Selected wetland soil properties correlate to Rift Valley fever livestock mortalities reported in 2009-10 in central South Africa.

Outbreaks of Rift Valley fever have devastating impacts on ruminants, humans, as well as on regional and national economies. Although numerous studies on the impact and outbreak of Rift Valley fever exist, relatively little is known about the role of environmental factors, especially soil, on the aestivation of the virus. This study thus selected 22 sites for study in central South Africa, known to be the recurrent epicenter of widespread Rift Valley fever outbreaks in Southern Africa. Soils were described, sampled and analyzed in detail at each site. Of all the soil variables analyzed for, only eight (cation exchange capacity, exchangeable Ca2+, exchangeable K+, exchangeable Mg2+, soluble Ca2+, medium sand, As, and Br) were statistically identified to be potential indicators of sites with reported Rift Valley fever mortalities, as reported for the 2009-2010 Rift Valley fever outbreak. Four soil characteristics (exchangeable K+, exchangeable Mg2+, medium sand, and Br) were subsequently included in a discriminant function that could potentially be used to predict sites that had reported Rift Valley fever-associated mortalities in livestock. This study therefore constitutes an initial attempt to predict sites prone to Rift Valley fever livestock mortality from soil properties and thus serves as a basis for broader research on the interaction between soil, mosquitoes and Rift Valley fever virus. Future research should include other environmental components such as vegetation, climate, and water properties as well as correlating soil properties with floodwater Aedes spp. abundance and Rift Valley fever virus prevalence.

Rift Valley Fever: Does Wildlife Play a Role?

Rift Valley fever (RVF) virus (RVFV) is an emerging vector-borne pathogen that causes sporadic epizootics and epidemics with multi-year, apparently quiescent, inter-epidemic periods. The epidemiology and ecology of the virus during these inter-epidemic periods is poorly understood. There is evidence for low-level circulation of the virus in livestock and wild ruminants; however, as of yet there is no evidence to identify a specific mammalian reservoir host. Using a systematic approach, this review synthesizes results from serosurveys, attempts at viral detection, and experimental infection of wildlife. These data demonstrate there is a gap in research conducted on RVF in wild ruminants. Specifically, there is very little published data on the pathogenicity of an RVFV infection in various wildlife species, validation of diagnostic assays for exposure to RVFV and understanding of epizootic or endemic disease dynamics in wild ruminants. We recommend that future research on RVFV incorporate a more systematic approach to understand the low-level cycling of the virus during inter-epidemic periods in both wild and domestic ruminant species.