Introduction
Lumpy skin disease (LSD) is a non-zoonotic re-emerging disease caused by a single strain of capripoxvirus from the family Poxviridae. Poxviridae is the family of the largest viruses which can cause disease in most domestic animals, except in dogs. Poxviridae possesses a large and complex genome consisting of a single, linear molecule of double-stranded DNA coding for around 200 proteins(Mulatu & Feyisa, 2018). LSDV is stable for long periods at ambient temperature in dried scabs. LSDV can be destroyed at 55°C for 2 hours and 65°C for 30 minutes and can also be recovered from skin nodules kept at –80°C for 10 years and infected tissue culture fluid stored at 4°C for 6 months(Tuppurainen et al., 2017). LSD virus demonstrates high susceptibility to the ether, chloroform, formalin, and some detergents, e.g. sodium dodecyl sulfate, phenol, sodium hypochlorite, Virkon® (2%) and, quaternary ammonium compounds(Gerilovych & Stegniy, 2016).
LSD is susceptible to cattle (Bos indicus and B. taurus ) and water buffalo (Bubalus bubalis ) resulting in high economic losses as it leads to reduced milk production(Gari, Bonnet, Roger, & Waret-Szkuta, 2011), infertility, abortion, and sometimes death(Davies, 1991). The serological surveys on wild ruminant species in Africa have not revealed a wildlife reservoir of LSDV and the virus appears to be highly host specific. But Young, Basson, & Weiss, (1970) revealed that impala (Aepyceros melampus ) and giraffe (Giraffa camelopardalis ) demonstrated the clinical signs of LSD after experimental inoculation with LSDV. A study in Ethiopia on differential breed susceptibility to LSD showed that Holstein Friesian or crossbred cattle exhibits higher morbidity and mortality compared to local zebu cattle(Brown C. & Torres A., 2008).