African Swine Fever
African swine fever virus (ASFV) belongs to the Asfivirus genus in the Asfarviridae family and is the only known DNA arbovirus (Gaudreault et al., 2020). ASFV is icosahedral, linear double‐stranded DNA virus with 170 to 190 kbp genome and an average diameter of 200 nm (Salas & Andrés, 2013). The virus is composed of the outer envelope, capsid, inner envelope, core-shell, and nucleoid (Salas & Andrés, 2013). Replication of the virus takes place in the macrophages initially in the nucleus followed by the cytoplasmic one (García-Beato et al., 1992). Even though various genes are used to characterize the virus, genotyping of ASFV is based on the nucleotide sequence of a 478 bp variable region in the C-terminus of the viral p72 gene (Achenbach et al., 2017; Gaudreault et al., 2020). Based on major capsid protein p72, there are 24 genotypes of ASFV and 8 serotypes based on viral hemagglutinin CD2-like protein (CD2v) and C-type lectin (Gaudreault et al., 2020).
Domestic pigs, wild suids, and soft ticks are the hosts of ASFV where the original vertebrate host is believed to be Warthogs (Phacochoerus africanus ) and the most important reservoir host in Africa (Costard et al., 2013). It is transmitted through direct contact with an infected animal, indirect contact with contaminated objects, consumption of infected meat, and also by the bites of tampans (Ornithodoros spp. ) (M. L. Penrith & Vosloo, 2009). Other sources of infection that are unlikely to spread the virus but are suggested to do so are water, rodents, and birds yet remain unproven and there is still no evidence of transfer of the virus from the sows to the fetus (M. L. Penrith & Vosloo, 2009). Transport of infected animal and infected products is one of the major reasons for the transmission and spread of the virus (Sanchez-Vizcaıno et al., 2015). Airborne transmission has also been identified as a possible route but only for a short distance (M. L. Penrith & Vosloo, 2009; Sánchez‐Vizcaíno et al., 2019). Stable fly (Stomoxys calcitrans ) can also act as a mechanical vector up to 48 hrs. after ingesting the virus (Mellor et al., 1987).Though the infected domestic pig can infect the other domestic pigs directly and indirectly (Thomson, 1985), the transmission of the ASFV from infected warthogs to the susceptible host in contact is rare (Golnar et al., 2019; Wilkinson, 1984). Even though the transmission of the virus through sexual contact is not defined, ASFV can be excreted in genital secretion (M. L. Penrith & Vosloo, 2009).
After the infection by the ASFV, the incubation period is 2-7 days although it differs according to the route of infection (Mebus, 1988). Even though the disease was categorized as per acute historically, it can be classified as a per acute, acute, subacute, and chronic disease (Wardley et al., 1983). In the per acute form, the animal can die without the presence of any clinical signs and symptoms, and minimal gross lesions but hemorrhages can be found during the post mortem inspection (Wardley et al., 1983). However, some may show a fever of 41-42°C, rapid respiration, hyperemia of the skin along with 100% mortality and morbidity (Mebus, 1988). Acute and subacute form are the commonly observed forms with highly virulent isolates causing the acute one and moderately virulent strain causing the subacute form (Mebus, 1988). The signs associated with the acute form are elevated body temperature (40-42°C), anorexia, apathy, inactivity, cyanosis in the extremities of legs, ears, and tail, and death with 90-100% mortality within 7-10 days (Sanchez-Vizcaıno et al., 2015; Sánchez‐Vizcaíno et al., 2019; Wardley et al., 1983). Diarrhea is also found to be associated with the acute form which may result due to the secondary bacterial infection (Mebus, 1988). Early leucopenia, splenomegaly, extensive necrosis, hemorrhage of lymphoid tissue, and rapid labored breathing due to pulmonary edema at the final stage can also be seen in the acute form (Sánchez‐Vizcaíno et al., 2019). Erythema, epistaxis, vomiting, and abortion can be related to the acute form where abortion can be the first sign of outbreak in many cases (Sanchez-Vizcaıno et al., 2015). The subacute form is indicated with signs shown in the acute form but a less severe form (Wardley et al., 1983). Reduction of feed intake and high body temperature of 40-42°C is present for 10-12 days (Mebus, 1988). But, hemorrhage and edema, the vascular changes associated with the subacute form are more intense than the acute form (Gómez-Villamandos et al., 2013). Mortality can be anywhere between 30-70% and the surviving animals can recover within 2-3 weeks (Sánchez‐Vizcaíno et al., 2019). Infection with low virulent strain causes a chronic disease that does not show any specific clinical signs and vascular lesions, but lesions can be observed in bacterial coinfection (Sanchez-Vizcaıno et al., 2015). It may persist for a longer duration of time and symptoms like pneumonia, stunting, emaciation, arthritis, and skin ulcers may be seen with hemorrhages during post mortem along with fibrinous pericarditis and pleuritis (Wardley et al., 1983). Poor growth, oscillating fever, skin lesions and soft painless swelling of joints are also associated with chronic form (Mebus, 1988).