African swine fever

From Pig
African swine fever. Hemorrhagic gastrohepatic lymph node. Courtesy of Dr. C.A.L.Oura
African swine fever. Generalized hyperemia of abdomen and legs. Courtesy of Dr. C.A.L.Oura
African swine fever. Hyperemia of the skin of the ears. Courtesy of Dr. C.A.L.Oura
African swine fever. Hemadsorption of red blood cells to macrophages. Courtesy of Dr. C.A.L.Oura

African swine fever (ASF) is a highly contagious hemorrhagic viral disease of pigs that produces a wide range of clinical signs and lesions that closely resemble those of classical swine fever. It is an economically important disease that is enzootic in many African countries and the Mediterranean island, Sardinia.


ASF virus is a large, enveloped DNA virus that replicates primarily in cells of the mononuclear phagocytic system. It is currently classified as the only member of a family called African swine fever-like viruses (Asfarviridae). The prolonged period during which ASF has been an enzootic disease in Africa has led to the selection of viruses of varying virulence. No distinct antigenic types have been identified, but distinct genotypes have been differentiated by restriction enzyme analysis of the genomes of viruses obtained from different geographic areas over a long period of time. The virus is highly resistant to a wide pH range and to a freeze/thaw cycle and can remain infectious for many months at room temperature or when stored at 4°C. Virus in body fluids and serum is inactivated in 30 min at 60°C, but virus in unprocessed pig meat, in which it can remain viable for several weeks, can be inactivated only by heating to 70°C for 30 min. Although ASF virus can be adapted to grow in cells from different species, it does not replicate readily in any species other than swine[1].

The disease is limited to all breeds and types of domestic pigs and European wild boar. All age groups are equally susceptible. In Africa, the virus produces inapparent infection in 2 species of wild swine—wart hog (Phacochoerus aethiopicus) and bush pig (Potamochoerus porcus) — and in the soft tick Ornithodoros moubata. When the disease was endemic in southern Spain and Portugal, a different species of soft tick, Ornithodoros erraticus, became infected with the virus. Several other Ornithodoros spp that are not usually associated with pigs or wild swine have been infected experimentally.

ASF has been reported in a large number of countries in Africa, south of the Sahara, either as an enzootic disease or as sporadic epidemics in domestic pigs. The first spread of the disease outside Africa was into Europe in 1957; this was almost certainly successfully eradicated. The second introduction in 1960 resulted in ASF becoming enzootic in Spain and Portugal and, subsequently (1978), in Sardinia. During the 1970s, it spread to the Caribbean and South America and serious, but limited, outbreaks in Europe occurred in Belgium (1985) and the Netherlands (1986). Rigorous eradication programs ended with the successful eradication of the disease from both Portugal (1993) and Spain (1995).

ASF virus is maintained in Africa by a natural cycle of transmission between wart hogs and the soft tick vector O moubata, which inhabits wart hog burrows and from which it is unlikely ever to be eliminated. The spread of virus from the wildlife reservoirs to domestic pigs can be either by the bite of an infected soft tick or by ingestion of wart hog tissues. Virulent viruses produce acute disease, and all body fluids and tissues contain large amounts of infectious virus from the onset of clinical disease until death. Pigs infected with less virulent isolates can transmit virus to susceptible pigs up to 1 mo after infection; blood is infectious up to 6 wk, and transmission can occur if blood is shed. Pigs usually become infected via the oronasal route by direct contact with infected pigs or by ingestion of waste food containing unprocessed pig meat or pig meat products. The primary route of infection is the upper respiratory tract, and virus replicates in the tonsil and lymph nodes draining the head and neck; generalized infection rapidly follows via the bloodstream. High concentrations of virus are then present in all tissues. The factors that produce the hemorrhagic lesions are not defined, but the severe disruptions to the blood clotting mechanism play a major role. Virus is excreted mainly from the upper respiratory tract and is also present in secretions and excretions containing blood.

Pigs that survive infection with the less virulent isolates are probably persistently infected for life and have circulating antibody, although they do not excrete virus or transmit virus to their offspring in utero. Their role in the epidemiology of the disease is not known, but they are resistant to disease when challenged with related virus genotypes. This challenge virus may replicate and be transmitted, either directly or indirectly, to other pigs.

The main factor in the persistence of the disease in domestic pigs in Africa is the presence of large numbers of free-ranging village pigs and, in some areas, soft tick vectors in pig pens.

Clinical signs

Peracute, acute, subacute, and chronic forms occur, and mortality rates vary from 0 to 100%, depending on the virulence of the virus with which pigs are infected. Acute disease is characterized by a short incubation period of 5-7 days, followed by high fever (up to 42°C) and death in 7-10 days. The least variable clinical signs are loss of appetite, depression, and recumbency; other signs include hyperemia of the skin of the ears, abdomen, and legs; respiratory distress; vomiting; bleeding from the nose or rectum; and sometimes diarrhea. Abortion is sometimes the first event seen in an outbreak. The severity and distribution of the lesions also vary according to virulence of the virus. Hemorrhages occur predominantly in lymph nodes, kidneys (almost invariably as petechiae), and heart; hemorrhages in other organs are variable in incidence and distribution. Some isolates produce an enlarged and friable spleen; straw-colored or blood-stained fluid in pleural, pericardial, and peritoneal cavities; or edema and congestion of the lungs. Some viruses of low virulence have been isolated in Europe and produce nonspecific clinical signs and lesions. Chronic disease is characterized by emaciation, swollen joints, and respiratory problems. This form of the disease is rarely seen in outbreaks.


ASF cannot be differentiated from classical swine fever (hog cholera) by either clinical or postmortem examination. Samples of blood, serum, spleen, tonsil, and gastrohepatic lymph nodes from suspected cases should be submitted to the laboratory for confirmation. Virus can be isolated by inoculation of primary cultures of pig monocytes, in which it produces hemadsorption of pig red cells to the surface of infected cells. Classical swine fever virus does not replicate in these cells. There are nonhemadsorbing viral isolates, some of which produce virulent disease. These isolates produce only a cytopathic effect in pig leukocytes. Confirmation of ASF in these cases has to be performed by either PCR or an antigen-detection ELISA. Viral antigen can be detected in infected tissue smears or sections by staining with labelled antibodies (several enzyme-labelled tests are available, eg, immunofluorescence), and viral DNA by PCR or hybridization of nucleic acid probes to tissue sections. The most appropriate tests for detecting antibody in serum or tissue fluids are the ELISA, indirect immunofluorescence, and counterimmunoelectrophoresis; a number of other useful tests are available.

Other differential diagnoses include hemorrhagic bacterial infections and certain types of poisons.


There is no treatment, and all attempts to develop a vaccine have been unsuccessful. Pigs that recover from infection with less virulent viral isolates are resistant to challenge with viruses of a different genotype in the absence of neutralizing antibody. Prevention therefore depends on ensuring that neither infected live pigs nor pig meat products are introduced into areas free of ASF. All successful eradication programs have involved the rapid diagnosis, slaughter, and disposal of all animals on infected premises. Sanitary measures must also be applied and include control of movement and treatment of waste food. Subsequently, a serologic survey of all pig farms within a specific control zone must be done to ensure that all infected pigs have been identified.