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Selected content from the Animal Health and Production Compendium (© CAB International 2013). Distributed under license by African Union – Interafrican Bureau for Animal Resources.

Whilst this information is provided by experts, we advise that users seek veterinary advice where appropriate and check OIE manuals for recent changes to regulations, diagnostic tests, vaccines and treatments.

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.


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Identity    Pathogen/s    Overview    Distribution    Distribution Map for Africa    Distribution Table for Africa    Host Animals    Systems Affected    Epidemiology    Impact : Economic    Pathology     Diagnosis    Disease Course    Disease Treatment    Prevention and Control    References    Links to Websites    OIE Reference Experts and Laboratories    Images

 

 Identity

Preferred Scientific Name
African swine fever

International Common Names
English acronym
ASF
PSA
French acronym
PPA
English
african swine fever - exotic
Spanish
peste porcina africana
French
peste porcine africaine

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 Pathogen/s

African swine fever virus

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Overview

African swine fever (ASF) is a highly contagious disease of pigs, first described in Kenya by Montgomery (1921). It is caused by a large DNA virus (170 to 190 kbp), classified as a unique member of the Asfarviridae family, and is considered by many experts to be one of the most complex viral diseases to affect domestic animals.

The disease is endemic in many African countries south of the Sahara desert. In Europe, it is endemic in Sardinia (Italy), but was successfully eradicated throughout the rest of Europe. However, ASF entered Europe again in 2007, in Georgia, and rapidly spread to neighbouring countries (Armenia, Azerbaijan and Russia), where it is now present without control.

ASF inflicts significant socio-economic impact on affected countries. The ASF virus affects both wild and domesticated pigs of all ages and breeds and is transmitted by soft ticks (Argasidae) of the genus Ornithodoros. Control of the disease is more difficult in outdoor systems than indoors, as this is usually achieved by the control of vectors. No treatment or effective vaccines are available.

This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's WAHID database on disease occurrence. Please see the AHPC library for further information on this disease from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: http://www.oie.int

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Distribution

ASF is present in Africa, particularly south of the Sahara, where the disease is mostly endemic. In Europe, ASF is endemic in Sardinia (Italy). In 2007, ASF entered Eastern Europe. First outbreaks were declared in Georgia, near the port of Poti (Beltrán-Alcrudo et al., 2008) and from there, the disease quickly spread to neighbouring countries (Armenia, Azerbaiyán and Russian Federation). Since the introduction of the disease in the area, hundreds of outbreaks have been reported and thousands of animals have been sacrificed, with huge economic losses associated. ASF is circulating in affected territories without control and this situation implies a risk, specifically for areas close by such as the European Union or China.

During 2011, ASF outbreaks were reported to AU-IBAR by 22 countries (see table below) with a total of 471 affected epidemiological units involving 144,950 cases, 135,712 deaths and a case fatality rate of 93.6%. Significantly, the Democratic Republic of Congo registered the highest number of outbreaks (84) accounting for about 17.8 % of the reported outbreaks and 79.4% of mortalities (AU-IBAR, 2011).

Although ASF was reported throughout the year in Africa, the highest number of outbreaks was recorded in May and January with 57 and 51 outbreaks, respectively.

Countries reporting African swine fever to AU-IBAR in 2011.

CountryOutbreaksCasesDeathsSlaughteredDestroyed
Benin25142681553652
Burkina Faso261518113400
Cameroon4146890NS
Central African Republic1799374200
Chad71891265954
Congo Brazzaville12200
DRC84105,614105,614969149
Ethiopia728190NS
Gambia519819800
Ghana756751015225
Kenya657530NS
Liberia112480
Madagascar19540540NS91
Malawi3619,75518,95611419
Mozambique165913800316
Nigeria117000
Rwanda606776002054647
South Africa1NSNSNSNS
Tanzania720631334NSNS
Togo802363115123540
Uganda5677883763158499
Zambia5422212NSNS
Total471144,950135,71214,4331392

 

NS: Not specified

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Distribution Map for Africa

 Distribution Map for AfricaDistribution Map for Africa

present, no further details = Present, no further details    widespread = Widespread    localised = Localised
confined and subject to quarantine = Confined and subject to quarantine    occasional or few reports = Occasional or few reports
evidence of pathogen = Evidence of pathogen    last reported = Last reported...    presence unconfirmed = Presence unconfirmed

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 Distribution Table for Africa

The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further information may be available for individual references in the Animal Health and Production Compendium. A table for worldwide distribution can also be found in the Animal Health and Production Compendium.
 
