African swine fever is a very dangerous infectious disease in pigs caused by a virus. The disease was first recorded in 1921 in Kenya, East Africa, and then rapidly spread to southern Africa. The disease first appeared in Europe in 1957, and has also been recorded in some Caribbean countries such as Cuba, Haiti, and the Dominican Republic. Wild boars are animals that carry the disease-causing virus, transmitting it to domestic pigs through ticks parasitizing wild boars. The virus causing African swine fever has been silently infecting wild boar herds in some European countries, and since 2018 the disease has broken out strongly in wild boar herds in Russia, Romania, Bulgaria, Belgium... and also in China.
There is currently no vaccine for prevention, and the morbidity and mortality rates are very high in pigs of all ages, causing severe losses in infected herds. In Vietnam, the first 3 outbreaks of African swine fever in farmed pigs in Hung Yen and Thai Binh were officially announced by the Ministry of Agriculture and Rural Development on February 20, 2019. This will be an extremely serious threat, causing enormous and incalculable consequences for Vietnam’s pig farming industry. Therefore, the entire livestock-veterinary system, including farmers, must raise vigilance, pay attention to control and prevent infection through the buying and selling and transport of pigs across borders, including across provinces, and thoroughly apply biosecurity measures to absolutely prevent the African swine fever virus from entering pig farms.
- Etiological agent
African swine fever is caused by a virus belonging to the family Asfarviridae, genus Asfivirus, which is relatively large, about 200 nm in diameter, with a double-stranded DNA genome and an outer envelope. ASFV is highly stable to changes in environmental temperature and a fairly wide pH range, and can withstand pH 4 or pH 13. The virus can survive in serum or blood for up to 18 months at room temperature, and can persist for many years at 4 °C - 20 °C. However, ASFV can be inactivated at 60 °C within 30 minutes and is sensitive to ultraviolet light, fat-soluble solvents, as well as many commercial disinfectants. Disinfectants such as 1% formaldehyde can kill ASFV after 6 days, and 2% NaOH in 1 day.
Unlike other viruses, ASF can replicate in both vertebrate and arthropod cells. The target cells of ASFV (African swine fever virus) are mononuclear white blood cells and macrophages; it enters cells by receptor binding and endocytosis. The virus replicates in the perinuclear region of the host cell and exits the cell by budding, and can cause cell death. Based on the gene encoding the p72 capsid protein of ASFV, 23 genotypes of ASFV have been identified.
Epidemiology
African swine fever is mainly present in Africa. For a long time, from the first recorded case in Kenya in the early 1900s, it was not until half a century later that the disease was recorded in Europe, and more recently it has reappeared in Europe (Ukraine, Poland, Latvia, Lithuania, Estonia and Moldova, the Czech Republic, Romania...) and in 2018, the first ASF outbreaks occurred in farmed pigs in China, causing very serious losses. ASFV only causes disease in animals of the pig family (Suidae). Domestic pigs and European wild boars are susceptible to ASFV and show clinical signs. African wild boars together with their parasitic ticks are the natural reservoir of ASFV.
ASF occurs at all ages. However, unlike classical swine fever, ASF spreads mainly through direct contact and through the blood, so it spreads rapidly within barns when pigs are kept at high density. When ASF first appears on a farm or in an area..., a high mortality rate will be recorded, possibly up to 100%. ASFV can enter farms through contact with wild boars (pig farms in areas with wild boars); introducing pigs already infected with ASFV; using meat from virus-infected pigs; or feeding pigs by-products contaminated with ASFV that have not been thoroughly cooked; or through the entry of people and vehicles contaminated with ASFV in outbreak areas.
Farm pigs infected with ASFV can shed large amounts of virus before clinical signs appear, through saliva, tears, nasal discharge, urine, feces, and vaginal discharge. The virus is also abundant in blood. ASFV can survive for a very long time in protein-rich environments (meat, blood, feces, bone marrow); and for many months in frozen meat. ASFV is transmitted mainly through the oral and nasal routes upon contact with the pathogen; in addition, ASFV can also infect through wounds and the bloodstream. ASFV can be transmitted directly from wild boars to domestic pigs and through the direct host of ticks parasitizing wild boars. Transmission between pigs occurs through direct contact with sick pigs, or through aerosol particles at close range, through contaminated feed, water, and bedding. People and transport vehicles are factors carrying ASFV to farther places. Blood-sucking flies can transmit the virus for at least 24 hours after feeding on ASF-affected pigs. During an outbreak, the virus can be transmitted through needles shared among multiple pigs.
Immunity
The immune characteristics of ASFV are complex antigenically, with many antigenic factors that can induce a neutralizing antibody response, which to date is still not well understood. ASFV is highly immunogenic. Pigs infected with ASFV will mount a strong antibody response that can be detected by testing. IgM and IgG antibodies can be detected in the serum of pigs 4–6 days after ASFV infection and remain at high titers for a long time after infection. The presence of antibodies in the blood is effective in preventing the onset of ASF, reducing viremia in infected pigs, and may protect pigs from ASF. However, due to the genetic and antigenic diversity of ASFV (up to 23 ASFV genotypes have been identified), tests based on ASFV-specific neutralizing antibodies have not yet achieved the desired results. In addition to humoral immunity based on antibodies, cell-mediated immunity based on cytotoxic T cells plays an important role in protecting pigs against ASF.
Due to the complex antigenic characteristics of ASFV, there is still no effective vaccine to prevent African swine fever.
