Rift Valley Fever

Endemic to Madagascar, eastern, and southern Africa is an RNA disease causing virus named for the area in which it was first reported in 1930 called Rift Valley Fever (RVF). The virus has since been detected as far north as Egypt and over to the Arabian Peninsula countries of Saudi Arabia and Yemen. Although an important pathogen in its native area affecting domestic ruminants and people, RVF is feared as a potential biological weapon capable of spreading the globe by the movement of infected people, animals, and insects.

Rift Valley Fever (RVF) is an arbovirus (arthropod-borne virus) and is classified in the family Bunyaviridae and the genus Phlebovirus. Being an arbovirus, RVF requires a blood sucking-arthropod for transmission. In Africa, the preferred arthropod for transmission is the mosquito. The virus can be found naturally in 23 species of mosquitoes. RFV virus has also been isolated from Culicoides species and Simulium species of flies. Culicoides and Simulium species are believed to be primarily mechanical vectors. Animal-to-animal transmission may occur but is not considered to be an important means of transmission under field conditions.

The role of ruminant wildlife as a reservoir of infection is unclear. Ruminant wildlife will often not show clinical signs of disease even while sharing the same grasslands with domestic animals that do exhibit the disease clinically. Ruminant wildlife have however been found with antibodies to the virus and it is possible that some species of wild ruminants may abort following what appears to be a non-clinical infection.

Nonhuman primates have been found to develop antibodies against RVF. Rhesus monkeys have been shown to develop hemorrhagic fever followed by recovery or death. Other species of African monkeys have not shown evidence of clinical illness. Wild rodents have been found to have limited resistance to the RVF virus.

In sub-Saharan East Africa, where RVF is endemic, the virus is proposed to have a rainfall-dependent biphasic maintenance cycle. Transovarial transmission (transmission of the virus through insect eggs to the next generation) of RFV in mosquito eggs is the most likely primary mechanism for maintenance of the virus during dry environmental conditions. Aedes mosquitoes have drought-resistant eggs that may survive several years without hatching. Low-level transmission of the virus to ruminant livestock, rodents, and nonhuman primates may also contribute to maintaining the virus during interepizootic periods (time between outbreaks of the disease). Interepizootic periods may last from 5 to 15 years in grassland areas and from 25 to 35 years in drier areas.

Wind dispersal of virus-infected insects has been implicated in the spread of RVF to new geographic areas. The distance traveled by these insects has been found to range from 110 to 1,350 Km (68 to 839 miles) during a 24 hour period due to wind dispersal. It is also feared that cargo containers could spread infected adult mosquitoes during a transcontinental ocean travel.

The virus has an extremely short incubation period of 30 to 72 hours and replicates rapidly in the cytoplasm of hosts cells, particularly those of the liver and other reticuloendothelial organs.

Clinically, there is a sudden onset of high fever, foul smelling diarrhea, icterus, and incoordination. Clinical signs are followed by collapse and death within 36 hours in 95 to 100% of affected lambs and in 70% of young calves. In adult sheep and cattle, the primary clinical sign is abortion but the mortality rate may be as high as 30% in adult sheep and as high as 10% in adult cattle. High temperatures, dysgalactia, emaciation and jaundice are seen in less severe cases in cattle. In fatal cases, death is preceded by high fevers by 1 to 2 days. Goats will show a febrile reaction but few other clinical signs of disease.

Serologic testing will demonstrate a severe leukopenia (lack of white blood cells). Antibodies will be demonstratable one week after infection. Serum is typically screened with hemagglutination-inhibition or ELISA tests. Samples testing positive for RVF on screening should be confirmed by virus neutralization tests.

There is no known treatment that is of any value and treatment is primarily supportive when conducted.

The cause of death is characteristically extensive hepatic (liver) necrosis.

Vaccines are available for use in endemic areas. Live attenuated vaccines give immunity for at least 28 months but are not recommended for pregnant animals because of fetal death and teratogenic properties (the ability to cause birth defects). There is also a concern with these vaccines that they could revert to virulent strains of the virus causing disease rather than prevention. Killed vaccines require repeat administration and may be used for pregnant and young animals.

Rift Valley Fever (RVF) is a zoonotic (capable of infecting humans) disease. This is a virus that causes a hemorrhagic fever and flu-like symptoms in humans with a high morbidity (the ability to cause infection) and a high mortality rate associated with infection in both humans and livestock. Humans may be readily infected by insects, aerosols from infected animals, and exposure to infected animal tissues or aborted fetuses. It is feared that terrorists could view the virus as a potential biological weapon or that infected humans could cause the spread of RVF to additional parts of the globe.

References:

Kahn, Cynthia, Editor. The Merck Veterinary Manual. Merck and Co. 9^th Edition. Pp. 617-619.

Kasari, Thomas and Deborah Carr et al. “Evaluation of Pathways for release of Rift Valley Fever Virus into Domestic Ruminant Livestock, Ruminant Wildlife and Human Populations in the Continental United States.” JAVMA, Vol 232, No. 4, February 15, 2008. P. 514-524.

Radostits, Otto ad Clive Gay. Veterinary Medicine. Saunders/Elsevier. 10^th Edition. Pp. 1205-1207.