African swine fever
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- African swine fever
International Common Names
- English: african swine fever - exotic
- Spanish: peste porcina africana
- French: peste porcine africaine
Local Common Names
- Italy: peste suina africana
OverviewTop of page
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. Until 2007, the Italian island of Sardinia was the only European ASF-infected area (Mur et al., 2016). However, in 2007, ASF was introduced into Georgia (Rowlands et al., 2008); from there it spread to neighbouring countries (Azerbaijan, Armenia and Russia) and subsequently to Ukraine, Belarus and Moldova.
ASF was introduced into the Baltic States (Estonia, Latvia, Lithuania) and then Poland in 2014 and the disease has continued to spread within these regions. In 2017, the virus spread further west and the first cases of disease were reported in the Czech Republic and Romania, in wild boar and domestic pigs, respectively (Olesen et al., 2018). ASF was detected in wild boar in Hungary in April 2018 (OIE report), in wild boar in Belgium in September 2018 (OIE report) and in wild boar in Bulgaria in October 2018 (OIE report).
In August 2018, ASF was reported for the first time in pigs in China. As China is the world’s largest pig producer and pork is the most important protein source for Chinese people, the outbreaks of ASF will have large consequences on both local and the world pig industry (Li and Tian, 2018).
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
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Sus scrofa (pigs)||Domesticated host, Experimental settings, Wild host||Pigs: All Stages|
Systems AffectedTop of page blood and circulatory system diseases of pigs
digestive diseases of pigs
multisystemic diseases of pigs
nervous system diseases of pigs
reproductive diseases of pigs
respiratory diseases of pigs
skin and ocular diseases of pigs
DistributionTop of page
[See: OIE reports on African swine fever for an overview of the latest situation.]
ASF is widespread 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. ASF was detected in Georgia, near the port of Poti (Beltrán-Alcrudo et al., 2008) and from there, the disease quickly spread to neighbouring countries (Armenia, Azerbaijan and Russian Federation) and subsequently to Ukraine, Belarus and Moldova. ASF spread into four EU member countries in 2014, namely Lithuania, Poland, Latvia, and Estonia; and in 2017, ASF was reported for the first time in Czech Republic and Romania (Jurado et al., 2018). In 2018, ASF was detected in wild boar in Hungary, Belgium and Bulgaria (for more information, see OIE’s World Animal Health Information Database (WAHIS) Interface).
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
Central African Republic
NS: Not specified
Distribution TableTop of page
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 details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Afghanistan||No information available||OIE, 2009|
|Armenia||Disease not reported||OIE, 2009|
|Azerbaijan||Disease not reported||OIE, 2009|
|Bahrain||Disease never reported||OIE, 2009|
|Bangladesh||Disease never reported||OIE, 2009|
|Bhutan||Disease never reported||OIE, 2009|
|Brunei Darussalam||Disease not reported||OIE Handistatus, 2005|
|Cambodia||No information available||OIE, 2009|
|China||Present||Li and Tian, 2018|
|-Henan||Present||Li and Tian, 2018|
|-Hong Kong||No information available||OIE, 2009|
|-Jiangsu||Present||Li and Tian, 2018|
|-Liaoning||Present||Li and Tian, 2018|
|-Zhejiang||Present||Li and Tian, 2018|
|Georgia (Republic of)||Present||OIE Handistatus, 2005; OIE, 2009|
|India||Disease never reported||OIE, 2009|
|Indonesia||Disease not reported||OIE, 2009|
|Iran||Disease never reported||OIE, 2009|
|Iraq||Disease never reported||OIE, 2009|
|Israel||Disease never reported||OIE, 2009|
|Japan||Disease never reported||OIE, 2009|
|Jordan||No information available||OIE, 2009|
|Kazakhstan||Disease not reported||OIE, 2009|
|Korea, DPR||Disease not reported||OIE Handistatus, 2005|
