Rift valley fever is an infectious disease caused by rift valley fever virus, an RNA virus that causes hemorrhagic fever in humans and animals, similar to Ebola, Lassa, Marburg, dengue and yellow fever viruses. Humans become infected via aerosols or by ingesting unpasteurized animal milk or after exposure to infected animal blood, body fluids or tissue or following mosquito or other insect bites.
Most infected individuals remain asymptomatic or develop a mild form of the disease, consisting of fever, muscle and joint pain, weakness, backache, and headache. The clinical picture may resemble meningitis with neck stiffness photophobia, anorexia, and vomiting. Still, symptoms may be difficult to recognize, especially if the epizootic context is unknown and diagnosis may depend on reliable laboratory techniques.
Severe illness consists of ocular disease, meningoencephalitis, and hemorrhagic fever. Ocular symptoms like blurred or decreased vision signify retinal or macular damage, that might spontaneously resolve or become permanent, leading to vision loss. Central nervous system disease manifests as an intense headache, hallucinations, confusion, seizures, lethargy, and coma, with persistence of neurologic deficit, whereas hemorrhagic fever signifies liver damage and manifests as jaundice, melena, hematemesis, menorrhagia, epistaxis or other mucosal hemorrhages, purpuric rash or ecchymosis. 50% of patients with hemorrhagic fever die within one week of symptom onset. Jaundice, neurologic and hemorrhagic forms have a higher incidence of mortality  . Central nervous system disease may be followed by permanent neurologic deficits.
Although abortion is the most prominent trait of this disease in animals, pregnant women, newborns, and small children usually are spared from this infection. The reason for this might be that they usually are not exposed to diseased animals and more efforts are made to prevent their exposure to mosquitoes; if other reasons exist, they are yet to be reported.
Rift valley fever (RVF) induces life-long immunity.
Ocular disease becomes apparent 7-21 days after infection and resolves after 10-12 weeks. Encephalitis may be suspected 1-4 weeks after initial general symptoms of the disease appear, while hemorrhages occurring much sooner i.e. 2-4 days following exposure, entail a poor prognosis.
Laboratory techniques used in order to establish the diagnosis include reverse transcriptase-polymerase chain reaction (RT-PCR)  , virus isolation in cell cultures , enzyme-linked immunoassay (ELISA) to detect viral antigens  , immunoglobulin IgM and IgG  and real-time reverse transcription-loop-mediated isothermal amplification assays (RT-LAMP)  , a new, highly specific and sensitive diagnostic test. Samples should be handled with caution and processed in specialized facilities, as they might be a bio- hazard. The virus is isolated from serum, liver, spleen or brain tissue. Rapid virus identification in severe cases is extremely important as patients need special management.
Immunological viral antigen detection methods include agar gel immunodiffusion and immunostaining on impression smears or on cryostat sections of liver, spleen, and brain, while histopathological examination reveals specific characteristics  . Sandwich ELISA for antigen detection (sAg-ELISA) is a new technique to identify the disease and it is less dangerous to laboratory personnel  .
Antibody detection methods include hemagglutination-inhibition, complement fixation, indirect immunofluorescence which aim to prove seroconversion and virus neutralization test which is considered to be the gold standard  .