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Copyright 2004 Tara K. Harper.  All rights reserved.

TKH Virology Notes:
Rift Valley Fever

•  Description      •  Mechanism      •  Outbreaks
•  Location      •  Incubation Period      •  Vaccine
•  Vector      •  Symptoms      •  Links
     •  Mortality Rates
     •  Treatment

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NOTE:  This file is for information only.  It is not intended for diagnosis.

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.

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Location.   Eastern and southern Africa, most countries of sub-Saharan Africa, and Madagascar.

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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.

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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.

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Incubation Period:  2-6 days.

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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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Mortality Rates.  Approximately 1% in humans.  Rates are significantly higher in livestock.  In addition, the fatality rate for fetuses in pregnant livestock is 100%, and the fatality rate for newborn lambs is 90%.

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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.  

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Outbreaks and History of Infection.  Outbreaks are often associated with periods of heavy rainfall, after which the mosquito population flourishes.  Outbreaks have been reported in Keyna, Sudan, Egypt, Cameroon, Central African Republic, Mali, Mauritania, Madagascar, Nigeria, Senegal, Somalia, South Africa, Tanzania, Zambia, and Zimbabwe.  One of the earliest reported outbreaks occurred in 1950-1951 in Kenya, resulting in the death of 100,000 sheep.  Imported European animals were especially susceptible to RVF.

The 1977 Egypt outbreak was thought to be caused by an unexplained spread from Sudan, possibly from the wind, imported camels or sheep, or by mosquitoes.  The epizootic affected 25% to 50% of all sheep and cattle.  Among humans, 200,000 fell ill, 18,000 clinical cases were confirmed, with 598 deaths from hemorrhagic fever.  Human infection rates ran as high as 35%.  Retrospective studies indicate that RVF was not present in Egypt before the 1977 outbreak.

In 1987, RVF broke out in Mauritania following the opening of Diama Dam at the mouth of the Senegal River, in an area where the virus was present but not generally recognized.  The dam project created additional breeding grounds for mosquitoes carrying the disease, and resulted in more than 200 human deaths from RVF.   The 1993 Egypt outbreak followed the opening of the Aswan dam.  Other outbreaks, such as the 1997 outbreaks in Kenya and Somalia, have been associated with periods of heavy rain, when standing floodwaters become available as breeding grounds for the RVF mosquito vectors.  The 1997 outbreak resulted in large losses of domestic animals, as well as more than 300 human deaths.

Some specific outbreaks:
   - 1950-1951, Kenya
   - 1967-1970, Nigeria
   - 1969, Central African Republic
   - 1976-1977, Sudan
   - 1977-1978, Egypt
   - 1987, Mauritania
   - 1990-1991, Madagascar
   - 1993, Egypt and Senegal
   - 1997, Kenya and Somalia

In July, 1999, scientists reported that they have developed a strategy for predicting outbreaks (Science, July 16, 1999).  Since heavy rains create conditions favorable to RVF vectors, scientists look at water temperatures in the Indian and Pacific Oceans to predict the heavy rains that, months later, affect East Africa and trigger the disease.

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Vaccine.   Killed RVFV vaccines and live-attenuated RVFV vaccines for animals (vetrinary use) are available, but they provide little protection for cattle, and they can cause birth defects and abortions in sheep.  These vaccines are available as killed RVFV vaccines and as live-attenuated RVFV vaccines.

A human live attenuated vaccine, MP-12, is currently undergoing trials, but is not approved for human use.  Other attenuated strains have been developed as potential live vaccines.  Formalin-inactivated vaccines have been used to protect laboratory workers.  A viral glycoprotein has also been developed.

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     •  Fact Sheet - Centers for Disease Control (CDC)
     •  Fact Sheet - CDC, Special Pathogens Branch

Copyright 2004 Tara K. Harper

All rights reserved.  It is illegal to reproduce or transmit in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, any part of this copyrighted file without permission in writing from Tara K. Harper.  Permission to download this file for personal use only is hereby granted by Tara K. Harper.

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