|Korea, Republic of||Disease never reported||OIE, 2009|
|Kuwait||Disease never reported||OIE, 2009|
|Kyrgyzstan||Disease never reported||OIE, 2009|
|Laos||Disease never reported||OIE, 2009|
|Lebanon||Disease never reported||OIE, 2009|
|Malaysia||Disease never reported||OIE, 2009|
|-Peninsular Malaysia||Disease never reported||OIE Handistatus, 2005|
|-Sabah||Disease never reported||OIE Handistatus, 2005|
|-Sarawak||Disease never reported||OIE Handistatus, 2005|
|Mongolia||No information available||OIE, 2009|
|Myanmar||Disease never reported||OIE, 2009|
|Nepal||Disease never reported||OIE, 2009|
|Oman||Disease never reported||OIE, 2009|
|Pakistan||No information available||OIE, 2009|
|Philippines||Disease never reported||OIE, 2009|
|Qatar||No information available||OIE, 2009|
|Saudi Arabia||Disease never reported||OIE, 2009|
|Singapore||Disease never reported||OIE, 2009|
|Sri Lanka||Disease never reported||OIE, 2009|
|Syria||Disease not reported||OIE, 2009|
|Taiwan||Disease never reported||OIE Handistatus, 2005|
|Tajikistan||Disease never reported||OIE, 2009|
|Thailand||No information available||OIE, 2009|
|Turkey||Disease never reported||OIE, 2009|
|Turkmenistan||Disease never reported||OIE Handistatus, 2005|
|United Arab Emirates||Disease never reported||OIE, 2009|
|Uzbekistan||Disease never reported||OIE Handistatus, 2005|
|Vietnam||Disease never reported||OIE, 2009|
|Yemen||No information available||OIE, 2009|
|Algeria||Disease never reported||OIE, 2012|
|Botswana||Disease not reported||OIE, 2009|
|Burkina Faso||Present||200805||OIE, 2012|
|Cape Verde||Present||OIE, 2012|
|Central African Republic||Last reported||2011||OIE, 2012|
|Congo Democratic Republic||Present||OIE, 2012|
|Côte d'Ivoire||Last reported||1996||OIE Handistatus, 2005|
|Djibouti||Disease never reported||OIE, 2012|
|Egypt||Disease never reported||OIE, 2009|
|Equatorial Guinea||Widespread||OIE, 1999|
|Eritrea||No information available||OIE, 2009|
|Gabon||Disease never reported||OIE, 2012|
|Guinea||No information available||OIE, 2009|
|Kenya||Present||Montgomery, 1921; OIE, 2012|
|Lesotho||Disease never reported||OIE, 2012|
|Libya||Disease never reported||OIE Handistatus, 2005|
|Mali||No information available||OIE, 2009|
|Morocco||Disease never reported||OIE, 2012|
|Namibia||Present||OIE, 2005; OIE, 2012|
|Réunion||Disease never reported||OIE Handistatus, 2005|
|Rwanda||Restricted distribution||OIE, 2012|
|Sao Tome and Principe||Last reported||1992||OIE Handistatus, 2005|
|Senegal||Last reported||2009||OIE, 2012|
|Seychelles||Disease never reported||OIE, 2012|
|Sierra Leone||Present||OIE, 2012|
|Somalia||Disease not reported||OIE, 2012|
|South Africa||Present||OIE, 2012|
|Sudan||Disease never reported||OIE, 2012|
|Swaziland||Disease never reported||OIE, 2012|
|Tunisia||Disease never reported||OIE, 2012|
|Zambia||Restricted distribution||OIE, 2012|
|Zimbabwe||Last reported||1992||OIE, 2012|
|Bermuda||Disease not reported||OIE Handistatus, 2005|
|Canada||Disease never reported||OIE, 2009|
|Greenland||Disease never reported||OIE, 2009|
|Mexico||Disease never reported||OIE, 2009|
|USA||Disease never reported||OIE, 2009|
Central America and Caribbean
|Barbados||Disease never reported||OIE Handistatus, 2005|
|Belize||Disease never reported||OIE, 2009|
|British Virgin Islands||Disease never reported||OIE Handistatus, 2005|
|Cayman Islands||Disease never reported||OIE Handistatus, 2005|
|Costa Rica||Disease never reported||OIE, 2009|
|Cuba||Disease not reported||OIE, 2009|
|Curaçao||Disease not reported||OIE Handistatus, 2005|
|Dominica||Disease not reported||OIE Handistatus, 2005|
|Dominican Republic||Disease not reported||OIE, 2009|
|El Salvador||Disease never reported||OIE, 2009|
|Guadeloupe||Disease never reported||OIE, 2009|
|Guatemala||Disease never reported||OIE, 2009|
|Haiti||No information available||OIE, 2009|
|Honduras||Disease never reported||OIE, 2009|
|Jamaica||Disease never reported||OIE, 2009|
|Martinique||Disease never reported||OIE, 2009|
|Nicaragua||Disease never reported||OIE, 2009|
|Panama||Disease never reported||OIE, 2009|
|Saint Kitts and Nevis||Disease never reported||OIE Handistatus, 2005|
