Rift Valley fever (RVF) is a viral disease that affects both animals and humans, mainly in Africa and the Middle East. It is caused by the Rift Valley fever virus, which belongs to the same group of viruses that include other insect-borne diseases.
The virus spreads mostly through the bites of infected mosquitoes, especially species like Aedes and Culex. People can also become infected through direct contact with the blood, body fluids, or tissues of sick animals such as cattle, sheep, and goats.
Outbreaks often happen after heavy rains and flooding, which allow mosquito populations to grow rapidly. In people, most cases are mild, causing fever, muscle pain, and headaches that usually clear up within a week. However, some infections can become severe, leading to liver problems, bleeding, eye damage, brain inflammation, or even death.
Prevention focuses on protecting animals and reducing mosquito exposure. Vaccines are available for livestock, but there is currently no approved vaccine for humans.
There is no specific cure for Rift Valley fever. Treatment is aimed at easing symptoms. For mild illness, over-the-counter pain relievers such as acetaminophen or ibuprofen can help reduce fever and body aches.
Definition and Classification
Rift Valley fever (RVF) is a viral zoonotic disease that affects both animals and humans, primarily in Africa and parts of the Middle East. A zoonotic disease is one that can spread between animals and humans. RVF is caused by the Rift Valley fever virus (RVFV), a member of the genus Phlebovirus within the family Phenuiviridae. This virus is an RNA virus and is classified among pathogens capable of causing viral hemorrhagic fevers, a group of illnesses characterized by fever and, in severe cases, bleeding and organ damage.
In animals, the disease mainly affects livestock such as sheep, cattle, goats, and camels. In humans, infection can occur through bites from infected mosquitoes or direct contact with the blood, body fluids, or organs of infected animals. The clinical spectrum ranges from mild, flu-like symptoms to severe complications, including hemorrhagic fever, encephalitis (inflammation of the brain), and ocular disease that can result in blindness.
History and Geographic Distribution
RVF was first described in 1931 during an outbreak among sheep in the Rift Valley of Kenya, from which the disease takes its name. Since then, RVF has been recognized as an important emerging disease affecting both public health and agriculture.
Outbreaks are strongly associated with periods of heavy rainfall and flooding, which create ideal breeding conditions for mosquito populations. During these times, RVF often occurs as simultaneous epidemics in humans and epizootics (outbreaks in animals). The disease is capable of causing high mortality in young livestock and widespread abortion in pregnant animals, leading to substantial economic losses.
Initially confined to East and Southern Africa, RVF has expanded geographically over time. Major outbreaks have been reported in Egypt (1977), Mauritania (1987 and 1998), Saudi Arabia and Yemen (2000), and Madagascar (2008). The Arabian Peninsula outbreaks marked the first confirmed transmission of RVF outside the African continent, raising concerns about the potential for further spread. Cases have since been detected in West and Central Africa, including countries such as Senegal, Mali, and Niger. The expansion of RVF has been linked to animal trade, livestock movement, and broader environmental and climate shifts.
Causative Agent
The causative agent, Rift Valley fever virus (RVFV), is a single-stranded RNA virus with a tripartite genome, consisting of three segments known as the L (large), M (medium), and S (small) segments. These segments encode viral proteins responsible for replication, structural components, and interactions with the host immune system.
RVFV belongs to the genus Phlebovirus, which includes other arthropod-borne viruses. Transmission occurs mainly through mosquitoes of the Aedes and Culex genera, although more than 30 mosquito species have been implicated as potential vectors. A unique feature of RVFV is its ability to persist in mosquito eggs through vertical transmission (from adult mosquitoes to their offspring). These eggs can remain dormant during dry conditions and hatch into infected mosquitoes when heavy rainfall and flooding occur, facilitating cyclical outbreaks.
Once inside the host, the virus primarily targets the liver, where it replicates extensively, causing tissue damage and necrosis. This accounts for many of the clinical manifestations observed in both humans and animals.