CountryDistributionLast ReportedOriginFirst ReportedInvasiveReferencesNotes
AFRICA
AlgeriaDisease never reported    OIE, 2012 
AngolaPresent    OIE, 2009 
BeninPresent    OIE, 2012 
BotswanaDisease not reported    OIE, 2009 
Burkina FasoPresent200805   OIE, 2012; OIE, 2003 
BurundiPresent    OIE, 2012 
CameroonPresent    OIE, 2012 
Cape VerdePresent    OIE, 2012 
Central African RepublicLast reported2011   OIE, 2012 
ChadPresent    OIE, 2012 
CongoPresent    OIE, 2009 
Congo Democratic RepublicPresent    OIE, 2012 
Côte d'IvoireLast reported1996   OIE Handistatus, 2005 
DjiboutiDisease never reported    OIE, 2012 
EgyptDisease never reported    OIE, 2009 
Equatorial GuineaWidespread    OIE, 1999 
EritreaNo information available    OIE, 2009 
EthiopiaPresent    AU-IBAR, 2011 
GabonDisease never reported    OIE, 2012 
GambiaPresent    AU-IBAR, 2011 
GhanaPresent    OIE, 2012 
GuineaNo information available    OIE, 2009 
Guinea-BissauPresent    OIE, 2012 
KenyaPresent    OIE, 2012; Montgomery, 1921 
LesothoDisease never reported    OIE, 2012 
LiberiaPresent    AU-IBAR, 2011 
LibyaDisease never reported    OIE Handistatus, 2005 
MadagascarPresent    OIE, 2012 
MalawiPresent    OIE, 2012 
MaliNo information available    OIE, 2009 
MauritiusPresent    OIE, 2012 
MoroccoDisease never reported    OIE, 2012 
MozambiquePresent    OIE, 2012 
NamibiaPresent    OIE, 2012; OIE, 2005 
NigeriaPresent    OIE, 2012 
RéunionDisease never reported    OIE Handistatus, 2005 
RwandaRestricted distribution    OIE, 2012 
Sao Tome and PrincipeLast reported1992   OIE Handistatus, 2005 
SenegalLast reported2009   OIE, 2012 
SeychellesDisease never reported    OIE, 2012 
Sierra LeonePresent    OIE, 2012 
SomaliaDisease not reported    OIE, 2012 
South AfricaPresent    OIE, 2012 
SudanDisease never reported    OIE, 2012 
SwazilandDisease never reported    OIE, 2012 
TanzaniaPresent    OIE, 2012 
TogoPresent    OIE, 2012 
TunisiaDisease never reported    OIE, 2012 
UgandaPresent    OIE, 2012 
ZambiaRestricted distribution    OIE, 2012 
ZimbabweLast reported1992   OIE, 2012 

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Host Animals

Animal name Context 
Sus scrofa (pigs) Domesticated host, Experimental settings, Wild host 

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Systems Affected

Blood and Circulatory System - Pigs
Digestive - Pigs
Multisystem - Pigs
Nervous - Pigs
Reproductive - Pigs
Respiratory - Pigs
Skin - Pigs

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Epidemiology

The ASF virus is found only in wild and domestic pigs and a number of soft ticks, mainly Ornithodoros moubata in Africa (Plowright et al., 1970) and Ornithodoros erraticus in the Iberian peninsula (Sanchez Botija, 1963). Ornithodoros corinaceus, a tick indigenous to the USA, has also been found to harbour and transmit ASF virus in experimental settings (Groocock et al., 1980), as has Ornithodoros savignyi which is present in Africa (Mellor and Wilkinson, 1985).

Some epidemiological differences have been observed between the transmission of ASF virus in Africa and Europe. In East and South Africa, ASF virus usually induces a non-apparent infection in three wild boar species: warthog (Phacochoerus aethiopicus), giant forest hog (Hylochoerus meinertzhageni) and bushpig (Potamochoerus porcus). Infection is characterised by low levels of virus in the tissues and low or undetectable levels of viremia. In the case of P. porcus, viremia has been observed between 35 and 91 days following infection and the virus can persist in lymphatic tissues for 34 weeks (Anderson et al., 1998). Viral infection normally moves from these animals to domestic pigs through a biological vector, Ornithodoros moubata, and not by direct transmission. In East and South Africa, ASF virus infection is maintained by a cycle of infection between wild boars and ticks, and only when domestic pigs are present is disease observed. In contrast, the European reservoir hosts is the wild boar (Sus scrofa), which is susceptible to ASF infection, exhibiting clinical symptoms and mortality similar to those observed in domestic pigs (Contini et al., 1982; Sanchez Botija, 1982). Similar results were observed in an experimental infection by ASF virus in feral pigs in Florida, USA (McVicar et al., 1981). Direct transmission by contact between sick and healthy animal is the most common mode of transmission, but in Europe indirect transmission by biological vectors, such as Ornithodoros erraticus, has been described in the Iberian Peninsula, especially in outdoor-reared pigs (Arias and Sánchez-Vizcaíno, 2002).

ASF virus infections in the African vector Ornithodoros moubata are transmitted by transovarial and transtadial routes, whilst only transtadial transmission has been observed in the European vector Ornithodoros erraticus.

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Impact : Economic

ASF is classified on OIE list A, which by definition contains only diseases that have the potential for very serious and rapid spread, producing serious socio-economic consequences (OIE, 1999). As there is no vaccine or treatment available for ASF, the identification and slaughter of sick and carrier animals is crucial to the control of the disease. The last five years (1985-1990) of the ASF Spanish eradication programme cost approximately US $92 million.

