Abstract:
Lumpy skin disease is recognized as a transboundary and emerging disease of
cattle, buffaloes and other wild ruminants. Being initially restricted to Africa, and
since 1989 the Middle East, the unprecedented recent spread across Eurasia
demonstrates how underestimated and neglected this disease is. The initial
identification of the causative agent of LSD as a poxvirus called LSD virus, was
well as findings on LSDV transmission and epidemiology were pioneered at
Onderstepoort, South Africa, from as early as the 1940s by researchers such
as Weiss, Haig and Alexander. As more data emerges from an ever-increasing
number of epidemiological studies, previously emphasized research gaps are
being revisited and discussed. The currently available knowledge is in agreement
with the previously described South African research experience that LSDV
transmission can occur by multiple routes, including indirect contact, shared
water sources and arthropods. The virus population is prone to molecular
evolution, generating novel phylogenetically distinct variants resulting from a
diverse range of selective pressures, including recombination between field and
homologous vaccine strains in cell culture that produce virulent recombinants
which pose diagnostic challenges. Host restriction is not limited to livestock, with
certain wild ruminants being susceptible, with unknown consequences for the
epidemiology of the disease.