Transmission of Rift Valley Fever
Rift Valley Fever (RVF) spreads primarily through insect vectors and direct contact with infected animals. Environmental conditions like rainfall and flooding also play a key role in the timing and location of outbreaks.
Mosquito Vectors
Mosquitoes are the main vectors of RVF. More than 30 species across multiple genera have been implicated, but Aedes and Culex mosquitoes are most important in sustaining and amplifying transmission.
- Aedes mosquitoes: Aedes species are regarded as the primary maintenance vectors. A distinctive feature is their ability to transmit RVFV vertically, from female mosquitoes to their eggs. These eggs can survive in dry soil for extended periods. When heavy rains or flooding occur, the dormant eggs hatch into infected adult mosquitoes capable of initiating new transmission cycles. This vertical transmission mechanism enables the virus to persist during inter-epidemic periods, even when conditions are not favorable for large mosquito populations.
- Culex mosquitoes: Culex species act as secondary, amplifying vectors during outbreaks. Unlike Aedes, they do not transmit the virus vertically but play a central role once the virus is circulating. After feeding on infected livestock, Culex mosquitoes transmit the virus to other susceptible animals and humans. Population surges in Culex mosquitoes are closely linked to wet seasons, standing water, and irrigation practices.
Other mosquito genera, including Anopheles and Mansonia, may also contribute to transmission under specific environmental conditions.
Animal-to-Human Transmission
Humans frequently become infected with RVFV through direct or indirect contact with infected animals. Livestock serve as amplifying hosts, often experiencing high levels of virus in their blood (viremia), which increases the risk of human exposure.
- Occupational exposure: People engaged in animal husbandry, veterinary medicine, slaughtering, or butchering face the greatest risk. Contact with animal blood, body fluids, or organs during these activities provides a direct route of transmission. Pregnant livestock that abort due to RVFV infection pose an especially high risk, as aborted material can contain large amounts of the virus.
- Aerosol transmission: Infection can occur through inhalation of aerosolized viral particles, particularly in laboratory environments or during veterinary procedures that generate aerosols. Although relatively uncommon in natural settings, this mode of transmission is significant for laboratory biosafety.
- Human-to-human transmission: Documented cases of human-to-human spread are extremely rare. RVF is not considered to have sustained person-to-person transmission, distinguishing it from other hemorrhagic fevers such as Ebola virus disease.
Protective measures such as gloves, masks, and other personal protective equipment (PPE) reduce occupational exposure risks.
Environmental Factors Influencing Spread
The ecology of RVF is closely tied to environmental conditions that favor mosquito breeding and virus amplification.
- Heavy rains and flooding events trigger hatching of dormant Aedes eggs and create abundant habitats for Culex mosquitoes. These environmental shifts often precede outbreaks by several weeks. In East Africa, RVF outbreaks are strongly associated with the El Niño–Southern Oscillation (ENSO) climate pattern, which increases rainfall and flooding across affected regions.
- High concentrations of livestock provide abundant hosts for mosquito feeding, facilitating viral amplification. The movement of animals for trade or grazing spreads the virus geographically, sometimes across borders. Outbreaks often begin in rural areas with dense livestock populations and can extend to urban areas through trade networks.
- Agricultural practices, irrigation schemes, and poor drainage systems create standing water that supports mosquito breeding. Farms near wetlands or floodplains are particularly vulnerable. Human settlements expanding into previously uninhabited areas may also increase contact between people, livestock, and vector populations.
Symptoms and Clinical Presentation
Rift Valley Fever (RVF) exhibits distinct symptoms in humans and animals with variations in severity. The disease progresses through defined stages marked by initial flu-like signs and possible complications.
Symptoms in Humans
Humans infected with Rift Valley Fever typically experience a sudden onset of fever, chills, headache, and muscle pain. Other common symptoms include weakness, dizziness, and joint pain lasting about one week.
In some cases, the illness progresses to severe manifestations such as hemorrhagic fever, encephalitis, or retinitis. Hemorrhagic signs include bleeding from the gums, nose, and other sites. Encephalitis presents with confusion, seizures, or coma. Vision problems may arise from retinal damage.