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Pathology

Post-mortem lesions and histopathological findings in ASFV infections vary widely depending on the virulence of the virus isolate and the species of pig infected; African wild pigs do not normally show lesions (Oura et al., 1988). Lesions are indistinguishable from those of hog cholera.

Three forms of ASF have been described: acute, sub-acute and chronic.

Acute form

The acute form of SAF is characterised by extensive haemorrhages in lymph nodes (mandibular, renal and gastro-hepatic), spleen and kidney and occasionally in the heart. Lymph nodes look like a red dark haematoma with oedema and a friable consistency. The spleen may show congestive splenomegaly when it is dark, enlarged, infarcted and friable. The kidneys usually have petechial haemorrhages of the renal cortex, in the medulla and renal pelvis. An intensive hydropericardium of sero-haemorrhagic liquid, and petechiae in the epicardium and endocardium are also frequently observed. Other lesions include petechiae in the mucous membrane of the urinary bladder, larynx and pleura. Congestion in the liver, fluid in the abdominal cavity and hydrothorax are also frequently observed (Sanchez Botija, 1982; Gomez-Villamandos et al., 1996).

Sub-acute form

The lesions observed in the sub-acute form of ASF are mild versions of those described for the acute form; that is large haemorrhages in lymph nodes and kidneys. An enlarged and haemorrhagic spleen, and congested and oedematous lung and in some cases an interstitial pneumonia are the lesions most frequently observed in the sub-acute form (Mebus et al., 1983).

Chronic form

The chronic form is characterised by enlarged lymph nodes and spleen, pleuritis and fibrous pericarditis. Focal caseous necrosis and mineralization of the lung have also been described (Mebus et al., 1983).

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Diagnosis

Introduction

Due to the great similarity of the clinical signs and lesions of ASF and those of other haemorrhagic pig diseases, laboratory diagnosis is an essential prerequisite for correct diagnosis (Sánchez-Vizcaíno, 2006).

Clinical Diagnosis

The clinical presentation varies depending on the virulence of the virus, the route of exposure, dose of virus and the species of pig infected, normally wild boar are more resistant (Sánchez-Vizcaíno, 2006).

Three forms of ASF have been described: acute, sub-acute and chronic.

The isolate currently circulating in the Russian Federation and Caucasus region belongs to genotype II (Rowlands et al., 2008) and only induces acute forms of the disease. Other forms of the disease can be observed in Sardinia (Italy) where ASF virus genotype I is circulating or in Africa where all the 22 ASF virus genotypes are circulating (Sánchez-Vizcaíno, 2006).

Acute form

Acute infections are characterised by high mortality (90-100%), fever (40-42ºC), leucopaenia and thrombocytopaenia. Reddening of the skin at the tips of ears, and chest and abdominal areas are frequently observed in white pigs. Vomiting and haemorrhagic diarrhoea may be observed. Abortion in pregnant sows is frequently described. One or two days before dying, the affected animals usually present anorexia, listlessness, cyanosis and incoordination (Mebus et al., 1983).

Sub-acute form

Sub-acute infections are produced by moderately virulent virus isolates, which present similar but less intense symptoms than those in the acute form. The mortality of the sub-acute form is approximately 30-70%, depending on the virus isolate. Illness and abortion is frequently observed.

Chronic form

Chronic infections result in low mortality (2-10%). Symptoms include weight loss, respiratory problems, arthritis, chronic skin ulcers or necrosis.

Lesions

See Pathology.

Differential Diagnosis

Differential diagnosis should consider the following diseases:

  • classical swine fever or hog cholera
  • erysipelas
  • salmonellosis
  • pasteurellosis

Laboratory Diagnosis

The samples that should be collected for ASF laboratory diagnosis are lymph nodes, kidneys, spleen, lung, blood and serum. Tissues are used for virus isolation (HA test) and viral antigen detection (PCR techniques and DIF test), while blood is used for virus isolation and PCR. Tissue exudates and serum are used for antibody detection by: IIF, ELISA or IB.

A wide variety of laboratory tests are available for ASF viral DNA and antibody detection (Sánchez-Vizcaíno, 2006). The most convenient, safe and specific tests for virus detection are: PCR techniques (both real time and conventional) (King et al., 2003; Agüero et al., 2004), direct immunofluorescence (DIF) (Bool et al., 1969) and haemadsortion (Malmquist and Hay, 1960).

The detection of the ASF virus genome by PCR has been developed with the use of sets of primers from a highly conserved region of the viral DNA, to detect all range of ASF isolates belonging to all the known virus genotypes including both non-haemadsorbing viruses and low virulence ones. This test is particularly useful for viral DNA identification from tissues which are poorly conserved, even if they have undergone putrefaction or the virus has been inactivated. It is an excellent and relatively rapid technique (results could be obtained in 5 hours) for ASF diagnosis, and is the most frequently technique used in worldwide laboratories for ASF virus detection. It needs good training and good laboratory practices to avoid contaminations and false positive results . Two types of PCR are validated by OIE for ASF diagnosis, conventional PCR (Agüero et al., 2003) and real-time PCR (King et al., 2003).

