Rift Valley fever is a peracute or acute mosquito-borne zoonotic disease of domestic and wild ruminants, largely confined to sub-Saharan Africa but with high potential for range expansion. It is characterized by abortions and neonatal mortality in ruminants and subclinical to mild febrile disease in most adult animals. Diagnosis depends on histopathological examination of samples of the liver and identification of the virus in tissues. Treatment is supportive only. Effective vaccines are available for livestock.
Rift Valley fever (RVF) is endemic in many parts of sub-Saharan Africa, Madagascar, some Indian Ocean islands, and part of the Arabian Peninsula. The disease is caused by infection with a Phlebovirus virus in the family Phenuiviridae.
Sporadic, sometimes very large, RVF outbreaks in ruminants are usually associated with heavy rainfall and localized flooding. In epidemic-prone areas, the virus can be maintained between epidemics by silent, low-level circulation between mosquito vectors and susceptible domestic or wild ruminants and/or by vertical transmission by certain floodwater-breeding Aedes spp mosquitoes. In some areas the virus can be hyperendemic, persisting at higher concentrations and resulting in herd immunity, with few or no outbreaks occurring.
During RVF epidemics, abortions in production animals and deaths among young animals, particularly lambs, together with an influenza-like disease in humans, are characteristic. However, infections in both animals and humans are frequently subclinical or mild.
Diagnosis of RVF is on the basis of identification of characteristic histopathological lesions in the liver and demonstration of the presence of the virus by immunohistochemical staining, PCR assay, and/or increasing antibody titer.
RVF is zoonotic: tissues and fluids from infected animals, particularly aborted fetuses, carry a high risk of infection for human handlers.
Treatment is supportive, and effective prevention can be achieved by vaccination of livestock. No human vaccine is currently available, although some are under development.
Etiology and Epidemiology of Rift Valley Fever
Rift Valley fever virus (RVFV), or Phlebovirus riftense, belongs to the order Hareavirales and family Phenuiviridae (1). An enveloped spherical particle of 80–120 nm in diameter, it has a three-segmented, single-stranded, negative-sense RNA genome with a total length of approximately 11.9 kilobases (kb). Each of the segments, L (large: 6.4 kb), M (medium: 3.9 kb), and S (small: 1.7 kb), is contained in a separate nucleocapsid within the virion (2).
Remarkably little genetic diversity has been found among RVFV isolates from many countries, and no noteworthy antigenic differences have been demonstrated. However, some differences in pathogenicity can occur.
Rift Valley fever is endemic in many tropical and subtropical regions of sub-Saharan Africa, Madagascar, Comoros, Mayotte, and the Arabian Peninsula. Thought to have been originally confined to the Rift Valley region of eastern and southern Africa, since the 1970s the virus has spread, with major outbreaks having occurred in Egypt since 1977, West Africa since 1987, Madagascar since 1990, and the Arabian Peninsula in 2000. Particularly large epidemics, including large numbers of human cases, occurred in Egypt in 1977–1978 and in Kenya in 2006–2007. Since about 2000, serological evidence of RVFV infection has emerged in north Africa, and there has also been serological evidence of RVFV exposure in parts of the Middle East, although not confirmed by virus neutralization testing (3, 4, 5, 6). (See .)
Map showing the distribution of Rift Valley fever virus, with areas that have experienced larger outbreaks indicated in red.
Geographic distribution of Rift Valley fever outbreak. World Health Organization. Accessed June 9, 2026. https://www.who.int/multi-media/details/geographic-distribution-of-rift-valley-fever-outbreak.
Sporadic epidemics of RVF occur at 5- to 10-year intervals in drier areas of East Africa as well as in the Sahel, particularly Senegal and Mauritania, and less frequently in southern Africa. Outbreaks are usually associated with periods of abnormally heavy rainfall or, in some cases, with localized flooding related to dam building or flood irrigation. Smaller outbreaks are likely to occur more often and can frequently be overlooked because of suboptimal veterinary surveillance and confusion with other causes of abortion and neonatal mortality.
RVF is considered a threat in other regions of the world, including Europe and North America, where competent mosquito vectors are present, and the potential exists for the virus to become endemic if introduced.
During interepidemic periods, RVFV is thought to remain dormant in transovarially infected eggs of floodwater-breeding Aedes spp mosquitoes (subgenera Neomelaniconion and Aedimorphus) in the dry soil of small, ephemeral wetlands (dambos or pans). In some areas, this transovarial transmission is believed to be the most important interepidemic survival strategy of the virus; however, this has seldom been demonstrated, and it is unknown how long RVFV can survive in this manner.
Inapparent cycling of RVFV between vectors and wild or domestic mammalian hosts also occurs, and this might be the most important survival strategy for the virus in many areas (see ). Serological evidence of exposure to RVFV has been found in many wildlife species, either associated with outbreaks in animals or in the absence of reported outbreaks (7).
