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).