two groups of ponies infected 16 weeks or 32 weeks after the first infection. Partial clinical protection persisted for over a year as demonstrated by the absence of coughing and a reduction in the number of febrile responses in a group of ponies infected 62 weeks after their first infection. These results contrasted with those observed in immunologically naive control ponies which developed pyrexia, dyspnoea and nasal discharge and coughing. The kinetics of virus specific antibody production in primary and secondary infections with equine influenza were studied by the single radial haemolysis test and a radioisotopic antiglobulin binding assay which measured virus specific IgGab antibody isotype. Antibody to the haemagglutinin, as measured by the single radial haemolysis test, declined rapidly after primary infection whereas the IgGab responses to whole virus antigens persisted for longer. The single radial haemolysis test was therefore particularly useful for the detection of antibody responses in multiple infections or exposures to influenza antigens. The radioisotopic antiglobulin binding assay was more sensitive for identifying infections which had occurred more than six months previously, as evidenced by anamnestic IgGab responses in ponies with low levels of antibody before rechallenge.

Following the success of the JP15 scheme and subsequent annual vaccination campaigns, East Africa was virtually free of rinderpest after the mid 1960s and the disease was considered beaten. However, economic difficulties have recently reduced the expensively maintained vaccine cover and the disease has reappeared throughout much of the region. In 1979 rinderpest was diagnosed in cattle in north eastern Uganda and caused considerable losses until finally brought under control in 1981. No field outbreaks of the disease in cattle have been seen in Kenya but there is serological evidence that the virus has recently infected unvaccinated sheep and goats and wild ungulates in that country. In 1982 rinderpest was confirmed in the laboratory as the cause of death of large numbers of buffaloes in northern Tanzania and implicated as the cause of a rinderpest-like disease of cattle which is reported to be still active in that area. Substantial aid is essential for further control and research if the virus is not again to become endemic in the region.

Malignant catarrhal fever virus was not isolated from samples of fetal membranes or fluid collected from 93 calving wildebeest (Connochaetes taurinus) in Kenya Maasailand. Cell-free strains of malignant catarrhal fever virus were very rapidly inactivated when exposed to the sun under field conditions, at least 3.0 log10 units/25 microliter being lost per hour at midday. It is suggested that wildebeest fetal membranes and fluids act as visual markers for areas of pasture which are particularly heavily contaminated with malignant catarrhal fever virus in oculonasal secretions of wildebeest calves. It is possible that starting to graze cattle one to two hours later each morning may be a useful measure for helping to protect cattle from malignant catarrhal fever in areas where they are forced to share pastures with calving wildebeest.

No abstract

No abstract