About Rift Valley Fever (RVF)
A quick overview for reporters, health workers, and the public.
What is RVF?
Rift Valley fever is a viral zoonosis that primarily affects animals but can also infect humans. Infection can cause severe disease in both animals and humans and leads to major economic losses due to death and abortion among infected livestock. The RVF virus is a Phlebovirus, first identified in 1931 during a sheep epidemic in Kenya’s Rift Valley.
- Most human infections come from contact with blood/organs of infected animals or from mosquito bites.
- No documented human-to-human transmission.
- Incubation in humans: 2–6 days.
- Animal outbreaks can be prevented with sustained vaccination programmes.
Key facts
- Primarily an animal disease; humans can be infected.
- Contact with animal blood/organs is the main risk.
- Infected mosquito bites can transmit RVF.
- No human-to-human transmission documented.
- Incubation: 2–6 days.
- Animal vaccination prevents outbreaks.
Overview & history
Outbreaks have occurred across sub-Saharan Africa. A major outbreak struck Egypt in 1977 after introduction via livestock trade. In 1997–98, heavy El Niño rains preceded a large outbreak in Kenya, Somalia and Tanzania. In September 2000, RVF spread to Saudi Arabia and Yemen—the first reports outside Africa—raising concerns about further spread into Asia and Europe.
Ecology & mosquito vectors
Many mosquito species can transmit RVF. Dominant vectors vary by region and may play different roles in sustaining transmission.
Among animals, RVF spreads mainly via bites of infected mosquitoes—especially Aedes, which can pass the virus to offspring via eggs.
RVF virus in host animals
RVF infects multiple species; severe disease occurs in cattle, sheep, camels and goats. Sheep/goats are more susceptible than cattle/camels.
Animal outbreaks often appear as a wave of unexplained abortions—an early warning of an epidemic.
Outbreak ecology: (1) Primary foci with vertical transmission in Aedes; (2) Spread to secondary foci via livestock movement or passive mosquito dispersal, with amplification by local mosquitoes such as Culex, Mansonia, and Anopheles. Irrigation areas favour secondary transmission.
Most infections arise from direct/indirect contact with blood or organs of infected animals during slaughtering, butchering, birthing, veterinary procedures, or carcass disposal. Ingesting unpasteurized or uncooked milk from infected animals may also pose risk.
Bites from infected mosquitoes—commonly Aedes and Culex—also infect humans; blood-feeding flies may play a role.
No human-to-human transmission has been documented, and with standard precautions, no health-care worker transmission has been reported.
Incubation: 2–6 days.
Mild disease: sudden fever, muscle/joint pain, headache; may include neck stiffness, photophobia, anorexia, vomiting (can resemble meningitis early).
Course: symptoms usually last 4–7 days; antibodies appear and virus clears from blood.
Severe forms (uncommon):
- Ocular (0.5–2%): retinal lesions 1–3 weeks after onset; vision may recover in 10–12 weeks, but macular lesions cause ~50% permanent vision loss.
- Meningoencephalitis (<1%): intense headache, memory loss, hallucinations, confusion, vertigo, seizures, coma; low mortality but frequent lasting deficits.
- Haemorrhagic fever (<1%): begins 2–4 days after onset, with severe liver impairment then bleeding (hematemesis, melena, rash, epistaxis, gum bleeding, menorrhagia, venepuncture bleeding); CFR ~50%, death usually day 3–6.
RVF can resemble malaria, typhoid, shigellosis, yellow fever, or other VHFs. Confirmation uses:
- RT-PCR
- IgG/IgM ELISA
- Virus isolation in cell culture
Patient samples are an extreme biohazard; non-inactivated testing must be done under maximum containment. Transport with triple-packaging.
Most human cases are mild and self-limited; no specific antiviral is available. Severe disease requires early intensive supportive care (fluids and symptom management).
An inactivated human vaccine exists but is not licensed or commercially available; used experimentally for high-risk veterinary/lab workers. Other candidates are under study.
Controlling RVF in animals
- Sustained preventive animal vaccination (live-attenuated and inactivated vaccines exist for veterinary use).
- Immunize before outbreaks; do not vaccinate during an outbreak due to contamination/re-use risks.
- Restrict/ban livestock movement to slow spread.
- Active animal health surveillance to provide early warning.
Public health education & risk reduction
- Promote safe animal husbandry and slaughter practices; use gloves/eye protection and hand hygiene.
- Avoid raw blood, unpasteurized milk, and undercooked animal products; cook thoroughly.
- Personal/community protection against mosquitoes: nets, repellents, light-coloured long clothing, avoid peak biting times.
- Vector control with larviciding where breeding sites are identifiable and limited.
Infection control in health care
Use standard precautions for suspected/confirmed cases; theoretical risk exists via blood/tissue exposure, but no HCW transmission reported with proper precautions.
Forecasting models using satellite imagery and climate data help predict conditions linked to outbreaks. In Africa, Saudi Arabia and Yemen, RVF correlates with above-average rainfall; in East Africa, with heavy El Niño rains.
Early warning enables faster animal case detection and targeted control to avert epidemics.
WHO supports at-risk countries with surveillance, diagnostics, patient care, and outbreak response.
WHO coordinates with FAO and WOAH to anticipate outbreaks and address the animal-human-ecosystem interface.