African swine fever virus (ASFV) is a double stranded DNA virus of the family Asfaviridae and genus Asfivirus that causes African swine fever (ASF). The disease can lead up to 100% mortality of infected domestic pigs causing farmers to incur enormous economic losses as a result of high pig mortalities and loss of market for pigs and pig products. First description of ASF as a disease of domestic pigs was documented in 1928 in East Africa. The disease is currently endemic in sub-Saharan Africa due to both pig-to-pig transmission and virus persistence in the sylvatic cycle involving asymptomatically infected wild pigs and soft tick of the genus Ornithodoros (Figure 1). The main mechanism of ASFV transmission from wild pigs to domestic pigs in Africa is trough infected tick bites.
Figure 1. ASFV transmission cycle
The main clinical manifestation includes high fever (40.5–42°C), loss of weight, increased respiratory rate and hemorrhages, erythema and necrosis in areas of skin, chronic skin ulcers, arthritis, and high mortality rates of up to 100% within a range of 1-13 days. The disease has also been reported outside Africa in Portugal (1957 and 1960), Italy (1967, 1980), France (1964, 1967), Malta (1978), Belgium (1985), Netherlands (1985, 1986), Cuba (1971 and 1980), Iberian Peninsula (1977-78), Dominican Republic (1978), Haiti (1979), Georgia (2007) and later on spread to Russia and Asia including China. The disease is one of the major pig diseases in Tanzania, with outbreaks being reported in different regions including Kigoma, Arusha, Morogoro, Dar es Salaam, Dodoma and Mwanza, Kilimanjaro, Rukwa, Iringa and Mbeya. Highest pig population in Tanzania is found in Mbeya region followed with Iringa, Ruvuma and Kilimanjaro regions.
Genotypes circulating in Tanzania and implication to control
The virus is a large enveloped double stranded DNA virus whose genome length ranges from 170 to 194 kilobase pairs (kbp). The genome is complex and may encode up to 165 genes out of which there is a number of novel genes whose functions have not yet been described. Genotyping of ASFV is primarily done by nucleotide sequencing of variable 3’-end of the B646L gene encoding the p72 capsid protein. Twenty-four (I-XXIV) p72 genotypes have been described so far in Sub-Saharan Africa (Eastern and southern Africa). Molecular characterization of ASFV in Tanzania has so far associated the outbreaks with genotype II, IX, X, XV and XVI (Figure 2). The genotypes in Tanzania are distributed based on zones: Lake zone (genotype IX), Northern zone (genotype XVI), Central zone (genotype X), Eastern zone (XV) and Southern zone (genotype II) (Figure 2). The ASFV genotyping studies have helped in establishing the epidemiological patterns of the disease and helped in making informed decisions regarding prevention, control and eradication measures of the disease.
Why is it difficult to control African Swine fever in Tanzania
Eradication of ASF in Tanzania has proved difficult as a result of complexity of sanitary, environmental and economic factors. There is no vaccine or treatment against ASF, and the only control measures include early detection, quarantine of infected live pigs and pig products followed by implementation of sanitary measures such as burning and burying. Strict biosecurity measures are also used to prevent human involvement in the spread of ASF. Access to pig keeping premises is restricted to only essential visitors like workers and veterinarians. Facilities for changing cloths to cloths that do not leave the premises must be put in place so as to prevent entry of virus through contaminated cloths. Major factors responsible for the spread of ASF in Tanzania has always been the illegal movement of pigs and swill feeding to pigs.
Why is it difficult to develop vaccine for ASF?
There are several attempts to develop vaccines for preventing ASF through vaccination which have not resulted in production of effective and safe vaccine so far. This is mainly because of complexity of the virus genome encoding more than 160 polypeptides most of which are responsible for invading and weaken host immunity. Due to high variability of ASFV isolates identified thus far, attenuated live vaccines produced have led to protection against homologous isolates. Inoculation of antibodies into pigs from ASFV-infected and recovered pigs has shown to offer protection against homologous ASFV through viremia reduction and delay of onset of the disease clinical signs.