Most human cases are mild or asymptomatic, but about 1% may develop severe complications. Symptoms generally appear 2 to 6 days after exposure.
Symptoms in Animals
In animals, particularly sheep, goats, cattle, and camels, RVF causes high fever and sudden death, especially in young animals. Pregnant animals frequently experience abortions and stillbirths.
Fever in affected animals is typically above 40°C (104°F). Other signs include weakness, loss of appetite, and nasal discharge. Liver damage is common and can lead to jaundice and hemorrhaging.
Mortality rates can reach 90% in young livestock. The infection spreads rapidly within herds during outbreaks, causing significant economic losses.
Disease Progression
The incubation period following infection is relatively short, typically lasting between two and six days before symptoms emerge.
Most human cases are mild, presenting with nonspecific symptoms that resemble influenza. These early manifestations commonly include fever, headache, muscle pain, and general malaise. In such cases, the illness generally resolves without complications within about a week, and patients recover fully.
A smaller proportion of individuals, however, progress to severe forms of RVF, which usually develop one to three weeks after the onset of initial symptoms. One of the most serious manifestations is hemorrhagic fever, marked by extensive bleeding such as nosebleeds, vomiting of blood, and blood in the stool. This form is often associated with significant liver damage, multi-organ failure, and high fatality rates. Neurological complications are another severe outcome, with encephalitis causing inflammation of the brain. Patients may develop confusion, hallucinations, seizures, or even fall into a coma. These neurological symptoms tend to arise after the acute febrile phase and may persist for weeks. Ocular disease, particularly retinitis, is also a recognized complication. It can cause blurred vision, blind spots, or in severe cases, complete loss of sight. Permanent vision impairment occurs in a proportion of affected individuals.
The prognosis for RVF is generally favorable, as most patients recover fully without lasting effects. However, those who develop severe disease forms may suffer long-term consequences, particularly from neurological damage or vision loss. While the overall case fatality rate is estimated at less than 1%, mortality is significantly higher among patients with hemorrhagic complications. Recovery from severe illness can be prolonged, often requiring several weeks before full health is restored.
Diagnosis of Rift Valley Fever
Accurate diagnosis of Rift Valley Fever (RVF) relies on identifying specific viral markers and clinical symptoms. Laboratory tests confirm infection, while clinical assessment and differentiation from other diseases guide appropriate management.
Laboratory Testing Methods
The cornerstone of RVF diagnosis is the detection of viral markers in blood or tissue samples. During the acute phase of infection, reverse transcription polymerase chain reaction (RT-PCR) is the most reliable method, as it identifies viral RNA directly and provides a rapid confirmation. RT-PCR is particularly useful within the first week of illness, when viral loads are highest.
Serological assays complement molecular testing by detecting antibodies produced in response to infection. Enzyme-linked immunosorbent assay (ELISA) can identify immunoglobulin M (IgM), which indicates recent infection, as well as immunoglobulin G (IgG), which reflects past exposure or recovery. Paired sera samples collected several weeks apart may be used to demonstrate a rising antibody titer, confirming active or recent infection.
Virus isolation through cell culture remains a possible but less common diagnostic approach, primarily due to the requirement for high-containment biosafety laboratories, as RVF is classified as a biosafety level 3 or 4 pathogen. In severe cases, additional laboratory investigations such as liver function tests and coagulation assays can provide supportive evidence by demonstrating hepatic damage or clotting abnormalities consistent with hemorrhagic disease.
Clinical Assessment
Patients with RVF present with fever, headache, muscle pain, and malaise. Severe forms include hemorrhagic symptoms, encephalitis, and ocular disease. Detailed history should focus on exposure to mosquitoes or infected animals.
Physical examination may reveal lymphadenopathy, photophobia, or jaundice. Progression to more serious symptoms requires prompt clinical evaluation to monitor for complications like hemorrhage or neurological deficits.
Clinical assessment helps determine severity, guides testing, and supports decisions for hospitalization or further care.