Cycle of transmission of the Rift Valley fever virus. Vectors (mainly Aedes and Culex spp) are able to transmit the virus to domestic and wild animals as well as humans. Direct transmission is possible among animals and from animals to humans. Vertical transmission has been described in animals and vectors. The role of vertical transmission for maintaining the virus during inter-epizootic periods is still under discussion.
Courtesy of Nielsen SS, Alvarez J, Bicout DJ, et al. Rift Valley fever – epidemiological update and risk of introduction into Europe. EFSA J. 2020;18(3):e06041. doi:10.2903/j.efsa.2020.6041.
RVF epidemiology occurs along a spectrum from the typically recognized epidemic scenario described above to a hyperendemic situation, where RVFV is permanently maintained in a reservoir system comprising mosquitoes together with domestic and/or wild ruminant populations. In such areas, outbreaks are small or nonexistent, mainly because of sustained herd immunity arising from more frequent exposure to RVFV.
RVFV can also be transmitted via movement of viremic animals, (eg, live animal trade, transhumance, and possibly windborne mosquitoes). When either the emergence of infected Aedes spp mosquitoes or the introduction of virus to an area coincides with abnormally wet conditions and the presence of a highly susceptible host population, a large epidemic can ensue. The virus is then amplified in ruminants and transmitted locally by many species of mosquitoes (particularly Culex spp), mechanically by other insects such as biting flies, or iatrogenically, such as by reuse of needles between infected animals.
The incidence of RVF peaks during the late rainy season. In areas with cold winters, both the disease and vectors can disappear after the first frost. In warmer and wetter climates where insect vectors are present continuously, seasonality is less pronounced, and outbreaks are likely to be smaller because of the maintenance of some level of herd immunity.
Humans are readily infected with RVFV via exposure to:
tissues or fluids from infected animals and aborted fetuses
aerosolized blood from infected animals during slaughter
mosquito bites, although this is considered less likely to result in clinical disease
Therefore, farmers, farm workers, slaughterhouse workers, and veterinarians are particularly at risk.
Clinical Findings of Rift Valley Fever
Clinical signs of Rift Valley fever tend to be nonspecific, rendering it difficult to recognize individual cases.
The incubation period for RVF is 12–36 hours in lambs, and a biphasic fever of up to 42°C (108°F) can develop (8). Affected animals are listless and reluctant to move or eat and can also show clinical signs of abdominal pain.Mortality in young lambs is high (90–100%), and animals usually die within 2–3 days (8). Adult sheep are less susceptible, with 10–30% mortality; the incubation period is 24–72 hours (8), and animals show a generalized febrile response, lethargy, hematemesis, hematochezia, and nasal discharge, although infection can also be inapparent.
Calves are less susceptible to RVFV than lambs; however, mortality can still be as high as 70% (8). Clinical signs are similar to those in sheep; however, icterus is more common. Disease in adult cattle is often inapparent; however, they can show anorexia, lacrimation, salivation, nasal discharge, dysgalactia, and bloody or fetid diarrhea, with a mortality of 5–10% (8).
Camelids, equids, pigs, dogs, and cats can be infected by RVFV and appear largely resistant to disease, whereas birds, reptiles, and amphibians appear to be refractory to infection.
Sometimes, abortion might be the only clinical sign of infection with RVFV; the aborted fetus is usually autolyzed. In pregnant ewes, abortion rates vary from 5% to almost 100% in different outbreaks and on different farms; abortion rates in cattle are usually < 10% (8).
Vaccination of ewes with live Smithburn strain vaccine can result in early embryonic death, congenital CNS anomalies and arthrogryposis, abortion, or stillbirth.
Clinical signs of RVF and abortions have also been reported in goats and occasionally in camels, water buffalo, and some wild ungulate species, including African buffalo (Syncerus caffer), springbok (Antidorcas marsupialis), blesbok (Damaliscus pygargus phillipsi), kudu (Tragelaphus strepsiceros), nyala (Tragelaphus angasii), sable (Hippotragus niger), and roan (Hippotragus equinus) (9).
In humans, RVF is usually inapparent or associated with a self-limiting febrile illness characterized by abrupt onset of malaise, myalgia, and arthralgia. Rarely, the condition progresses to ocular disorders, meningoencephalitis, or a hemorrhagic form (which can have a 50% case fatality rate) (10, 11).
