African swine fever virus (ASFV) infects domestic swine and other members of the family Suidae, including warthogs (Phacochoerus aethiopicus), bushpigs (Potamochoerus porcus) and wild boar (Sus scrofa ferus). All efforts to infect other animals have been unsuccessful. The virus does not infect humans. The disease is limited to all breeds and types of domestic pigs and European wild boar, with all ages being equally susceptible to the virus. In Africa, the virus produces inapparent infection in warthogs, bushpigs, and in the soft tickOrnithodoros moubata. When the disease was endemic in southern Spain and Portugal, a different species of soft tick (O erraticus) became infected with the virus. Several other Ornithodoros spp that are not usually associated with pigs or wild swine have been infected with ASFV experimentally.
African swine fever (ASF) was considered a disease confined to subSaharan Africa until 1957, when an outbreak occurred on the Iberian Peninsula (Portugal) as a result of waste from airline flights being fed to pigs near Lisbon airport. A further introduction of ASF to Portugal was reported in 1960. ASF remained endemic in the Iberian peninsula until the mid-1990s. Outbreaks of ASF were reported in a number of other European countries during the 20th century, including Malta (1978), Italy (1967, 1980), France (1964, 1967, 1977), Belgium (1985), and the Netherlands (1986). The virus was eradicated by slaughter from each of these countries but has remained endemic in Sardinia since its introduction in 1978. During the 1970s and 80s, ASFV spread to the Caribbean and South America (Brazil), where outbreaks were stamped out after they had devastated the swine industries in the affected countries.
The virus appeared again in continental Europe in 2007, initially in Georgia, from where it spread to western parts of Russia, Armenia, Azerbaijan, Ukraine, Belarus, Lithuania, Latvia, Poland, and Estonia. In 2018, the virus spread to China, from where it rapidly spread to many neighbouring Asian countries, including Mongolia, Cambodia, India, Laos, Vietnam, the Philippines, North and South Korea, Myanmar, Timor-Leste, and Papua New Guinea. The virus has also spread further west in Europe, infecting pigs in Romania, Serbia, Slovakia, Bulgaria, and Greece, as well as infecting wild boar in Belgium, Czech Republic, and Hungary. However ASF was successfully eradicated from Belgium and the Czech Republic. As of July 2020, reports from FAO and OIE indicate that many millions of pigs have either died or been culled as a direct result of the ASF outbreak across Europe and Asia and this has had a large impact on global pork supplies.
Etiology and Pathogenesis of African Swine Fever
African swine fever virus is a large, enveloped, double-stranded DNA virus that is the sole member of the genus Asfivirus within the family Asfarviridae. ASFV is distantly related to virus families of lower eucaryotes including the family Faustoviridae and genus Kaumoebavirus. Together with other viruses that have a replicative stage in the cytoplasm, the Asfarviridae have been classified in the Phylum "Nucleocytoviricota" (ICTV Master Species List 2019.v1).
The primary route of infection is the upper respiratory tract, where the virus replicates in the tonsils and lymph nodes draining the head and neck. Generalized infection rapidly follows via the bloodstream, leading to high concentrations of virus in all tissues. The factors that produce the hemorrhagic lesions are not fully defined, but severe disruption to the blood clotting mechanism plays a major role. Virus is excreted mainly from the upper respiratory tract and is present in all secretions and excretions containing blood.
Epidemiology and Transmission of African Swine Fever
The prolonged period during which African swine fever has been an enzootic in Africa is likely to have led to the selection of viruses of varying virulence. Distinct genotypes of ASFV have been differentiated by sequence analysis of viral genomes obtained from different geographic areas over a long 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 minutes at 60°C, but virus in unprocessed pig meat, in which it can remain viable for several weeks or months, can be inactivated only by heating to 70°C for 30 minutes.
Two distinct patterns of transmission occur: a sylvatic cycle in warthogs and ticks in Africa, and epizootic and enzootic cycles in domestic swine and wild boar. ASFV is maintained in Africa by a sylvatic cycle of transmission between warthogs and the soft tick vector O moubata, which inhabits warthog burrows and from which it is unlikely ever to be eliminated. Ornithodoros ticks are biological vectors for the virus. The spread of virus from the wildlife reservoirs to domestic pigs can be by the bite of an infected soft tick or by ingestion of warthog tissues.
Once the virus has been introduced in domestic pigs or wild boar, infected animals constitute the most important source of the virus for susceptible swine. 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. In acutely infected swine, 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 for as long as 1 month after infection; blood is infectious for as long as 6 weeks, and transmission can occur if blood is shed. Pigs that survive infection may be persistently infected, however their role in the epidemiology of the disease is not fully understood.
Clinical Signs, Lesions, and Necropsy Findings of African Swine Fever
Peracute, acute, subacute, and chronic forms of ASF occur, and mortality rates vary from 0% to 100%, depending on the virulence of the virus with which pigs are infected. The acute and peracute forms of the disease are characterized by a severe hemorrhagic disease with close to 100% mortality. After a short incubation period of 3 –7 days, swine develop high fever (up to 42°C), followed rapidly by inappetence, incoordination, and prostration. Swine may die at this stage without exhibiting other clinical signs. Surviving swine will then exhibit reddening or cyanosis of the ears and snout, followed rapidly by more generalized reddening of the body and bleeding from the nose and anus. Infected pigs may also show dyspnea, vomiting, and abortion if pregnant.