Differential Diagnosis
RVF symptoms overlap with other viral hemorrhagic fevers such as Crimean-Congo hemorrhagic fever and dengue. Malaria and bacterial septicemia are also common differentials in endemic areas.
Differentiation depends on laboratory confirmation and epidemiological factors including mosquito exposure and recent outbreaks. Distinguishing RVF from leptospirosis and other zoonoses is critical to avoid misdiagnosis.
Accurate differentiation ensures targeted treatment and appropriate public health responses.
Treatment and Management
Rift Valley Fever (RVF) treatment primarily involves managing symptoms and preventing complications. Care strategies focus on supporting vital functions, addressing severe symptoms, and exploring antiviral options.
Supportive Care
Supportive care constitutes the foundation of RVF management. Patients presenting with mild, self-limiting disease are generally treated on an outpatient basis with rest, adequate hydration, and symptomatic relief. Intravenous fluid administration is crucial for those experiencing dehydration due to fever, vomiting, or reduced oral intake. Pain and fever can be managed with acetaminophen or paracetamol, while the use of nonsteroidal anti-inflammatory drugs (NSAIDs) is discouraged because of their potential to exacerbate bleeding tendencies.
Monitoring vital signs closely is essential, especially in severe cases. Patients should avoid nonsteroidal anti-inflammatory drugs (NSAIDs) to reduce the risk of bleeding complications.
Management of Complications
Severe manifestations of RVF require specialized interventions. Patients with hemorrhagic fever may develop coagulopathy and require transfusions of blood products such as platelets, packed red blood cells, or fresh frozen plasma to correct clotting abnormalities and stabilize circulation. Intensive care support may be necessary for multi-organ failure.
Neurological complications, including encephalitis and seizures, demand close monitoring and may necessitate anticonvulsant therapy, sedation, or mechanical ventilation in extreme cases.
Ocular complications such as retinitis should be promptly referred to ophthalmologists, as early evaluation may help limit permanent vision loss. Secondary bacterial infections can occur in critically ill patients and should be treated with appropriate antimicrobial therapy based on clinical suspicion or laboratory confirmation.
Antiviral Therapies
At present, no antiviral agent has been formally approved for the treatment of RVF. Ribavirin, a broad-spectrum antiviral, has demonstrated partial efficacy in laboratory and animal studies, but its clinical effectiveness in human cases remains unproven, and routine use is not recommended outside of research or emergency contexts. Experimental antiviral compounds and immune-modulating therapies continue to be investigated, with some showing potential in preclinical trials.
Prevention and Control Strategies
Effective prevention and control of Rift Valley Fever (RVF) require coordinated efforts in immunization, vector management, and community awareness. Each approach targets a specific aspect of the disease’s transmission cycle to reduce outbreaks and human exposure.
Vaccination Programs
Vaccination of livestock is one of the most effective means of controlling RVF, as domestic animals such as sheep, goats, cattle, and camels serve as the primary amplifying hosts for the virus. Several types of animal vaccines are available, including live attenuated and inactivated formulations. Live attenuated vaccines, such as the Smithburn vaccine, provide long-lasting immunity but carry risks of causing abortions or teratogenic effects in pregnant animals. Inactivated vaccines are safer for use in breeding stock but require multiple doses and booster shots, making them less practical for large-scale use in resource-limited settings.
Mass vaccination campaigns are most effective when conducted before the rainy season, which coincides with increased mosquito breeding and viral circulation. Timing is critical, as immunization after the onset of outbreaks may have limited impact. Successful vaccination programs depend on strong veterinary infrastructure, adequate funding, cold chain maintenance, and effective distribution systems to reach remote farming communities.
Human vaccines remain experimental and have been used only under emergency conditions for laboratory personnel and high-risk occupational groups such as veterinarians and abattoir workers.
Vector Control Measures
Mosquito control is another central pillar of RVF prevention, as mosquitoes are the primary vectors responsible for transmitting the virus between animals and from animals to humans. Vector control strategies target both larval and adult mosquito populations.
