Unravelling the mechanisms of Rift Valley fever virus (RVFV) maintenance in endemic areas during interepidemic periods is critical for enhancing early detection and response. Unfortunately, data on key epidemiological parameters, such as incidence rates, which are crucial for risk assessments and designing targeted interventions, are almost nonexistent. We conducted a longitudinal study of 1,938 pastoral livestock and 814 livestock keepers in an endemic region of northern Kenya from March 2022 to May 2023 to estimate the incidence rate of RVFV exposure and determine risk factors for infection. We assessed exposure to RVFV in humans and livestock using an anti-RVF immunoglobulin enzyme-linked immunosorbent assay. RVFV incidence was calculated in livestock and humans as the number of new seroconversions over the total animal and person time at risk, respectively. An interval-censored regression model was employed to compute the baseline hazard and identify risk factors. We observed 113 new livestock infections over 805 animal-years at risk, translating to an annual livestock incidence rate of 0.14 per animal-year (95% CI: 0.12-0.17). Multivariable analysis found species, acaricide use, and period of sampling were significant factors that influence RVFV incidence in livestock. In humans, 15 RVFV seroconversions were observed over 629 person-years at risk, yielding an incidence rate of 24 per 1000 person-years (95% CI: 13-39). Age and sex were not significant predictors of RVFV human exposure. Seroconversion in livestock and humans suggests that low-level transmission between vertebrate hosts and vectors could be the primary mechanism for RVF viral persistence in endemic areas. Our findings highlight the need for routine serosurveillance and continuous public health education on RVF infection and prevention during interepidemic periods.
Rift Valley fever, a zoonotic mosquito-borne viral disease caused by a Phlebovirus in the family Phenuviridae, is most prevalent in East Africa's Great Rift region, where the virus (RVFV) was first identified in 1931. The disease has also been detected and is believed to be enzootic in various regions of Africa and the Arabian Peninsula. Outbreaks have historically been confined to these areas, but the spread and persistence of the virus in new territories, including the Global North, poses a viable threat due to the presence of competent vectors in these regions.
RVF is primarily transmitted to animals through mosquito vectors, with at least 30 species across eight genera believed to have RVFV transmission potential. Aedine mosquitoes are thought to play a crucial role in initiating transmission during the early stages of the epidemic phase, while other mosquito genera, like Culex, are believed to play a vital role in propagating infection when the population of Aedes mosquitoes recedes in the latter stages of outbreaks. A range of other arthropods, like phlebotomine sandflies, Culicoides biting midges, and ticks, have been identified as possible mechanical vectors of RVFV under experimental conditions, but their role in nature remains unascertained.
In livestock, RVF majorly presents with non-specific symptoms such as inappetence, debilitation, and diarrhoea; however, the classical syndromes indicative of an outbreak are mass abortions affecting all stages of pregnancy and high perinatal mortality rates. Humans primarily get infected through contact with infected animals or their tissues and fluids, although mosquito-borne transmission is also plausible but rare. Human cases majorly present with constitutional symptoms, but one to two percent of cases advance to a more severe form that clinically varies depending on the system affected. Ocular, hepatic, neurologic, and hemorrhagic disease and death are common manifestations of severe RVF in humans.
The epidemiology of RVF is complex and multifaceted. A confluence of ecological abiotic and biotic factors, intrinsic host factors such as immunity, and human practices such as migration and irrigation are all known to influence RVFV emergence. However, the mechanisms of how these factors interact are poorly understood. While it is generally agreed that outbreaks are linked to weather events that support vector amplification and increased transmission, there is debate on how and where RVFV is maintained during the decades-long interepidemic periods (IEP) that precede outbreaks. A pioneering theory suggests that the virus could be maintained through vertical transmission in Aedes eggs, which remain buried and viable for years until the right ecological conditions trigger the hatching of RVFV-infected progeny. Although this is the principal theory cited in literature, limited data supports the same. An alternative theory is that the virus is maintained primarily through a low-level mosquito-host infection cycle that causes sub-clinical disease in susceptible ruminant livestock and wildlife. Evidence of acute livestock, human, and wildlife infections in endemic and non-endemic regions of Africa during IEPs strongly supports this theory. However, it remains unclear whether either of these mechanisms is sufficient to maintain RVFV endemicity independently. Unravelling the epidemiological complexity around RVFV maintenance requires answering questions on livestock and human incidence rates and the risk factors for infection during IEPs. Unfortunately, most of the available data are limited to cross-sectional serological studies and routine passive surveillance data, which lack the causal insights needed to elucidate maintenance and transmission dynamics of RVFV in endemic environments. As a result, the endemicity of RVF is not in question, but data on population-level incidence, which is key to detecting cryptic transmission rates during IEPs, are almost nonexistent. Incidence rates, defined as the proportion of new cases or events occurring over a specified period in a population at risk, are an important measure of morbidity. Incidence rates provide a direct estimate of the risk of disease spread among susceptible individuals, which is critical in understanding disease transmission dynamics, identifying populations at highest risk, assessing temporal trends in transmission, and evaluating interventions.
Nearly a century since RVF was reported in Kenya, this paper presents the first estimates of human and livestock RVF incidence rates, providing evidence of interepidemic transmission in humans and livestock. The findings underscore the need for sustained RVF surveillance and interventions, even during interepidemic periods.