African swine fever was confined to Africa until 1957 when infection spread through Portugal, Spain, Southern France and Italy. Infection persists in Sardinia, Italy, but has been eradicated from the Italian mainland.
Outbreaks have occurred in domestic pigs in a number of African countries outside the areas commonly reporting disease. The occurrence of the disease in Georgia in 2007 has resulted in outbreaks in the countries and Russian regions of the Caucasus and its current spread to areas of Russia, the Ukraine and Belarus.
The African swine fever virus is a large, complex, ether-sensitive DNA Asfivirus. Isolates of African swine fever virus from Africa are genetically variable, although a single genotype was involved in the European, American and West African outbreaks. The virus in the current Caucasian/Russian outbreak is of the same genotype as that in Madagascar, Mozambique, Tanzania and Zambia.
The virus grows in cell cultures in the laboratory. But in the field it is found in pigs and multiplies in ticks and pig lice and is found in the blood of wild pigs in Africa, such as warthogs. The virus is very resistant and survives putrefaction and sunlight. It can survive 2 hours at 56 degrees C, 6 months in carcasses held at 4 degrees C, 2 years when dried at room temperature and almost indefinitely when frozen in meat at -20 degrees C. It is stable between pH 3 and pH 10 but is inactivated by 1 percent formaldehyde in 6 days and by 2 percent NaOH in 24 hours.
The main route of infection in domestic pigs is via the upper respiratory tract and initial virus replication occurs within 24 hours of infection in the pharyngeal tonsil to give viraemia (virus in the blood). Tick borne infections lead directly to viraemia. The virus affects the vascular endothelium. After 4-5 days damage to blood vessel walls occurs and death ensues due to pulmonary oedema.
The virus multiplies in monocytes, macrophages, hepatocytes, endothelial cells and some epithelial cells throughout the body, and it may be shed within 24 hours of the onset of fever. Surviving pigs are persistently infected and viraemia persists in spite of the presence of high levels of circulating antibody. Antibody may be detected first at 11 days post-infection and from that time virus levels in the plasma fall, to disappear by day 46 post-infection. Protection against re-infection appears to be related to cellular immunity which may develop within 7-10 days of infection.
The incubation period averages 1 week (5-15 days) and is followed by fever (40-42 degrees C) for a period of 48 hours during which affected pigs remain bright and continue eating. Clinical signs begin as the temperature drops and consist of dullness, anorexia, huddling together, incoordination, dyspnoea and coughing (30 percent of cases), skin cyanosis and occasional vomiting or diarrhea, sometimes with bloody discharges from the eyes and nose. Death occurs within 7-10 days of the onset of clinical signs and in classic outbreaks the mortality rate is 95-100 percent. Chronic cases appear emaciated with lameness, swollen joints and skin ulceration. Abortion may occur in sows in all stages of pregnancy 5-8 days after infection or 1-3 days after fever develops. A high proportion of such mildly affected animals may recover.
Severe hemorrhages are widespread throughout the body. The lymph nodes are so hemorrhagic that they resemble pieces of spleen; the ecchymoses on serous membranes are severe, especially on the heart, pleura and peritoneum. Hemorrhages may also be found in the myocardium, lung, liver, kidney and bladder.
The gall bladder is oedematous and the hepatic lymph node is hemorrhagic even in cases of mild disease. There may be oedema of the lung. Hemorrhagic ulceration may develop in the large intestine, but button ulcers are rare and laryngeal hemorrhages and turkey egg kidney are uncommon. In chronic cases, pericarditis, pleuritis, pneumonia, arthritis and cutaneous ulcers are seen.
Some African isolates may only cause petechiation of the kidney and visceral lymph nodes with an increase in abdominal fluid. Aborted fetuses have extensive placental and fine cutaneous hemorrhages. Histological findings include meningitis, thickening of blood vessels, severe damage to their linings and hemorrhages around them. A fall in the number of lymphocytes is common. Virus can be demonstrated throughout the body.
Infected pigs have a persistent viraemia and the virus is present in all body fluids, secretions and excretions. The virus is shed for 7-10 days after the onset of fever, can form aerosols but is present in greatest amounts in feces. It persists in blood for up to 8 weeks and in lymphoid tissues for 12 weeks or more and carriage has been recorded for up to 21 weeks.
Virus has been demonstrated in blood for more than 500 days by polymerase chain reaction. Pigs which have recovered are immune to challenge with the same virus but can succumb to other strains of virus. Maternal immunity may protect for up to 7 weeks.
Transmission is by the following routes in order of importance:
a) Direct contact with pigs excreting virus
b) Ingestion of infected improperly cooked meat products
c) Bites of biological vectors such as Ornithodoros erraticus (Iberia), O.moubata or O. porcinus (Africa). Ticks remained infective in disused piggeries for 5 years (Iberia).
d) Bites of mechanical vectors such as biting flies, lice etc.
e) Parenteral inoculation which allows infection from low titres of virus.
In Africa, infection may be derived from carrier warthogs which are the source of infection for ticks or occur as a warthog-independent infection in domestic pigs. Where the disease has become enzootic as in Sardinia, the clinical signs are less dramatic and chronic infection may occur so that carrier pigs are important in the spread of the disease.
Onward transmission from recovered animals is not inevitable as many antibody-positive animals are virus-negative. Wild boar are infected in Sardinia, Southern Russia and the Caucasus, and in 1990, 1.5 percent of wild boar sampled in Sardinia were seropositive. The relationship between infected ticks, wild boar and domestic pigs is not clear in some areas, but it is now clear that Ornithodorus ticks may carry the disease for up to 4 years, transmitting the virus from one generation to the next. Spanish wild boars have not maintained infection after eradication of the virus from domestic pigs. The virus is introduced to countries in pig products and then spread by the methods noted above. In Belgium (1985) spread by infected materials was particularly important.
African swine fever should be suspected where a highly infectious syndrome causes 95-100 percent mortality in pigs of all ages accompanied by fever and hemorrhages. Mild forms of the disease may be more difficult to diagnose. At post-mortem examination, findings of multiple hemorrhages, petechiated kidneys, hemorrhagic lymph nodes (especially the hepatic, in chronic or wild pig cases) and splenic infarcts also suggest one of the swine fevers.
Material for investigation should include clotted blood and blood in EDTA, lymph node, kidney, spleen and lung. In abortion from African swine fever, infection is more easily demonstrable in the sow rather than the fetus. Placenta is the best product of abortion for diagnosis.
The tests used are as follows:
a) Demonstration of antibody in tissue or body fluids
b) Demonstration of virus in tissue
c) Virus isolation in cultures of buffy coat leucocytes or macrophages
d) Animal transmission-the ultimate confirmation, especially of new introductions and to distinguish it from classical swine fever
African swine fever must be notified to government agencies. Outbreaks of the disease are controlled by slaughter and destruction of all pigs on the infected farm and any farms in direct contact. Affected farms are disinfected and sentinel pigs introduced prior to restocking depopulated farms.
Movement of pigs and meat from infected areas is prohibited. Measures such as the prohibition of feeding waste foods and the import of infected pigs or meat can safeguard countries, but infected meat appears to have been responsible for the initial outbreak in Georgia.
Vaccines have been studied experimentally by infection with attenuated strains and subsequent challenge with virulent strains, but universally protective vaccines have not yet been marketed. Genetic resistance is being explored.