Rift Valley Fever
Description. An acute, febrile, viral disease that affects livestock (such as cattle,
buffalo, sheep, goats, and camels) and people. Rift Valley virus is a member of the
family Bunyaviridae, genus Phlebovirus. It was first identified in 1931 in East Africa
during major epizootics of sheep and cattle, but remained an unclassified arbovirus
described as flu-like with occasional retinitis. Prior to 1977, it was considered
primarily a veterinarian's disease. It wasn't until the Marburg filovirus attained
international attention that Rift Valley fever was also identified as a cause of human
hemorrhagic fever.
Location. Eastern and southern Africa, most countries of sub-Saharan Africa, and
Madagascar.
Vectors. There are three main vectors of RVF: transcutaneous transmission, aerosol
transmission, and mosquito or other insect bite. Aedes vexans, Ae. ochraceus, and Ae.
dalzieli mosquitoes, as well as other mosquitoes and blood-sucking insects, such as
the sandfly Phlebotomus duboscqui. Three mosquito species (Ae. cumminsii, Ae.
circumluteolus, and Ae. mcintoshi) are known vectors for RVF, but their role in
transmitting the virus is not yet known. Following periods of heavy rains, shallow
depressions in the ground, called dambos, are filled with water. Flood-water
mosquito populations flourish, and the virus reemerges. During dry periods, the virus
lies dormant in drought-resistant mosquito eggs over much of the African continent.
RVF has been isolated from both male and female mosquitoes. Sleeping outside
significantly increases the chances of contracting RVF. The virus is also transmitted
via contact with the blood, secretions, or excretions of infected animals. Because the
virus affects livestock, contact with diseased animals can be via slaughtering or
handling of infected animals, herding and animal husbandry tasks, touching
contaminated meat from infected animals, and so on. Aerosol transmission of the
disease, via contact with laboratory specimens, has also been documented.
Mechanism. Rift Valley fever is cytopathic. It forms plaques, replicates to high
titer, and tends to target the liver (focal necrosis) and brain (necrotic encephalitis). It
is thought that, after a mosquito bite, the virus moves from the skin to draining lymph
nodes, where it replicates. Efferent lymphatics spread the virus throughout the body.
As the liver is rapidly invaded, hepatocytes (parenchymal cells of the liver) become
involved. The virus may also cross the blood-brain barrier and infect neurons and
glia. Meningoencephalitis and retinitis develop 2 to 3 weeks after onset of infection,
and are highly inflammatory. Immune-system response may mediate the effects of
these latter conditions.
Symptoms. Some patients show no symptoms. Others show sudden onset of mild
fever with a biphasic course, and symptoms of liver and kidney disorder. The most
common complication is retinitis with a central scotoma. Paramacular retinal
hemorrhages and edema may also occur. Between 1%-10% of convalescents have
some permanent vision loss. In general, patients recover from the disease 2 to 7 days
after onset of symptoms. In severe cases, the disease becomes serious. Symptoms
include fever, myalgias, and encephalitis, including headache, coma, and seizures.
Other symptoms include: backpain, dizziness, and extreme weight loss. In extreme
cases, the patient hemorrhages, vascular collapse occurs, followed by shock and
death. Severe cases of RVF fall into three categories: Liver necrosis with orrhaging
• Retinitis with visual impairment Meningoencephalitis
Treatment. Ribavirin, which is used to treat Lassa fever, has shown some promise
as an antiviral. Other treatments also show promise, such as: interferon, immune
modulators, and convalescent-phase plasma. However, the Egyptian strain of RVF
appears to be not only more virulent, but also to be resistant to interferon. Currently,
there is no specific treatment for the disease.