Reaction of goats to infection with infectious bovine rhinotracheitis virus.

Intranasal exposure of goats to infectious bovine rhinotracheitis virus resulted in mild respiratory disease and virus reisolation from nasal secretions. No disease was produced in goats exposed to the same virus by the genital or ocular routes. There was serological evidence of contact transmission of infection from infected goats to cattle. Virus recrudescence was not detected in goats treated with dexamethasone two months after virus inoculation.

Observations on rinderpest in Kenya, 1986-1989.

Rinderpest was confirmed in Kenya in 1986, 1987, 1988 and 1989. Three epidemiologically distinct events appear to have occurred: repeated outbreaks in West Pokot district related to cross-border movement of stock, an outbreak in Marsabit district in 1987 (thought to have been caused by illegal movement of cattle, possibly in vehicles, from countries further north) and a series of related outbreaks in and near Nairobi between 1988 and 1989 due to the unauthorized movement from abattoirs and holding grounds of slaughter stock possibly introduced from West Pokot or Marsabit. In West Pokot the disease affected unvaccinated calves and yearlings. In Marsabit cattle of all ages were affected. In August 1988, a major outbreak was confirmed in Kiambu and Kajiado districts in central Kenya, near Nairobi. At the same time a provisional diagnosis of rinderpest was made in a herd of cattle at a slaughterhouse in Nairobi. Rinderpest virus was isolated from sick cattle in all the outbreaks. Experimental infection of susceptible cattle with the Kiambu isolate demonstrated this to be of low virulence. Emergency vaccination and quarantine measures instituted immediately after confirmation eliminated clinical disease within three to four weeks in West Pokot, Kiambu and Nairobi. In Kajiado, however, the disease persisted for at least nine months, during which time a series of virus isolates was recovered. There was no evidence of infection in susceptible wildlife. This increase in the incidence of rinderpest in Kenya in recent years serves to highlight the problems of control and the need for concerted efforts to eradicate the threat of the disease from East Africa.

Development and distribution of rinderpest virus antigen in experimentally infected goats.

Three goats, experimentally infected with rinderpest virus were examined for the development and distribution of precipitating antigens in various tissues and secretions using the agar gel immunodiffusion test. Virus antigens were detected in ocular secretions and lymph node biopsies from the second to the fourth and fifth days of pyrexia, respectively, but were not detected in nasal secretions. Precipitating antigens were demonstrated in various lymphoid organs, the lung and abomasum of a goat killed on the fourth day of pyrexia. These findings are discussed in relation to the epidemiology of rinderpest in goats in Africa.

Preliminary observations on rinderpest in pregnant cattle.

A Kabete 'O' strain of rinderpest virus enhanced in virulence was inoculated subcutaneously into four cows which were between six and eight months pregnant. All the cows developed clinical signs of rinderpest from the third day after inoculation and shed high titres of virus in their ocular and vaginal secretions during the course of the clinical disease. Three of the cows died of rinderpest on the third day after the onset of fever but no virus was isolated from their fetuses which were examined post mortem. The fourth cow showed complete clinical and virological recovery by the eighth day after the onset of fever and aborted an eight-and-a-half-month-old fetus on the 12th day after it recovered. Rinderpest virus was demonstrated in a wide range of the aborted fetal tissues. Virus was also detected in the maternal vaginal discharges up to 24 hours after abortion. The only gross pathological change observed was a severe necrotising placentitis.

Re-emergence of rinderpest as a threat in East Africa since 1979.

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.

Continuing presence of rinderpest virus as a threat in East Africa, 1983-1985.

The re-emergence of rinderpest virus in East Africa in 1979 caused widespread outbreaks of disease and subclinical infection throughout the region until mid-1983. Subsequent massive emergency vaccination campaigns have been successful in eliminating clinical rinderpest from Tanzania and preventing its spread southwards. Unfortunately the virus is still endemic in north-eastern Uganda and has recently caused epidemic outbreaks with high mortality in cattle in that country. In Kenya, buffaloes (Syncerus caffer) in and around the Masai Mara game reserve have developed antibodies to rinderpest virus as recently as late 1984. Although there have been no outbreaks of clinical disease in Tanzania or Kenya from April 1983 to the end of 1985 this serological evidence plus the increasing incidence of clinical outbreaks in Uganda indicate that rinderpest virus still threatens East Africa. The substantial aid which has been provided to the region for rinderpest control must be maintained.