Clinical signs and lesions
ASFV causes fever and hemorrhage in infected pigs. Clinical signs usually appear about 5–15 days after pigs are infected with ASFV. Depending on the virulence of the infecting virus strain, the disease may appear in acute, chronic, or subclinical form. Highly virulent ASFV strains can cause 100% mortality in sick pigs; moderately virulent strains can cause up to 50% mortality in sick pigs.
4.1 Clinical signs
* Acute form
In the acute form, sick pigs show high fever (41-42OC), lethargy, loss of appetite, pigs lying piled on top of each other, rapid breathing, congested to bluish-purple or hemorrhagic skin, especially in the abdomen and extremities, unsteady gait, weak hind legs, and may convulse. Sick pigs have white, thick nasal discharge that may be blood-tinged, eyes may have discharge, severely congested mucous membranes may hemorrhage, abdominal pain and vomiting, and some pigs may have constipation or bloody diarrhea. Pregnant sows may abort at any stage. Pigs with the acute form will die within 7 days after clinical signs appear. Pigs that die in the acute form are usually in fairly good body condition.
* Chronic form
Pigs are thin and weak, with long, rough hair. Pigs with chronic ASF will die after a few weeks or months.
4.2 Lesions
* Acute form
Lesions are mainly observed in the spleen, lymph nodes, kidneys, and heart. Necropsy reveals brown effusion in the thoracic and abdominal cavities, hemorrhages in many organs; enlarged, infarcted, friable spleen; swollen hemorrhagic lymph nodes; edematous lungs with abundant foam on cut surface, trachea full of foam and possibly blood-tinged; pinpoint hemorrhages in the kidneys; pinpoint hemorrhages and congestion in the heart; hemorrhagic and possibly ulcerated stomach, hemorrhagic intestines, and congested liver and gallbladder.
* Subacute form
Necropsy reveals effusion in body cavities, sudden death due to heart failure, swollen hemorrhagic lymph nodes, fibrinous inflammation of the lungs and heart, inflamed, firm, mottled lungs, and swollen joints containing fluid and fibrin.
* Chronic form
Typical lesions recorded are arthritis, swollen lymph nodes, and kidney failure
Diagnosis
5.1 Clinical diagnosis
The clinical signs of African swine fever are very similar to those of classical swine fever, PRRS, erysipelas, pasteurellosis... in pigs. Therefore, in cases where sick and dead pigs are recorded in large numbers at all ages with clinical signs and widespread hemorrhagic lesions similar to other “red diseases” (classical swine fever, PRRS, erysipelas, pasteurellosis), African swine fever should be suspected. Farms in outbreak areas at risk of African swine fever infection must pay close attention to early diagnosis, isolation, and rapid destruction of suspected pigs.
5.2 Laboratory diagnosis
* Antigen diagnosis
Applied to acute cases (during outbreaks). Test for virus or viral DNA in lymph node or spleen samples taken from pigs that have just died or been necropsied within 12 hours. PCR is used to detect ASFV DNA. Immunofluorescence on lymph node or spleen smears, or immunoperoxidase staining of lymph node or spleen histological slides, or virus culture on pig macrophage cells are used to identify ASFV. PCR is widely used because it provides faster test results than other techniques.
*Antibody diagnosis
Only applied to subacute, chronic, or latent forms. Test for antibodies in the blood of pigs that survive the outbreak using ELISA to determine the persistence of ASFV infection
5.3 Differential diagnosis
Differential diagnosis is needed with the following diseases: classical swine fever, PRRS, erysipelas, pasteurellosis, disease caused by Salmonella, or high-level mycotoxin poisoning (aflatoxin and stachybotryotoxin).
6. Prevention and treatment
* No outbreak yet
Currently there is no vaccine to prevent African swine fever, so preventive measures mainly rely on biosecurity measures to control cross-border, inter-regional, and farm-to-farm transmission; do not use by-products of pig origin or only use them after thorough cooking, at least 30 minutes of boiling. When there is a risk of an outbreak, sanitation and disinfection inside and outside barns and farms should be intensified twice a week (chlorine, iodine, formalin, sodium chloride, potassium peroxymonosulfate, o-phenylphenol, 2-benzyl-4-chlorophenol...); do not allow people and vehicles from outside to enter the farm unless they have been disinfected.
. Farm staff must also strictly comply with sanitation and disinfection procedures when entering pig housing areas.
* During an outbreak
Strictly implement disease control measures: report, cordon off, isolate, destroy suspected pigs, clean and disinfect the entire farm, equipment, and transport vehicles; impose absolute lockdown on farm staff and do not allow outsiders into the farm area.
Assoc. Prof. Dr. Nguyen Ngoc Hai – Lecturer, University of Agriculture and Forestry, Ho Chi Minh City
References
- P.J. Sánchez-Cordón1, M. Montoya, A.L. Reis, L.K. Dixon. African swine fever: A re-emerging viral disease threatening the global pig industry. The Veterinary Journal 233 (2018) 41–48 *
- Alonso, C., Borca, M., Dixon, L., Revilla, Y., Rodriguez, F., Escribano, J.M., and ICTV Report Consortium. 2018. ICTV Virus Taxonomy Profile: Asfarviridae. Journal of General Virology, 99: 613–614.
- Barbara E. Straw Jeffery J. Zimmerman Sylvie D’Allaire David J. Taylo. Diseases of swine. 9th edition, ©2006 Blackwell Publishing All rights reserved.
- FAO, 2000. Recognizing African swine fever. A field manual. http://www.fao.org/.