|Saint Vincent and the Grenadines||Disease never reported||OIE Handistatus, 2005|
|Trinidad and Tobago||Disease never reported||OIE Handistatus, 2005|
|Argentina||Disease never reported||OIE, 2009|
|Bolivia||Disease never reported||OIE, 2009|
|Brazil||Disease not reported||OIE, 2009|
|Chile||Disease never reported||OIE, 2009|
|Colombia||Disease never reported||OIE, 2009|
|Ecuador||Disease never reported||OIE, 2009|
|Falkland Islands||Disease never reported||OIE Handistatus, 2005|
|French Guiana||Disease not reported||OIE, 2009|
|Guyana||Disease never reported||OIE Handistatus, 2005|
|Paraguay||Disease never reported||OIE Handistatus, 2005|
|Peru||Disease never reported||OIE, 2009|
|Uruguay||Disease never reported||OIE, 2009|
|Venezuela||Disease never reported||OIE, 2009|
|Albania||Disease never reported||OIE, 2009|
|Andorra||Last reported||1975||OIE Handistatus, 2005|
|Austria||Disease never reported||OIE, 2009|
|Belarus||Present||Gallardo et al., 2014|
|Belgium||Disease not reported||OIE, 2009|
|Bosnia-Hercegovina||Disease never reported||OIE Handistatus, 2005|
|Bulgaria||Disease never reported||OIE, 2009|
|Croatia||Disease never reported||OIE, 2009|
|Cyprus||Disease never reported||OIE, 2009|
|Czech Republic||Present||Kučínský, 2017|
|Denmark||Disease never reported||OIE, 2009|
|Estonia||Present||Nurmoja et al., 2017|
|Finland||Disease never reported||OIE, 2009|
|France||Disease not reported||OIE, 2009|
|Germany||Disease never reported||OIE, 2009|
|Greece||Disease never reported||OIE, 2009|
|Hungary||Present||Štukelj and Plut, 2018|
|Iceland||Disease never reported||OIE, 2009|
|Ireland||Disease never reported||OIE, 2009|
|Isle of Man (UK)||Disease never reported||OIE Handistatus, 2005|
|Italy||Restricted distribution||OIE, 2009|
|-Sardinia||Localised||Contini et al., 1982; OIE, 1999|
|Jersey||Disease never reported||OIE Handistatus, 2005|
|Latvia||Present||Oļševskis et al., 2016|
|Liechtenstein||Disease not reported||OIE, 2009|
|Lithuania||Present||Gallardo et al., 2014|
|Luxembourg||Disease never reported||OIE, 2009|
|Macedonia||Disease never reported||OIE, 2009|
|Malta||Disease not reported||OIE, 2009|
|Moldova||Present||Jurado et al., 2018|
|Montenegro||Disease never reported||OIE, 2009|
|Netherlands||Disease not reported||OIE, 2009|
|Norway||Disease never reported||OIE, 2009|
|Poland||Present||Pejsak et al., 2014|
|Portugal||Disease not reported||OIE, 2009|
|Romania||Present||Olesen et al., 2018|
|Russian Federation||Present||OIE, 2009|
|Serbia||Disease never reported||OIE, 2009|
|Slovakia||Disease never reported||OIE, 2009|
|Slovenia||Disease never reported||OIE, 2009|
|Spain||Disease not reported||OIE, 2009|
|Sweden||Disease never reported||OIE, 2009|
|Switzerland||Disease never reported||OIE, 2009|
|UK||Disease never reported||OIE, 2009|
|-Northern Ireland||Disease never reported||OIE Handistatus, 2005|
|Ukraine||Present||Goller et al., 2015|
|Yugoslavia (former)||Disease never reported||OIE Handistatus, 2005|
|Yugoslavia (Serbia and Montenegro)||Disease never reported||OIE Handistatus, 2005|
|Australia||Disease never reported||OIE, 2009|
|French Polynesia||Disease never reported||OIE, 2009|
|New Caledonia||Disease never reported||OIE, 2009|
|New Zealand||Disease never reported||OIE, 2009|
|Samoa||Disease never reported||OIE Handistatus, 2005|
|Vanuatu||Disease never reported||OIE Handistatus, 2005|
|Wallis and Futuna Islands||No information available||OIE Handistatus, 2005|
PathologyTop of page
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.
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).
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).
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).
DiagnosisTop of page
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).
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 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 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 infections result in low mortality (2-10%). Symptoms include weight loss, respiratory problems, arthritis, chronic skin ulcers or necrosis.