Lesions of Rift Valley Fever
RVF hepatic lesions are similar across affected species and vary mainly with the age of the affected individual. The most severe lesions occur in aborted fetuses and newborn lambs, where the liver is moderately to markedly enlarged, soft, friable, and mottled by irregular areas of congestion (see and images). Numerous gray-white necrotic foci are invariably present; however, they might not be readily visible because of congestion or autolysis. Additional findings commonly include widespread petechial and ecchymotic hemorrhages as well as pulmonary congestion and edema (see and images). Less frequently observed lesions include enlarged, edematous lymph nodes, gallbladder edema and hemorrhage, serosanguinous ascites, and occasional hemorrhages on the serosal surfaces of the GI tract.
Macroscopically, the liver contains discrete foci of hemorrhage and necrosis (arrows), although these lesions can be obscured by autolysis and congestion and are therefore easily overlooked.
Courtesy of Prof. Lieza Odendaal, University of Pretoria.
The liver contains multifocal, randomly distributed foci of hepatocellular necrosis (arrows), accompanied by hemorrhage and mild infiltrates of neutrophils and macrophages. Portal tracts are mildly expanded by edema and lymphocytes (arrowhead), with occasional lymphocytic karyorrhexis. H&E stain, magnification 100X.
Courtesy of Prof. Lieza Odendaal, University of Pretoria.
Macroscopically, the lungs are markedly congested, edematous, and increased in weight. Fluid exudes from the cut surfaces, and copious amounts of foam fill the trachea and bronchi. Mild to moderate hydrothorax is commonly present.
Courtesy of Prof. Lieza Odendaal, University of Pretoria.
The lungs exhibit congestion, occasional hemorrhage, emphysema, and both intra-alveolar (arrow) and interstitial edema (arrowheads). H&E stain, magnification 100X.
Courtesy of Prof. Lieza Odendaal, University of Pretoria.
Histologically, the liver lesions are severe and extensive, with hepatocellular necrosis representing the hallmark lesion of RVF. This is consistently accompanied by pulmonary edema and necrosis of the adrenalcortex and splenic germinal centers (see image).
Pearls & Pitfalls
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The spleen exhibits lymphocytolysis and necrosis within the germinal centers of lymphoid follicles (arrow) and also affecting the white pulp. H&E stain, magnification 200X.
Courtesy of Prof. Lieza Odendaal, University of Pretoria.
Diagnosis of Rift Valley Fever
Abortions and death (especially neonatal) associated with heavy rainfall and flooding
Characteristic histological lesions in liver specimens (necrotic hepatitis)
Immunohistochemistry, PCR assay, or viral isolation
Demonstration of seroconversion
Virus neutralization testing
Note that Rift Valley fever is a notifiable disease in many countries and is a WOAH-reportable disease. State veterinary authorities should be notified whenever RVF is suspected.
RVF should be suspected when abnormally heavy rains and flooding are followed by abortions and neonatal mortalityin domestic ruminants, particularly sheep, with necrotic hepatitis. Concurrent influenza-like disease in humans handling animals or their products should increase the index of suspicion for RVF.
Necropsy of infected animals poses considerable risk to the operator and should be performed only by trained personnel using appropriate personal protective equipment.
Pearls & Pitfalls
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The Rift Valley fever virus can be readily isolated from tissues of aborted fetuses and blood of infected animals. However, definitive diagnosis of RVFV infection is now routinely performed via detection of viral nucleic acid by conventional reverse transcriptase-PCR assay or by real-time (quantitative) PCR assay. RVFV presence can also be demonstrated in organ sections using immunohistochemical stains.
A variety of serological tests can detect antibodies against RVFV; they are helpful in epidemiological studies and in showing seroconversion during active infection. Commercial ELISA test kits are available for detection of either total immunoglobulin (IgG and IgM) or IgM only. An IgM ELISA can demonstrate recent infection using a single serum sample, with IgM detectable for 1.5–3 months after infection (12, 13).
Serological surveys can be complicated by lack of specificity, possibly because of cross-reactivity between RVFV and other phleboviruses, leading to false-positive results. Positive reactions, particularly when the seroprevalence is low, should ideally be confirmed with a virus neutralization test (VNT), which is highly specific and generally regarded as the gold-standard assay. This would be particularly important to do when a positive serological test is obtained in a geographical region where RVF has not previously been detected.
Pearls & Pitfalls
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A disadvantage of most VNTs is the requirement for high levels of biosafety because of the use of virulent virus; however, safe VNTs with lower biosafety requirements have been developed by using laboratory-produced avirulent RVFV strains.
RVF must be considered in light of other differential diagnoses. Wesselsbron disease and other insect-borne viral diseases tend to occur under the same climatic conditions that favor explosive proliferation of arthropod vectors. RVF mortality associated with hepatic lesions should also be distinguished from hepatotoxic plant and algal intoxications; bacterial septicemias such as pasteurellosis, salmonellosis, and anthrax; and other viral infections such as Nairobi sheep disease and peste des petits ruminants. When abortion is the only finding, other important diseases such as brucellosis, leptospirosis, chlamydiosis, campylobacteriosis, toxoplasmosis, Coxiella burnetii infection, and salmonellosis should be eliminated.
