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The article reviews the outbreaks and distribution of African swine fever (ASF) in South Africa since the first probable outbreak that occurred in the Koedoesrand Ward in 1926. Retrospective data on the ASF outbreaks in South Africa were obtained from the World Organisation for Animal Health (OIE) disease database and the South African veterinary services annual reports in addition to published articles and online sources. South Africa has experienced many outbreaks that can be divided into 2 time periods: the period before the development of the OIE diseases database (1993) and the period after. More than 141 outbreaks of ASF were reported during the first period. Since the development of OIE disease database, 72 outbreaks directly involving 2968 cases, 2187 dead and 2358 killed pigs mainly in smallholder pig farms were reported. The median number of cases for a given ASF outbreak is 17, but in 50% of outbreaks no pigs were killed for prevention. The most important ASF outbreak was reported in April 2014 in the Greater Zeerust district (North West province) involving 326 cases and 1462 killed pigs. However, the outbreak with highest mortality involving 250 pigs was reported in 2016 (Free State province). According to phylogenetic analysis, nine p72 genotypes (I, III, IV, VII, VIII, XIX, XX, XXI and XXII) have been identified in South Africa. Season-wise, more outbreaks were recorded during summer. It was also observed that the OIE disease database could contain errors that would have been introduced through compiled forms at country level. Spatiotemporal studies on ASF outbreaks in South Africa are therefore required in order to assess statistically and quantitatively the clustering of outbreaks over space and time.

African swine fever (ASF) is a devastating haemorrhagic fever of pigs that causes up to 100% mortality, for which there is no vaccine. It is caused by a unique DNA virus that is maintained in an ancient cycle between warthogs and argasid ticks, making it the only known DNA arbovirus. ASF has a high potential for transboundary spread, and has twice been transported from Africa to other continents--Europe and subsequently the Caribbean and Brazil (1957, 1959) and the Caucasus (2007). It is also a devastating constraint for pig production in Africa. Research at Onderstepoort Veterinary Institute has made and is making important contributions to knowledge of this disease, focusing on the cycle in warthogs and tampans and transmission from that cycle to domestic pigs, resistance to its effects in domestic pigs, and the molecular genetic characterisation and epidemiology of the virus.

African swine fever (ASF) is the most important disease that constrains pig production in Mozambique. Until 1994 it was apparently restricted to the central and northern provinces, but since 1994 outbreaks have been experienced throughout the country. ASF causes severe economic losses both in the small commercial sector and among the large numbers of small-scale producers in the family sector in rural and peri-urban areas. The history of ASF in Mozambique since its first confirmation in 1960 is briefly reviewed, recent outbreaks are reported, and the available information on the virus genotypes that have been responsible for some of the outbreaks is presented. Epidemiological factors that contribute to ASF outbreaks and strategies for limiting the negative effects of the disease in the different pig farming sectors in Mozambique, including raising farmer and community awareness, are discussed.

Wildlife mortality involving bongos, Tragelaphus eurycerus, and other ungulates was investigated in the north of the Congo Republic in 1997. Four bongos, one forest buffalo, Syncerus caffer nanus, and one domestic sheep were examined and sampled. Although an outbreak of rinderpest had been suspected, it was found that the animals, which had been weakened by an Elaeophora sagitta infection and possibly also by adverse climatic conditions, had been exsanguinated and driven to exhaustion by an unusual plague of Stomoxys omega.

Tuberculosis, caused by Mycobacterium bovis, was recently diagnosed in a cheetah (Acinonyx jubatus), two lions (Panthera leo) and a chacma baboon (Papio ursinus) from the Kruger National Park (KNP). It is assumed that they contracted the disease directly or indirectly from tuberculous buffaloes in the park. Tuberculous granulomatous lesions in the lungs were extensive and constituted the predominant changes in all three animal species. These pulmonary lesions included tuberculous bronchiolitis and cavitation which would facilitate dissemination of M. bovis into the environment. Spread of the disease to free-ranging species (in which it has not previously been reported) that may act as maintenance hosts of the infection, is a matter of serious concern.

An outbreak of paralysis in finisher pigs in South Africa after ingestion of feed containing 54,581 mg/kg of selenium is described. The main and entirely consistent lesion was bilaterally symmetrical focal poliomalacia of the ventral horns of the spinal cord, which was most severe and consistent in the lumbar intumescence. Acute and subacute lesions were characterized by malacia with large numbers of gitter cells. The main features of chronic lesions were loss of neurons and gliosis. Focal degeneration and necrosis of the myocardium and skeletal muscles were also consistent, but there were fewer specific changes. Endothelial swelling, mild fibrinoid degeneration and perivascular leukocytic infiltration were present in the acute stage. Dermatitis, coronitis and hoof sloughing, usually present in more chronic cases of intoxication, were not a feature of the present outbreak, although alopecia and crusting were evident on the backs of a few pigs several weeks after the episode of intoxication. Serum-and tissue-selenium levels were elevated in the early stages after intoxication. Serum levels were nearly normal in chronic cases two months after the episode, while liver and kidney levels were still higher than normal. Higher levels were found in liver, kidney and serum than in muscle, with the highest levels in the kidney. Less than 20% of affected pigs recovered sufficiently to be marketed.

Cloacas of male ostrich chicks that had suffered prolapse of the phallus and cloaca were compared with cloacas of normal ostrich chicks of both sexes from the same area. Heavy infection of the cloacal and bursal tissue with Cryptosporidium sp. was present in all the cases of prolapse, while no cryptosporidia were observed in the normal chicks. Histopathological lesions as described in cryptosporidial infection in other species were present in the infected cloacas. These included loss of the microvillous border and epithelial hyperplasia and degeneration, which was indicated ultrastructurally by vacuolation of the apical cytoplasm, swelling of organelles, and nuclear changes. It is suggested that these lesions, in combination with the anatomy of the male ostrich cloaca, may be responsible for prolapse of the phallus and cloaca.