Significance Rift Valley fever (RVF) is an emerging, zoonotic hemorrhagic fever, affecting mainly livestock and humans in Africa. Despite its growing global concern, the impact of control measures on epidemic dynamics using empirical data has not been assessed. By combining a unique RVF epidemic dataset covering both livestock and human data in a closed ecosystem (Mayotte island) with a dynamic model, we estimate viral transmission potential among livestock, and from livestock to humans. We also quantify the impact of vaccination in decreasing the epidemic size. We demonstrate that reactive livestock vaccination is key. We present a reference case study for RVF and illustrate the value of a One Health quantitative approach to surveillance and control of zoonotic infectious diseases.
Peste des petits ruminants (PPR), a devastating viral disease of sheep and goats, has been targeted by the global community for eradication within the next 15 years. Although an efficacious attenuated live vaccine is available, the lack of knowledge about the transmission potential of PPR virus (PPRV) may compromise eradication efforts. By fitting a metapopulation model simulating PPRV spread to the results of a nationwide serological survey in Ethiopia, we estimated the level of viral transmission in an endemic setting and the vaccination coverage required for elimination. Results suggest that the pastoral production system as a whole acts as a viral reservoir, from which PPRV spills over into the sedentary production system, where viral persistence is uncertain. Estimated levels of PPRV transmission indicate that viral spread could be prevented if the proportion of immune small ruminants is kept permanently above 37% in at least 71% of pastoral village populations. However, due to the high turnover of these populations, maintaining the fraction of immune animals above this threshold would require high vaccine coverage within villages, and vaccination campaigns to be conducted annually. Adapting vaccination strategies to the specific characteristics of the local epidemiological context and small ruminant population dynamics would result in optimized allocation of limited resources and increase the likelihood of PPR eradication.
Significance Between June 2014 and February 2015, thousands of Ebola treatment beds were introduced in Sierra Leone, alongside other infection control measures. However, there has been criticism of the timing and focus of this response, and it remains unclear how much it contributed to curbing the 2014–2015 Ebola epidemic. Using a mathematical model, we estimated how many Ebola virus disease cases the response averted in each district of Sierra Leone. We estimated that 56,600 (95% credible interval: 48,300–84,500) Ebola cases were averted in Sierra Leone as a direct result of additional treatment beds. Moreover, the number of cases averted would have been even greater had beds been available 1 month earlier.
Background Lassa fever (LF), a haemorrhagic illness caused by the Lassa fever virus (LASV), is endemic in West Africa and causes 5000 fatalities every year. The true prevalence and incidence rates of LF are unknown as infections are often asymptomatic, clinical presentations are varied, and surveillance systems are not robust. The aim of the Enable Lassa research programme is to estimate the incidences of LASV infection and LF disease in five West African countries. The core protocol described here harmonises key study components, such as eligibility criteria, case definitions, outcome measures, and laboratory tests, which will maximise the comparability of data for between-country analyses. Method We are conducting a prospective cohort study in Benin, Guinea, Liberia, Nigeria (three sites), and Sierra Leone from 2020 to 2023, with 24 months of follow-up. Each site will assess the incidence of LASV infection, LF disease, or both. When both incidences are assessed the LASV cohort (n min = 1000 per site) will be drawn from the LF cohort (n min = 5000 per site). During recruitment participants will complete questionnaires on household composition, socioeconomic status, demographic characteristics, and LF history, and blood samples will be collected to determine IgG LASV serostatus. LF disease cohort participants will be contacted biweekly to identify acute febrile cases, from whom blood samples will be drawn to test for active LASV infection using RT-PCR. Symptom and treatment data will be abstracted from medical records of LF cases. LF survivors will be followed up after four months to assess sequelae, specifically sensorineural hearing loss. LASV infection cohort participants will be asked for a blood sample every six months to assess LASV serostatus (IgG and IgM). Discussion Data on LASV infection and LF disease incidence in West Africa from this research programme will determine the feasibility of future Phase IIb or III clinical trials for LF vaccine candidates.
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