Direct immunofluorescence (DIF) is based on the detection of viral antigen in impression smears or frozen tissue sections with a fluorescein labelled immunoglobulin directed against the ASF virus. It is a very rapid (one hour) and economic test with high sensitivity to the acute form of ASF. However, for sub-acute or chronic infections, the DIF test has a sensitivity of only 40%. This decrease in sensitivity seems to be related to the formation of antigen-antibody complexes, which do not facilitate the reaction with the ASF conjugate (Sánchez-Vizcaíno, 1986). The use of DIF together with an indirect immunofluorescence test (IIF) makes it possible to detect 85 to 95% of all ASF cases (acute, sub-acute and chronic) in less than three hours (Sánchez-Vizcaíno, 1986).

The haemadsorption test (HA) is a technique used as the gold standard test for ASF virus identification due to its sensitivity and specificity. This test is usually only performed in ASF reference laboratories in order to confirm any new outbreak and when other tests have yielded negatives. HA is based on the haemadsorption characteristics that most ASF virus isolates induce when pig macrophages are infected in the presence of erythrocytes. A characteristic rosette around the infected macrophages develops before the cytopathic effect appears. A small number of field strains have shown cytopathic effect without producing the haemadsorption phenomenon (Sanchez Botija, 1982); these strains are identified using the DIF test on the sediments of these cell cultures. HA is relatively economical but access to ASF-free pigs and sterile facilities are also needed.

The lack of an effective vaccine against ASF virus and the long duration of the specific ASF-IgG reaction in infected pigs (detectable in blood on days 6-10 post-inoculation and subsequently for protracted periods, even years) has made the study of ASF antibody reactions an important prerequisite for the detection of sub-acute and chronic forms of ASF, and for ASF eradication programs (Arias and Sánchez-Vizcaíno, 2002). Several techniques have been adapted for ASF antibody detection, but the most common, practical and inexpensive tests are ELISA (Sánchez-Vizcaíno et al.,1986), immunoblotting (IB) (Pastor et al., 1987) and IIF (Bool et al., 1969).

The IIF test is a fast technique and has high sensitivity and specificity for the detection of ASF antibodies from either sera or tissue exudates (Sanchez Botija et al., 1970). It is based on the detection of ASF antibodies that bind to a monolayer of cell lines (by MS) infected with an adapted ASF virus. The antibody-antigen reaction is detected by a fluorescein labelled protein A. ELISA testing is the most useful method for large-scale serological studies. It is highly sensitive and specific, simple, rapid and economic and commerical kits are available. It is based on the detection of ASF antibodies bound to the viral proteins which are attached to a solid phase by addition of protein A-conjugated with an enzyme that produces a visible colour reaction when it reacts with the appropriate substrate.

The IB test is a highly specific, sensitive and easy to interpret technique which has been successfully used as a confirmatory method to IIF for low or doubtful ELISA sera (Sánchez-Vizcaíno, 2006).

Immunology

The immune response to ASF virus infection is still poorly understood. The main difficulty encountered has been the lack of neutralising antibodies and the great variability of the virus isolates. These characteristics made the production of an effective vaccine impossible to date.

Monocytes and macrophages are the main target cells for ASF virus replication; no evidence of virus replication in T or B lymphocytes has been observed (Minguez et al., 1988; Gomez-Villamandos et al., 1995). However, a lymphopenia, due to apoptosis of lymphocytes, mainly in the T area of the lymphatic organs, have been described (Carrasco et al., 1996).

Another characteristic of the response to ASFV is the lack of viral neutralisation. ASF virus-specific neutralised antibodies have never been demonstrated to entirely fulfil the classic definition of antibody neutralisation. It has proved impossible to neutralise 100% of the homologous virus, even with sera from recovered animals infected with attenuated ASF isolate; in this case a 10% fraction of non-neutralising virus is observed to persist (Ruiz et al., 1986). In contrast, animals that have recovered from ASFV infections can produce neutralised antibodies to foot and mouth virus (De Boer, 1967), and T cytotoxic lymphocytes (CD 8+) from recovered pigs are able to destroy macrophages infected with ASFV (Martin and Leitao, 1994).

ASF virus is very antigenic, inducing antibodies to a great number of viral proteins. IgM is detectable in animal sera at 4-6 days post inoculation and IgG is detectable at 6-9 days post inoculation with low or medium virulent ASF isolates (Sánchez-Vizcaíno, 2006).

Humoral and cell-mediated immunity does not seem to be affected in pigs infected with ASF virus.

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Disease Course

ASF virus normally infects the pig through the oral or nasal passages, but infection may also occur by cutaneous scarification or by intramuscular, subcutaneous, intraperitoneal or intravenous injections and by the bite of an infected tick (Colgrove et al., 1969; Plowright et al., 1969; McVicar, 1984). Primary virus replication begins in monocytes and macrophages of the lymph nodes near the site of infection; in oral infection, replication starts in the tonsils and mandibular lymph nodes. After initial replication the virus spreads through the blood (associated with the erythrocyte cell membrane) and/or lymphatic vessels to reach the target organs, where secondary replication takes place. The organs most usually affected are the lymph nodes, bone marrow, spleen, kidney, lungs and liver.

