Abstract

Lumpy skin disease (LSD) is a viral disease of cattle caused by lumpy skin disease virus (LSDV). LSDV shares high degree of sequence homology with goatpox virus (GTPV) and sheeppox virus (SPPV), the two other members of the genus Capripoxvirus of the family Poxviridae. Genetically LSDV is a double-stranded DNA genome of approximately 151 kbp. LSD is an economically important and notifiable animal disease by the World Organisation for Animal Health (OIE). Clinically LSD is characterized by fever and the appearance of nodules on the skin and mucous membranes. In severe and chronic cases, nodular skin lesions cover the entire body and become deep scab and eroded. Transmission of the disease occurs predominantly by insects possibly through mechanical vectors, contaminated feed and water, infected saliva, and rarely natural contact. LSD is endemic in many African countries and mostly coexists with sheeppox and goatpox. Recently, LSD has been rapidly spreading to the Middle East, Turkey, and Russia, the Balkan and European Union countries. Diagnosis is mainly based on observation of clinical signs and the detection of virus genome using conventional and real-time PCR methods. In Africa, prevention and control of LSD relies on vaccination using live attenuated vaccines derived from Kenyan or South African LSDV strains. Vaccine that can allow the differentiation of infected from vaccinated animals (DIVA) and high-throughput serological method for the detection of specific antibody need to be developed. Alternatively, a 12 nucleotide deletion that exists only on the G-protein-coupled chemokine receptor gene of LSDV field isolates can be used to differentiate wild-type from vaccine strains by sequencing and real-time PCR.

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