Rift Valley fever (RVF) virus is a mosquito-borne virus associated with epidemics in livestock and humans [1
]. Since the 1970s, periodic epidemics of RVF associated with heavy rainfall and flooding have been reported in an increasing number of countries of eastern and southern Africa where the virus became endemic, including Kenya, Somalia, Sudan, Tanzania, Zimbabwe, South Africa, and Madagascar [2
]. The RVF epidemics have also occurred in countries where virus activity was not previously detected, such as Egypt in 1977, Mauritania in 1983, and Saudi Arabia and Yemen in 2000 [2
]. In these naïve ecologies, propagation of the epidemic appears to be the result of spread of the newly introduced virus across nonimmune livestock and human populations through animal movement and mosquito vectors. This conclusion is supported by molecular epidemiological data showing that RVF virus strains recovered during epidemics in naïve ecologies belonged to a single lineage with minimal genetic diversity [9
]. For example, comparison of 6 RVF virus isolates from the Egyptian epidemic of 1977 identified a single lineage of virus with <.33% nucleotide (nt) and <.1% amino acid (aa) sequence differences, and 3 RVF virus isolates from the Mauritanian epidemic of 1983 had similarly low genetic differences [9
]. In contrast, the mechanisms associated with propagation of the epidemic in ecologies where the virus is endemic are not well understood; there are minimal data on the genetic diversity of RVF virus strains recovered from various areas of endemic countries during an epidemic [9
]. A study that compared RVF virus isolates from livestock in Kenya during the 2006–2007 epidemic suggested the presence of multiple lineages of the viruses [12
]. However, due to inadequate surveillance in livestock, the extent of the epizootic in livestock was not well documented.
Severe RVF epizootics in countries where the virus is endemic occur after a period of between 3 and 7 years [13
]. For instance, in Kenya, where the highest number of epizootics have been reported to date, the average interepizootic period is 3.6 years, a period likely representing the time required for the immunity of livestock populations to decrease to levels that are permissive to virus spread [13
]. Recurrent RVF epidemics in regions where the virus is endemic may be due to amplification of virus residing in each ecological zone, the virus being maintained through either persistence in eggs of floodwater Aedes
mosquito species or via low-level cycling among vertebrates. Alternatively, as in naïve ecologies, a single virus lineage may be introduced and amplified from the first epicenter of the epidemic and subsequently spread across the geographic region.
The RVF epidemic of 1997–1998 that affected Kenya, Somalia, and Tanzania was characterized by outbreaks that started in the North Eastern Province of Kenya in November 1997 and ended with cases reported from the north central region of Tanzania in June 1998 [14
]. Spatial mapping of these outbreaks and molecular analysis of viruses involved in the outbreaks were not performed due to late confirmation and response to the epidemic. Another RVF epidemic occurred in 2006–2007 in these 3 countries, once again starting from the North Eastern Province of Kenya and continuing to Tanzania, where the last livestock and human cases were reported in June 2007 [14
]. During an 8-month period, >1100 suspected cases in humans resulting in 350 deaths were reported across the 3 countries, as well as thousands of livestock abortions and deaths [14
]. The early detection of the epidemics in each country enabled us to perform spatial mapping of the sequential outbreaks across 3 countries and to isolate and genetically characterize RVF virus strains from most of the outbreak foci.