Swine that survive acute infection may appear healthy or chronically diseased. Some viruses of low virulence have been isolated that produce nonspecific clinical signs and lesions often characterized by emaciation, swollen joints, and respiratory problems.
The severity and distribution of the lesions caused by ASFV vary according to the virulence of the virus. In acutely fatal cases, gross lesions are most prominent in the lymphoid and vascular systems. Hemorrhages occur predominantly in lymph nodes, which may resemble blood clots, and in the kidneys (usually as petechiae) and heart. The spleen is often large and friable, and there may be straw-colored or blood-stained fluid in pleural, pericardial, and peritoneal cavities and congestion of the lungs.
Diagnosis of African Swine Fever
Laboratory testing is used to differentiate from classical swine fever
Rapid, early laboratory diagnosis is essential for timely control
The clinical signs of African swine fever can be similar to those of several diseases, including bacterial septicemia (eg, erysipelas Swine Erysipelas Erysipelas in swine is caused primarily by Erysipelothrix rhusiopathiae, a bacteria carried by up to 50% of pigs. Possible clinical manifestations are cutaneous erythema, including characteristic... read more and acute salmonellosis Intestinal Salmonellosis in Pigs Enteropathogenic salmonellae cause inflammation and necrosis of the small and large intestines, resulting in diarrhea. Infection with certain serotypes may be accompanied by generalized sepsis... read more ), but the major diagnostic problem is in distinguishing it from classical swine fever Classical Swine Fever (hog cholera). Any febrile disease in swine associated with disseminated hemorrhage and high mortality should raise suspicion of African swine fever.
Diagnosis of chronic infections of African swine fever is problematic, because the clinical signs and lesions in chronically infected pigs are highly variable. Laboratory confirmation is essential, and samples of blood, spleen, kidney, lymph nodes, and tonsils, in particular, should be collected for virus isolation, detection of antigen, or PCR testing for viral DNA. Virus isolation is carried out in swine bone marrow or peripheral blood leukocyte cultures, in which hemadsorption of red blood cells on the surface of the infected cells can be demonstrated. There are nonhemadsorbing viral strains that produce a cytopathic effect in pig leukocytes. Antigen detection can also be achieved by immunofluorescence staining of tissue smears, immunodiffusion using tissue suspensions as the source of antigen, or antigen-detection ELISA. Antibodies can be detected by ELISA and indirect immunofluorescence, but in acute cases of ASF, the pigs may die before antibodies are produced.
Treatment, Control, and Prevention of African Swine Fever
No effective treatment or vaccine
There is no treatment for ASF, and attempts to develop a vaccine are ongoing.. Many laboratories around the world are working to develop a vaccine, with some promising results, but more work is required to ensure the safely and efficacy of these prototype vaccines before registration. Researchers in China have reported results of field trials to determine safety recently.
The prevention and control of ASF is complicated by several factors, including the transmission of virus in fresh meat and some cured pork products, the possible persistent infection in some swine, the presence of wildlife reservoirs of virus including wild suids and soft ticks in some parts of the world, and diagnostic confusion with agents that cause similar clinical signs, such as classical swine fever (hog cholera). Prevention depends on ensuring that neither infected live domestic or wild swine nor swine meat products are introduced into areas free of ASF.
The presence of the virus in ticks and warthogs in many countries of sub-Saharan Africa makes it difficult, if not impossible, to break the sylvatic cycle of the virus. However, domestic swine can be reared in Africa if the management system avoids feeding uncooked waste food scraps and prevents the access of ticks and contact with warthogs, usually by double fencing, with a wire mesh perimeter fence extending beneath the ground.
Countries free of ASF maintain their virus-free status by prohibiting the importation of live swine and swine products from infected countries and by monitoring the destruction of all waste food scraps from ships and aircraft involved in international routings.
If disease does occur in a previously noninfected country, control depends first on early recognition and rapid laboratory diagnosis. Once ASF is confirmed in a country that has been free of disease, prompt action is required to control and then eradicate the infection. The strategy for eradication involves slaughter of infected swine and swine in contact with them, and safe disposal of carcasses. If wild boar are present and being infected, this significantly complicates control programs. In these cases. direct contact between wild boar and domestic pigs must be avoided through enhanced biosecurity in backyard farms. Movement of swine between farms is controlled, and feeding of waste food is prohibited. Where soft ticks are known to occur, infested buildings are sprayed with acaricides, and restocking of farms should only be allowed if sentinel swine do not become infected.
African swine fever is a highly infectious, often rapidly fatal viral disease of pigs.
The virus is endemic to subSaharan Africa, where it is transmitted from warthogs and bushpigs by soft ticks.
An outbreak that began in Georgia in 2007 has since spread to numerous countries in Asia and Europe.
There are no vaccines available, although multiple candidates are being tested.