Rift Valley fever is a mosquito-borne viral zoonosis caused by a member of the Phlebovirus genus, first recognized in 1931 during a sheep epidemic in Kenya's Rift Valley [1][2]. The infection principally circulates among animals but is capable of spilling over to humans through vector bites or contact with infected animal tissues [1][2].
Disease overview
Rift Valley fever is a viral zoonosis caused by a Phlebovirus that primarily affects livestock but can also infect humans, producing a spectrum from mild febrile illness to severe hemorrhagic fever [1][2]. The disease has expanded beyond sub-Saharan and North Africa to the Arabian Peninsula and is associated with significant animal and human health burdens as well as economic losses [1][2]. It is regarded as an emerging, neglected arboviral disease with widening geographic scope [3].
Read the full clinical and epidemiological profile 6
In humans the illness ranges from asymptomatic or mild flu-like fever with muscle and joint pain, headache, vomiting, and light sensitivity to severe hemorrhagic fever that may be fatal [2][4]. Pooled analyses of laboratory-confirmed cases describe febrile, renal, hepatic, hemorrhagic, visual, neurologic, and obstetric syndromes, with fever reported in about 81% and death in roughly 21% of cases [4]. In animals, particularly sheep, goats, cattle, camels, and livestock, infection causes severe disease with high mortality in young animals and abortion waves in pregnant females [1][2].
The virus was first identified in 1931 in Kenya and subsequently caused outbreaks across sub-Saharan Africa, with an explosive 1977 event in Egypt linked to livestock trade along the Nile and a 1997–98 regional outbreak after El Niño flooding [1]. In 2000 it spread via infected livestock to Saudi Arabia and Yemen, marking its first occurrence outside Africa [1][2].
The RVF virus is transmitted among animals mainly through bites of infected mosquitoes such as Aedes species, and female mosquitoes can pass the virus to offspring via eggs [1]. Humans may be infected by mosquito or blood-feeding fly bites, but most cases arise from contact with blood or organs of infected animals, or ingestion of unpasteurized milk [2]. No human-to-human transmission has been documented, and domesticated animals serve as secondary amplification hosts [2][3].
Preventive veterinary vaccination before outbreaks can halt epizootics, whereas vaccination during an active animal outbreak is discouraged due to risks of intensifying spread through multi-dose vial and needle reuse [1]. Restricting or banning livestock movement helps slow geographic expansion from infected to uninfected areas [1]. An inactivated human vaccine exists but is unlicensed and used only experimentally for high-risk veterinary and laboratory personnel, with other candidates under study [1].
- 1 World Health Organization. Rift Valley fever [Internet]. cited 23 Oct 2026. Available from: https://www.who.int/news-room/fact-sheets/detail/rift-valley-fever
- 2 World Health Organization. Rift Valley fever [Internet]. cited 23 Oct 2026. Available from: https://www.who.int/health-topics/rift-valley-fever
- 3 Weaver SC et al. Zika, Chikungunya, and Other Emerging Vector-Borne Viral Diseases. Annu Rev Med. 2018 Jan 29. PMID: 28846489. doi: 10.1146/annurev-med-050715-105122. PubMed: https://pubmed.ncbi.nlm.nih.gov/28846489/
- 4 Anywaine Z et al. Clinical manifestations of Rift Valley fever in humans: Systematic review and meta-analysis. PLoS Negl Trop Dis. 2022 Mar. PMID: 35333856. doi: 10.1371/journal.pntd.0010233. PubMed: https://pubmed.ncbi.nlm.nih.gov/35333856/
- A92.4
- 1D47
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