The incubation periods of natural or experimental infection vary widely depending on the virus isolate, route of infection and quantity of virus inoculated. This period will vary in natural infections between 4-8 days for the shortest incubation period and 15-19 days for the longest. In experimental infections, the incubation period is usually shorter than in natural infections, varying from 2 to 5 days.

Viremia in ASF infection generally starts 6-8 days post-infection, and due to a shortage of neutralizing antibodies may remain for a long time, even several months. Antibodies are detectable in sera and tissue exudates 7-10 days post-infection. In sera, they may be present for long periods, sometimes for more than a year post-infection.

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Disease Treatment

No effective treatment or vaccine against ASF virus is yet available. Live-attenuated vaccines that have been widely used experimentally, protect some animals against challenge infection with a homologous virus, but not with a heterologous one and most of them become carriers with ASF virus in several lymph nodes. Inactivated vaccine or viral protein vaccine does not appear to induce any protection. The role that some ASF virus genes may play in the modulation of protection is already being researched. These studies are opening new opportunities for the production of an ASF virus vaccine, but until now the only treatment for ASF is eradication, based on the control of animal transport and vectors as well as the early detection and slaughter of infected and carrier animals.

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Prevention and Control

As no vaccine for ASF is available, the control of this disease is based on rapid laboratory diagnosis and the enforcement of strict sanitary measures. Depending on the epidemiological status of disease in a particular region, different measures are recommended.

Epizootiological studies have shown that the most frequent source of ASF contamination in infection-free countries is refuse from international airports or ports. All leftover food from aeroplanes and ships should be routinely incinerated or efficiently sterilised. Import policy for animals and animal products should consider the disease status of the exporting nation. In infected European areas such as Sardinia (Italy) where the disease is enzootic and where mild or non-apparent clinical signs can be observed, the most important aspects of ASF prevention are the control of animal movement and the use of extensive serological surveys to detect carrier pigs. In endemic areas of Africa, the most important factor is to control the natural tick vectors and wild pig reservoirs, and/or limit their contact with domestic pigs.

During disease outbreaks, the rapid and efficient slaughtering of all pigs and the proper disposal of carcases and all waste material is critical. Other important aspects to consider are the cleaning and disinfecting of affected farms, designation of the infected area and increased control of animal movements. Serological surveys should be undertaken in the surrounding area. In the presence of any suspicious haemorrhagic pig disease, a differential laboratory diagnosis should be undertaken; as low virulence ASF strains do not produce significant lesions.

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References

African Union-Interafrican Bureau for Animal Resources, 2011. Panafrican Animal Health Yearbook 2011. Pan African Animal Health Yearbook, 2011:xiii + 90 pp. http://www.au-ibar.org/pan-african-animal-health-yearbook

Agüero M, Fernández J, Romero L, Sánchez Mascaraque C, Arias M, Sánchez-Vizcaíno JM, 2003. Highly sensitive PCR assay for routine diagnosis of African swine fever virus in clinical samples. Journal of Clinical Microbiology, 41(9):4431-4434.

Agüero M, Fernández J, Romero LJ, Zamora MJ, Sánchez C, Belák S, Arias M, Sánchez-Vizcaíno JM, 2004. A highly sensitive and specific gel-based multiplex RT-PCR assay for the simultaneous and differential diagnosis of African swine fever and Classical swine fever in clinical samples. Veterinary Research, 35(5):551-563.

Alcaraz C, Alvarez A, Escribano JM, 1992. Flow cytometric analysis of African swine fever virus-induced plasma membrane proteins and their humoral immune response in infected pigs. Virology (New York), 189(1):266-273; 42 ref.

Anderson EC, Hutchings GH, Mukarati N, Wilkinson PJ, 1998. African swine fever virus infection of the bushpig (Potamochoerus porcus) and its significance in the epidemiology of the disease. Veterinary Microbiology, 62(1):1-15; 21 ref.

Arias M, Sanchez-Vizcaino JM, 1992. Manual de diagnóstico serológico de la Peste porcina africana. Monografias INIA, 83:5-44.

Arias M, Sánchez-Vizcaíno JM, 2002. African swine fever. In: Trends in emerging viral infections of swine [ed. by Morilla, A.\Yoon, K. J.\Zimmerman, J. J.]. Ames, USA: Iowa State Press, 119-124.

Ayoade GO, Adeyemi IG, 2003. African swine fever: an overview. Revue d'Elevage et de Medecine Veterinaire des Pays Tropicaux, 56(3-4):129-134.

Beltran-Alcrudo D, Lubroth J, Depner K, Rocque Sde la, 2008. African swine fever in the Caucasus. EMPRES Watch, 2008(April):8 pp.

