Mokola virus infection: description of recent South African cases and a review of the virus epidemiology.

Five cases of Mokola virus, a lyssavirus related to rabies, are described. The cases occurred in cats from the East London, Pinetown and Pietermaritzburg areas of South Africa from February 1996 to February 1998. Each of the cats was suspected of being rabid and their brains were submitted for laboratory confirmation. Four of the cases were positive, but with atypical fluorescence, and 1 was negative. Mokola virus infection was identified by anti-lyssavirus nucleocapsid monoclonal antibody typing. As in rabies cases, the predominant clinical signs were of unusual behaviour. Aggression was present, but only during handling. Four of the 5 cats had been vaccinated for rabies, which is consistent with other studies that show that rabies vaccination does not appear to protect against Mokola virus. Since Mokola may be confused with rabies, the incidence of Mokola virus may be more common in Africa than is currently reported. As human infections may be fatal, the emergence of this virus is a potential threat to public health.

Molecular epidemiology of rabies virus in South Africa: evidence for two distinct virus groups.

In order to derive phylogenetic relationships between rabies virus isolates from different geographical locations and host species in South Africa, two genome regions of the virus, viz. the cytoplasmic domain of the glycoprotein and the G-L intergenic region (pseudogene), were sequenced. A high level of nucleic acid sequence conservation indicated a close phylogenetic relationship between virus isolates from domestic dogs, jackals and bat-eared foxes, i.e. Canidae. These isolates appeared to be distinct from but closely related to European strains of rabies virus. However, a phylogenetically distinguishable and distant group, which contained isolates from mongooses (i.e. Viverridae) was identifiable. The latter group appears to be distantly related to European and vaccine strains of rabies virus and may have evolved uniquely on the central plateau of South Africa. Our data also indicate that spillover from mongooses (or other viverrids) to canid hosts occurs occasionally.

Canid and viverrid rabies viruses in South Africa.

Historical records suggest that in South Africa rabies was present in viverrids in the early 1800s. In the early 1950s a wave of canine rabies spread from Namibia through Botswana into the northern Transvaal and by 1961 a second front had penetrated south from Mozambique into Swaziland and northern Natal. Today, rabies is regularly confirmed in a number of canid and viverrid species in most regions of South Africa. A panel of anti-nucleoprotein monoclonal antibodies was used to examine 83 virus isolates from these species. Two major reaction patterns, one chiefly confined to viruses from canids and the other to viruses from viverrids, were obtained. In addition, some variation in the reaction patterns of viverrid viruses was observed and spill-over of viverrid virus into canids and vice versa was recorded. Rabies in South Africa appears to behave as two distinct disease entities.

Rabies in southern Africa.

The first confirmed outbreak of rabies in Africa, believed to have followed the importation of an infected dog from England in 1892, occurred in the eastern Cape Province of South Africa, and was brought under control in 1894. An unconfirmed epidemic of rabies in dogs occurred in western Zambia in 1901. By the following year the disease had apparently spread along a major trade route, to cause an outbreak in Zimbabwe which engulfed most of the country before being eradicated in 1913. The existence of endemic rabies of viverrids (mongooses and genets) was confirmed in South Africa in 1928, and since then the viverrid disease has continued to occur widely on the interior plateau of the country with spill-over of infection to cattle and a variety of other animals. From about 1947 onwards, an invasive form of dog rabies spread from southern Zambia and/or Angola into Namibia, across northern and eastern Botswana into Zimbabwe and the northern Transvaal by 1950, entered Mozambique in 1952, and spread from there to Swaziland in 1954. Dog rabies extended from southern Mozambique into Natal in 1961 to cause a major epidemic which was brought under control in 1968. The disease re-entered northern Natal from Mozambique in 1976 and since then dog rabies has proved difficult to control in the peri-urban settlements of Natal-KwaZulu. The disease spread from Natal to Lesotho in 1982, and into the Transkei region of the eastern Cape Province in 1987, to reach the Ciskei by 1990. The spread of the disease in dogs was followed by the emergence of rabies of jackals and cattle in central Namibia, northern Botswana, Zimbabwe and the northern Transvaal. A unique outbreak of rabies in kudu antelope occurred in central Namibia from 1977 to 1985, apparently involving oral spread of infection between individuals. A few cases of rabies in the bat-eared fox were recognized each year in Namibia from 1967 onwards, and from the 1970s the occurrence of the disease in the fox has emerged as a distinct problem in the northern Cape Province and spread to the west coast. The rabies-related viruses, Lagos bat, Mokola and Duvenhage, associated with bats, shrews and rodents in Africa, are known to have caused isolated cases of disease in South Africa, and on one occasion a small outbreak involving six cats and a dog in Bulawayo, Zimbabwe.(ABSTRACT TRUNCATED AT 400 WORDS)

Rabies in bat-eared foxes in South Africa.

Rabies in bat-eared foxes was first recognized in South Africa in 1955 and is likely to have been derived from canine rabies introduced to South Africa in 1950. Since then it has become established in this species in the drier western half of the country and the south-western Cape so that rabies now occurs in bat-eared foxes adjacent to the peri-urban canine population of Cape Town. Peak incidence was recorded in the early 1980s and the incidence is seasonal with most cases occurring in winter.

The suitability of a rolled BHK21 monolayer system for the production of vaccines against the SAT types of foot-and-mouth disease virus. I. Adaptation of virus isolates to the system, immunogen yields achieved and assessment of subtype cross reactivity.

In an examination of 34 southern African SAT-type foot-and-mouth disease viruses, all but 1 attained satisfactory levels of infectivity within 6 passages in rolled BHK21 monolayer cell cultures. However, there were marked differences between adapted viruses with respect to the mass of immunogen (146S material) produced. Several isolates which consistently produced levels greater than or equal to 2 micrograms/ml were identified. In cross neutralization tests using post-vaccinal sera, SAT-1 and SAT-2 isolates showed considerable diversity and none of the viruses tested would be expected to produce a broad-spectrum response if incorporated into a vaccine. On the other hand, when 2 of the SAT-2 isolates were incorporated into the same vaccine a distinctly broader response resulted.

An outbreak of ovine listeriosis associated with poor flock management practices.

An outbreak of listerial meningo-encephalitis involving sheep in the Western Cape Province is recorded. Poor management practices which are described were thought to be principal precipitating cause.