Larval control involves reducing breeding habitats through environmental management, including draining stagnant water, filling depressions, and improving drainage around farms. Chemical larvicides may also be applied to standing water sources. Adult mosquito populations can be reduced through targeted insecticide spraying, although the sustainability of such measures depends on monitoring insecticide resistance and maintaining adequate coverage.
For human protection, insecticide-treated bed nets, repellents, and protective clothing are recommended in endemic areas, particularly for those working with livestock. Housing improvements, such as window screens and reduced exposure to outdoor biting times, further lower infection risks.
Public Health Education
Raising awareness about RVF in affected regions helps reduce human infections. Education programs focus on explaining transmission routes, symptoms, and preventive behaviors.
Key messages include avoidance of contact with infected animals, proper handling and disposal of animal products, and use of personal protective equipment for those in direct contact with livestock.
Epidemiology and Outbreaks
Rift Valley Fever (RVF) has caused significant outbreaks in Africa and the Arabian Peninsula. Its transmission is strongly linked to climate, vector populations, and animal movements, influencing patterns of spread and risk exposure.
Major Past Outbreaks
Large-scale RVF outbreaks have been documented since the early 20th century. The 1997–1998 outbreak in Kenya, Tanzania, and Somalia was among the most severe, killing an estimated 100,000 livestock and more than 500 people, with case fatality rates (CFRs) for humans ranging between 0.5% and 2% in most reports. The 2006–2007 outbreak in East Africa affected Kenya, Somalia, Sudan, and Tanzania, with over 1,000 confirmed human cases and at least 300 deaths. Livestock mortality rates during this outbreak exceeded 70% in some herds.
In 2000, RVF spread beyond Africa for the first time, with outbreaks in Saudi Arabia and Yemen. These epidemics caused more than 2,000 human cases and approximately 245 deaths, in addition to significant losses in the livestock sector due to both deaths and trade restrictions. The introduction of RVF into the Arabian Peninsula raised international concern about the potential for further spread into Asia or Europe, particularly through the livestock trade.
Smaller but significant outbreaks have continued, such as those reported in Mauritania (2012, 2015), Niger (2016), Uganda (2016), and South Africa (2018).
Patterns of Spread
The virus primarily spreads through mosquito vectors, notably Aedes and Culex species. Aedes mosquitoes act as transovarial reservoirs, passing the virus to offspring via eggs that can survive in dry soil for years. When heavy rainfall or flooding occurs, these eggs hatch en masse, releasing infected mosquitoes that initiate transmission cycles. Culex mosquitoes then amplify the outbreak by transmitting the virus more efficiently between animals and humans.
Transmission follows a classic epizootic-epidemic pattern:
- Initial amplification occurs when infected Aedes mosquitoes bite livestock after hatching during flooding events.
- Secondary amplification follows as Culex and other mosquitoes feed on infected livestock, spreading the virus to more animals and eventually to humans.
- Human spillover occurs through vector bites or direct exposure to animal blood, tissues, or aborted fetuses.
The movement of livestock, both for trade and seasonal migration, is a major driver of geographic spread, sometimes introducing RVF into regions with no prior history of the disease.
Risk Factors
Several environmental, occupational, and socioeconomic factors increase RVF risk:
- Heavy seasonal rains and flooding create optimal habitats for mosquito proliferation. Outbreaks often follow periods of unusually high rainfall linked to El Niño–Southern Oscillation (ENSO) events. Satellite-based rainfall and vegetation monitoring have been used to predict high-risk periods with moderate accuracy.
- High concentrations of cattle, sheep, and goats facilitate rapid viral amplification, particularly in mixed farming systems.
- Farmers, herders, veterinarians, and abattoir workers are at elevated risk due to direct contact with infected blood or tissues during slaughtering or animal birthing. In some outbreaks, over 50% of human cases occurred in individuals with such occupational exposure.
- Limited laboratory diagnostic capacity in rural areas, delayed outbreak recognition, and inadequate vaccination coverage contribute to widespread transmission and higher mortality.
- Communities reliant on livestock for food security and income are disproportionately affected, with outbreaks often leading to trade bans, food shortages, and long-term economic disruption.