Blasco R, Agüero M, Almendral JM, Vinuela E, 1989. Variable and constant regions in African swine fever virus DNA. Virology (New York), 168(2):330-338; 40 ref.

Bool P, Ordas A, Sanchez Botija C, 1969. The diagnosis of African swine fever by immunofluorescence. Bull. Off. Int. Epizoot., 72:819-839.

Breese S, De Boer CJ, 1966. Electron microscope observation of Africa swine fever virus in tissue culture cells. Virology, 28:420-428.

Carrasco L, Chacon M, Lara J, Martin J, Gomez J, Hervas J, Wilkinson P, Sierra M, 1996. Virus association with lymphocytes in acute African swine fever. Veterinary Research, 27:305-312.

Colgrove G, Haelterman EO, Coggins L, 1969. Pathogenesis of African swine fever virus in young pigs. Am. J. Vet. Res., 30:1343-1359.

Contini A, Cossu P, Rutili D, Firinu A, 1982. African swine fever in Sardinia. In: Wilkinson PJ, ed. African swine fever, EUR 8466 EN, Pro. CEC/FAO Research seminar, Sardinia, September, 1981, 1-6.

De Boer CV, 1967. Studies to determine neutralizing antibody in sera from animals recovered from Africa swine fever and laboratory animals inoculated with Africa swine fever virus with adjuvants. Arch Gesamte Virusforsch, 20:164-179.

Gomez-Villamandos J, Bautista M, Hervas J, Carrasco J, Cahcon F, Perez J, Sierra M, 1996. Subcellular changes in platelets in acute and subacute African swine fever. J. Comp. Pathol., 59:146-151.

Gomez-Villamandos J, Hervas J, Mendez A, Carrasco L, Villeda C, Wilkinson P, Sierra M, 1995. Experimental African swine fever: apoptosis of lymphocytes and virus replication in other cells. J. Gen. Virol., 76:2399-2405.

Groocock CM, Hess W, Gladney G, 1980. Experimental transmission of African swine fever virus by Ornithodoros coriaceus, an argasid tick indigenous to United States. Am. J. Vet. Res., 41:591-594.

Hess WL, Cox BF, Heuschele WP, Stone SS, 1965. Propagation and modification of African swine fever virus in cell cultures. Am. J. Vet. Res., 26:141-146.

King DP, Reid SM, Hutchings GH, Grierson SS, Wilkinson PJ, Dixon LK, Bastos ADS, Drew TW, 2003. Development of a TaqMan® PCR assay with internal amplification control for the detection of African swine fever virus. Journal of Virological Methods, 107(1):53-61.

Lubisi BA, Bastos ADS, Dwarka RM, Vosloo W, 2005. Molecular epidemiology of African swine fever in East Africa. Archives of Virology, 150(12):2439-2452. http://springerlink.metapress.com/link.asp?id=100423

Malmquist WA, Hay D, 1960. Hemadsorption and cytophathic effect produced by African swine fever virus in swine bone marrow and buffy coat cultures. Am. J. Vet. Res., 21:104-108.

Martin C, Leitao A, 1994. Porcine immuno responses to African swine fever virus infection. Veterinary Immunology and Immunopathology, 34:99-106.

McKercher PD, Yedloutschnig RJ, Callis JJ, Murphy R, Panina GF, Civardi A, Bugnetti M, Foni E, Laddomada A, Scarano C, Scatozza F, 1987. Survival of viruses in Prosciutto di Parma (Parma ham). Canadian Institute of Food Science and Technology Journal, 20(4):267-272; 13 ref.

McVicar JW, 1984. Quantitative aspects of the transmission of African swine fever. American Journal of Veterinary Research, 45(8):1535-1541; 29 ref.

McVicar JW, Mebus C, Becker HN, Belden RC, Gibbs EP, 1981. Induced African swine fever virus in feral pigs. J. Am. Vet. Med. Assoc., 179:441-446.

Mebus CA, McVicar JW, Dardiri AH, 1983. Comparison of the pathology of high and low virulence African swine fever virus infections. African swine fever., 183-194; [Report EUR 8466 EN]; 14 ref.

Medbus CA, House C, Gonzalvo FR, Pineda JM, Tapiador J, Pire JJ, Bergada J, Yedloutschnig RJ, Sahu S, Becerra V, Sanchez-Vizcaino JM, 1993. Survival of foot-and-mouth disease, African swine fever, and hog cholera viruses in Spanish Serrano cured hams and Iberian cured hams, shoulders and loins. Food Microbiology, 10(2):133-143; 6 ref.

Mellor PS, Wilkinson PJ, 1985. Experimental transmission of African swine fever virus by Ornithodoros savignyi (Audouin). Research in Veterinary Science, 39(3):353-356; 16 ref.

Mínguez I, Rueda A, Domínguez J, Sánchez-Vizcaíno JM, 1988. Double labeling immunohistological study of African swine fever virus-infected spleen and lymph nodes. Veterinary Pathology, 25(3):193-198; 25 ref.

Montgomery RE, 1921. On a form of swine fever ocurring in British East Africa (Kenya Colony) J. Comp. Pathol., 34:159-191.