Control and Prevention of Rift Valley Fever
Prediction can provide early warning
Vaccination of susceptible animals in advance of risk periods
Once an outbreak of Rift Valley fever has started, any efforts to mitigate its course are usually futile. Control of vectors, movement of stock to high-lying areas, and confinement of stock in insect-proof stables are usually impractical, instituted too late, and of little value.
Treatment of individual clinically affected animals should be on the basis of clinical signs, and the high risk of zoonotic transmission to humans via tissues or fluids and mosquito bites should be considered.
Immunization remains the only effective way to protect animals from RVF. The mouse neuroadapted Smithburn strain of Rift Valley fever virus can be readily produced in large quantities, is inexpensive, and induces a durable immunity 6–7 days after inoculation in sheep. However, it produces a relatively poor antibody response in cattle. It should typically not be administered for protection of pregnant animals, because it can cause abortion, congenital defects, and hydrops amnii in the ewe; however, its use can be considered during an outbreak when possible adverse effects are outweighed by the dangers of natural infection.
Although not proven, it is theoretically possible for an attenuated virus to revert to virulence. Therefore, it is not advisable to use live attenuated vaccines in nonendemic countries or regions.
A formalin-inactivated vaccine is safe to use in pregnant animals; however, it induces short-lived immunity and requires booster doses (14). A naturally attenuated avirulent isolate of RVFV, clone 13, has been used in a commercially available vaccine and is reportedly safer to administer to pregnant animals (15, 16). Future recombinant DNA vaccines and viral strains with deletions of the major virulence genes could offer improved options.
Because large RVF outbreaks occur only very occasionally in any particular area, and areas at risk are often in underresourced countries, it is difficult to motivate farmers or authorities to vaccinate animals regularly to prevent outbreaks. As a result, vaccination is often employed as an emergency measure in the face of an outbreak, resulting in vaccine shortages, apparent vaccine failure, and iatrogenic transmission within herds/flocks because of reuse of needles on already-viremic animals.
The development of multivalent recombinant capripox-vectored vaccines, combining RVF with lumpy skin disease and/or peste des petits ruminants vaccines, might improve vaccine uptake in many areas of Africa affected by these diseases.
Much effort has been directed toward prediction of RVF outbreaks. This includes use of meteorological and remote-sensing data to identify high-risk areas and time periods. This analysis has been somewhat successful in predicting outbreaks in eastern Africa; however, it is less so in southern Africa, and work on predictive models is ongoing. However, outbreaks cannot yet reliably be predicted and are usually of sudden onset.
Routinely immunizing lambs for RVF at 6 months old, which likely affords lifelong protection, is advisable. The offspring of susceptible ewes can be immunized at any age. Pregnant ewes and cattle can be vaccinated with a formalin-inactivated vaccine, which elicits a better immunity in cattle and is safe in pregnancy; however, revaccination after 3 months is advisable to induce an immunity that will last > 1 year and to confer colostral immunity to the offspring (17).
Zoonotic Risk of Rift Valley Fever in Animals
Because Rift Valley fever virus can cause severe and potentially fatal disease in humans, workers involved in the food-producing animal industry should be made aware of the potential dangers of exposure to RVFV-infected animals and tissues. Appropriate protective measures should be taken when investigating cases of abortion, handling potentially infected animals, and collecting diagnostic samples.
Key Points
Rift Valley fever is a mosquito-borne zoonotic disease currently largely confined to sub-Saharan Africa but with potential for global spread.
Abortions and death in domestic ruminants associated with heavy rainfall and flooding should suggest possible RVF, particularly if influenza-like symptoms occur concurrently in humans.
Vaccination is the only effective prevention or control method for RVF, and ruminant livestock in areas at risk should be vaccinated, particularly if high rainfall is expected.
Strict precautions should be taken to prevent zoonotic transmission via close contact with tissues or fluids from diseased animals or aborted fetuses.
For More Information
Coetzer JAW, Paweska JT, Bird B, Swanepoel R, Odendaal L, Fafetine J. Rift Valley fever. Anipedia. Published online May 31, 2021.
Linthicum KJ, Britch SC, Anyamba A. Rift Valley fever: an emerging mosquito-borne disease. Annu Rev Entomol. 2016;61:395-415. doi:10.1146/annurev-ento-010715-023819
Nielsen SS, Alvarez J, Bicout DJ, et al. Rift Valley fever – epidemiological update and risk of introduction into Europe. EFSA J. 2020;18(3):e06041.
Rostal MK, Thompson PN, Anyamba A, et al. Rift Valley fever epidemiology: shifting the paradigm and rethinking research priorities. Lancet Planet Health. 2025;9(9):101299.
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