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 Rift Valley Fever
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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 hemorrhaging
• Retinitis with visual impairment
• Meningoencephalitis
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