Murphy F, Fauquet C, Bishop D, Ghabrial S, Harvis A, Martinelli G, Mayo M, Summer M, 1995. Virus taxonomy. Sixth report of the International Committee on taxonomy of viruses. Archives of Virology, Suplement 10.

OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.

OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.

OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.

OIE, 1999. Bulletin - November-December 1999. [International disease statistics]. Bulletin - Office International des Epizooties 1999, No. 6, 112 pp.

OIE, 2003. African swine fever in Burkina Faso. Disease Information, 16, No. 35.

OIE, 2005. African swine fever in Namibia. Follow-up report No. 1. Disease Information, 18(1).

OIE, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.

OIE, 2009. World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int

OIE, 2012. World Animal Health Information Database. Version 2. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int/wahis_2/public/wahid.php/Wahidhome/Home

Oura CA, Powell PP, Anderson E, Parkhouse RM, 1988. The pathogenesis of African swine fever in the resistant bushpig. J. Gen. Viro., 1439-1443.

Pastor MJ, Laviada MD, Sanchez-Vizcaino JM, Escribano JM, 1987. Detection of African swine fever virus antibodies by immunoblotting assay. Can. J. Vet. Res., 53:105-107.

Plowright W, Parker J, Peirce MA, 1969. The epizootiology of African swine fever in Africa. Vet. Rec., 85:668-674.

Plowright W, Perry CT, Peirce MA, 1970. Experimental infection of the Argasid tick, Ornithodoros moubata porcinus, with African swine fever virus. Arch. Ges. Virusforsch, 31:33-50.

Rowlands RJ, Michaud V, Heath L, Hutchings G, Oura C, Vosloo W, Dwarka R, Onashvili T, Albina E, Dixon LK, 2008. African swine fever virus isolate, Georgia, 2007. Emerging Infectious Diseases, 14(12):1870-1874. http://www.cdc.gov/eid

Ruiz Gonzalvo F, Carnero M, Caballero C, 1986. Inhibition of African swine fever infection in the presence of immune sera in vivo and in vitro. Am. J. Vet. Res., 47:1125-1131.

Sanchez Botija C, 1963. Reservorios del virus de la Peste Porcina Africana. Investigacion del virus de la PPA en los artropodos mediante la prueba de la hemoadsorcion. Bull. Off. Int. Epizoot., 60:895-899.

Sanchez Botija C, 1982. African swine fever. New developments Rev. Sci. Techol. Off. Int. Epizoot., 1:1065-1094.

Sanchez Botija C, Ordas A, Gonzalez J, 1970. La inmunofluorescencia indirecta aplicada a la investigacion de anticuerpos de la Peste porcina africana. Su valor para el diagnostico. Bull. Off. Int. Epizoot., 74:397-417.

Sanchez-Vizcaino JM, 1986. Africa Swine Fever diagnosis. In: Becker J, ed. African swine fever, Martinus Nijhoff Publishing, Boston, 63-71.

Sanchez-Vizcaino JM, 1999. African swine fever. In: Leman AD, Straw BE, Mengeling WL, Dallaire S, Taylor DJ, eds. Diseases of swine. 8th edition. Iowa State University.

Sánchez-Vizcaíno JM, 2006. African swine fever. In: Straw BE, Zimmerman JJ, D'Allaire S, Taylor DJ, eds. Diseases of Swine, 9th edition. Ames, Iowa: Blackwell Publishing, 291-298.

Sánchez-Vizcaíno JM, Martinez-López B, Martinez-Avilés M, Martins C, Boinas F, Vial L, Michaud V, Jori F, Etter E, Albina E, Roger F, 2009. Scientific Review on African Swine Fever. Report for European Food Safety Authority, 1-141.

Sanchez-Vizcaino JM, Tabares E, Salvador E, Ordas A, 1982. Comparative studies of two antigens for the use in the indirect Elisa test for the detection of ASF antibodies. In: Wilkinson PJ, ed. African swine fever, EUR 8466 EN Proc CEC/FAO Research seminar, Sardinia, September, 1981, 195-325.

Shirai J, Kanno T, Tsuchiya Y, Mitsubayashi S, Seki R, 2000. Effects of chlorine, iodine and quaternary ammonium compound disinfectants on several exotic disease viruses. Journal of Veterinary Medical Science, 62(1):85-92.

Sogo JM, Almendral JM, Talavera A, Vinuela E, 1984. Terminal and internal inverted repetitions in African swine fever virus DNA. Virology, 133(2):271-275; 14 ref.

Tabares E, Marcotegui MA, Fernandez M, Sanchez Botija C, 1980. Proteins specified by African swine fever virus I. Analysis of viral structural proteins and antigenic properties. Arch. Virol., 66:107-117.

Wilkinson PJ, Wardley RC, 1978. The replication of ASFV in pig endothelial cells. Br. Vet. J., 134:280-282.

Yañez R, Rodriguez J, Nogal L, Enriquez C, Rodriguez J, Viñuela E, 1995. Analysis of the complete nucleotide sequence of Africa swine fever virus. Virology, 208:249-278.