Some antigenic and cultural properties of border disease and bovine viral diarrhoea viruses.

In vitro comparison of the replication cycles of three strains of border disease virus and one strain of bovine viral diarrhoea virus showed similar growth curve patterns and a tendency of cell-free virus to exceed cell-associated virus. Each virus was antigenically distinguishable from the others in cross-neutralisation tests.

The shedding of a virulent Kabete O strain of rinderpest virus by cattle.

A Muguga substrain of the virulent Kabete O strain of rinderpest virus was demonstrated in the ocular, nasal, oral and rectal swabs collected from infected cattle. Ocular shedding was detected at the onset of viraemia and before the onset of clinical signs whilst virus shedding in nasal, oral and rectal discharges appeared at the same time as lesions. It is suggested that virus isolation from ocular and nasal swabs should be considered in the diagnosis of rinderpest in addition to the other methods currently employed, as virus was isolated from swabs collected from dead animals.

A recent outbreak of rinderpest in East Africa.

Rinderpest was brought under control in Kenya in 1976 but in April 1986 an outbreak of the disease occurred in cattle in Western Kenya, five kilometres from the Kenya-Uganda border. This was the first confirmed field outbreak of the disease in Kenya after a lull of over 10 years. Clinical disease was confined to unvaccinated zebu calves aged six to eight months from which rinderpest virus was isolated. High titres of antibodies to rinderpest virus were demonstrated in sera collected from sheep and goats that were grazing together with the affected cattle herds; there was, however, no evidence of clinical disease in these small ruminants and wildlife species in the affected area. The disease outbreak was rapidly stamped out by quarantine and vaccination.

Confirmation of rinderpest in experimentally and naturally infected cattle using microtitre techniques.

Virulent rinderpest virus was detected by immunoperoxidase staining of microtitre bovine kidney cell cultures within 24 to 48 hours of inoculation with prescapular lymph node and spleen homogenates from experimentally infected steers. Rinderpest virus specific cytopathic effects were evident from 48 hours in microtitre plates and from 72 hours in rolled tube cultures. Nasal and ocular secretions collected from cattle naturally infected with rinderpest and inoculated into bovine kidney cell cultures did not readily yield cytopathic virus in both tubes and microtitre plates, but immunoperoxidase staining of microtitre cultures on the fourth day of inoculation detected replication of virus in cultures inoculated with ocular and nasal secretions from seven of 17 cattle tested.

Immunohistological localisation of rinderpest virus in formalin-fixed, paraffin-embedded tissues from experimentally infected cattle.

Six Freesian steers were subcutaneously inoculated with the virulent rinderpest virus strain Kabete "0" and sacrificed at the height of fever. Sections of formalin-fixed, paraffin-embedded tissues were stained according to the peroxidase anti-peroxidase (PAP) technique. Labelling of viral antigen, both in the cytoplasm and in the nuclei of infected cells, was observed in the epithelial cells of the upper and lower alimentary tract and in lymphoid organs, i.e. spleen, lymph nodes, pharyngeal tonsils, Peyer's patches and thymus. Electron microscopy studies confirmed the results.

Development and stability of rinderpest virus antigens in cattle tears and lymph nodes.

Diffusible rinderpest virus antigens were demonstrated in increasing quantities in ocular and lymph node biopsies from rinderpest-infected cattle using agar gel immunodiffusion (AGID) and counterimmunoelectrophoresis (CIEP) tests. Positive samples were detected from the second day of pyrexia to two days after death. The antigens in ocular secretions and lymph nodes were thermolabile being destroyed within five minutes at 56 degrees C and within two weeks at 4 degrees C.

Detection of antibody to mycoplasma F38 in goat sera by an enzyme-linked immunosorbent assay.

An indirect enzyme-linked immunosorbent assay (ELISA) was developed to screen goat sera at a single dilution for antibody to mycoplasma F38. Antibody was detected in sera of six convalescent goats following experimental infection. Antibody was also detected in 34 sera three to four weeks after vaccination. No antibody was detected in 164 sera from goats without a history of vaccination or infection with contagious caprine pleuropneumonia. The ELISA was more sensitive than the complement fixation test in detecting antibody in vaccinated goats.