Differential diagnosis should consider the following diseases:
- classical swine fever or hog cholera
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).
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.
List of Symptoms/SignsTop of page
|Cardiovascular Signs / Increased strength of pulse||Pigs:All Stages||Sign|
|Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate||Pigs:All Stages||Sign|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Pigs:All Stages||Sign|
|Digestive Signs / Bloody stools, faeces, haematochezia||Sign|
|Digestive Signs / Dark colour stools, faeces||Pigs:All Stages||Sign|
|Digestive Signs / Decreased amount of stools, absent faeces, constipation||Sign|
|Digestive Signs / Diarrhoea||Pigs:All Stages||Sign|
|Digestive Signs / Hepatosplenomegaly, splenomegaly, hepatomegaly||Pigs:All Stages||Diagnosis|
|Digestive Signs / Melena or occult blood in faeces, stools||Sign|
|Digestive Signs / Mucous, mucoid stools, faeces||Sign|
|Digestive Signs / Vomiting or regurgitation, emesis||Pigs:All Stages||Sign|
|General Signs / Abnormal proprioceptive positioning, knuckling||Sign|
|General Signs / Ataxia, incoordination, staggering, falling||Pigs:All Stages||Sign|
|General Signs / Cyanosis, blue skin or membranes||Pigs:All Stages||Diagnosis|
|General Signs / Dehydration||Pigs:All Stages||Sign|
|General Signs / Dysmetria, hypermetria, hypometria||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Pigs:All Stages||Sign|
|General Signs / Forelimb swelling, mass in fore leg joint and / or non-joint area||Pigs:All Stages||Sign|
|General Signs / Generalized weakness, paresis, paralysis||Sign|
|General Signs / Haemorrhage of any body part or clotting failure, bleeding||Sign|
|General Signs / Icterus, jaundice||Sign|
|General Signs / Inability to stand, downer, prostration||Pigs:All Stages||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Pigs:All Stages||Sign|
|General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes||Pigs:All Stages||Diagnosis|
|General Signs / Pale mucous membranes or skin, anemia||Sign|
|General Signs / Paraparesis, weakness, paralysis both hind limbs||Sign|
|General Signs / Petechiae or ecchymoses, bruises, ecchymosis||Pigs:All Stages||Diagnosis|
|General Signs / Reluctant to move, refusal to move||Pigs:All Stages||Sign|
|General Signs / Sudden death, found dead||Pigs:All Stages||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sign|
|General Signs / Weight loss||Pigs:All Stages||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Nervous Signs / Seizures or syncope, convulsions, fits, collapse||Sign|
|Nervous Signs / Tremor||Pigs:All Stages||Sign|
|Ophthalmology Signs / Blindness||Sign|
|Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling||Sign|
|Ophthalmology Signs / Conjunctival, scleral, injection, abnormal vasculature||Sign|
|Ophthalmology Signs / Conjunctival, scleral, redness||Sign|
|Ophthalmology Signs / Corneal edema, opacity||Pigs:All Stages||Sign|
|Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes||Pigs:All Stages||Sign|
|Ophthalmology Signs / Purulent discharge from eye||Pigs:All Stages||Sign|
|Pain / Discomfort Signs / Skin pain||Sign|
|Reproductive Signs / Abortion or weak newborns, stillbirth||Pigs:All Stages||Sign|
|Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs||Pigs:All Stages||Sign|
|Respiratory Signs / Coughing, coughs||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Pigs:All Stages||Sign|
|Respiratory Signs / Epistaxis, nosebleed, nasal haemorrhage, bleeding||Pigs:All Stages||Sign|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Sign|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Pigs:All Stages||Sign|
|Respiratory Signs / Nasal mucosal ulcers, vesicles, erosions, cuts, tears, papules, pustules||Pigs:All Stages||Sign|
|Respiratory Signs / Purulent nasal discharge||Sign|
|Skin / Integumentary Signs / Skin erythema, inflammation, redness||Pigs:All Stages||Diagnosis|
|Skin / Integumentary Signs / Skin ulcer, erosion, excoriation||Pigs:All Stages||Sign|
|Urinary Signs / Haematuria, blood in urine||Pigs:All Stages||Sign|
Disease CourseTop of page
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.
EpidemiologyTop of page
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.
Impact: EconomicTop of page
ASF has potential for rapid spread, producing serious socioeconomic 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.
Disease TreatmentTop of page
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.
Prevention and ControlTop of page
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.
ReferencesTop of page
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Distribution MapsTop of page
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