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Links to Websites

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OIE Reference Experts and Laboratories

(http://www.oie.int, accessed 5 June 2013)

Dr Baratang Alison Lubisi
Onderstepoort Veterinary Institute
Agricultural Research Council
Private Bag X05
Onderstepoort 0110
SOUTH AFRICA
Tel: +27-12 529 91 17 Fax: +27-12 529 94 18
Email: This email address is being protected from spambots. You need JavaScript enabled to view it.

Dr José Manuel Sánchez-Vizcaíno
Centro de Vigilancia Sanitaria Veterinaria (VISAVET)
Facultad de Veterinaria
HCV Planta sótano
Universidad Complutense de Madrid (UCM)
Avda Puerta de Hierro s/n
28040 Madrid
ESPAÑA
Tel: +34-91 394.40.82 Fax: +34-91 394.39.08
Email: This email address is being protected from spambots. You need JavaScript enabled to view it.

Dr Linda Dixon
Institute for Animal Health
Ash Road, Pirbright
Woking, Surrey, GU24 0NF
UNITED KINGDOM
Tel: +44-1483 23 24 41 Fax: +44-1483 23 24 48
Email: This email address is being protected from spambots. You need JavaScript enabled to view it.

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Images


Skin erythema on the ear of a pig affected by acute disease. © J.M. Sanchez-Vizcaino (CISA)Skin erythema on the ear of a pig affected by acute disease. © J.M. Sanchez-Vizcaino (CISA) 
Reddened skin on the extremities is a non-specific lesion associated with a septicemic/viremic condition. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection ServiceReddened skin on the extremities is a non-specific lesion associated with a septicemic/viremic condition. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection Service
 
  A greatly enlarged dark red to black spleen from a pig infected with a highly virulent ASFV isolate. There are petechial haemorrhages in the renal cortex. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection ServiceA greatly enlarged dark red to black spleen from a pig infected with a highly virulent ASFV isolate. There are petechial haemorrhages in the renal cortex. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection Service   Very enlarged dark red (haemorrhagic) gastrohepatic lymph nodes from a pig infected with a highly virulent isolate of ASFV. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection Service Very enlarged dark red (haemorrhagic) gastrohepatic lymph nodes from a pig infected with a highly virulent isolate of ASFV. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection Service
 Swine lymph nodes: normal (A), affected by acute African swine fever (B), and affected by hog cholera (C).|Swine lymph nodes: normal (A), affected by acute ASF (B), and affected by hog cholera (C). © J.M. Sanchez-Vizcaino (CISA)Swine lymph nodes: normal (A), affected by acute African swine fever (B), and affected by hog cholera (C).|Swine lymph nodes: normal (A), affected by acute ASF (B), and affected by hog cholera (C). © J.M. Sanchez-Vizcaino (CISA) Spleen of swines: acute hog cholera (A), acute African swine fever (B), normal (C).|Spleen of swines: acute hog cholera (A), acute ASF (B), normal (C). © J.M. Sanchez-Vizcaino (CISA)Spleen of swines: acute hog cholera (A), acute African swine fever (B), normal (C).|Spleen of swines: acute hog cholera (A), acute ASF (B), normal (C). © J.M. Sanchez-Vizcaino (CISA)
  Swine macrophages infected with ASF virus showing hemadsorption. © J.M. Sanchez-Vizcaino (CISA)Swine macrophages infected with ASF virus showing hemadsorption. © J.M. Sanchez-Vizcaino (CISA)  Enlarged dark red renal lymph nodes, petechial haemorrhages in the renal cortex and perirenal oedema. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection ServiceEnlarged dark red renal lymph nodes, petechial haemorrhages in the renal cortex and perirenal oedema. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection Service
 Petechial haemorrhages on the serosal surface are indicative of a viremic/septicemic condition. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection ServicePetechial haemorrhages on the serosal surface are indicative of a viremic/septicemic condition. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection Service Oedema of the gall bladder. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection ServiceOedema of the gall bladder. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection Service
 Chronic ASF; consolidated lobules in the lung. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection ServiceChronic ASF; consolidated lobules in the lung. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection Service Enlarged bronchial lymph nodes are part of a generalized lymphadenopathy in chronic ASF. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection ServiceEnlarged bronchial lymph nodes are part of a generalized lymphadenopathy in chronic ASF. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection Service
 Necrosis of the skin is a frequent lesion in chronic ASF. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection ServiceNecrosis of the skin is a frequent lesion in chronic ASF. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection Service Necrosis of the skin in chronic ASF can be focal; the areas begin as raised hyperemic areas and progress to areas of necrosis. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection ServiceNecrosis of the skin in chronic ASF can be focal; the areas begin as raised hyperemic areas and progress to areas of necrosis. © USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal & Plant Health Inspection Service
  

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Date of report: 28/05/2013

© CAB International 2013. Distributed under license by African Union – Interafrican Bureau for Animal Resources.

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This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.