Facts about Rift Valley fever

factsheet

Rift Valley fever (RVF) is an acute viral disease that affects domestic animals (such as cattle, buffalo, sheep, goats, and camels). The disease is caused by the RVF virus, generally found in regions of eastern and southern Africa, but also in most countries of sub-Saharan Africa, Madagascar, Saudi Arabia and Yemen.

Humans may become infected through direct or indirect contact with the blood or organs of infected animals. While most human cases are relatively mild, a small percentage of patients develop a much more severe form of the disease. The uncomplicated cases are characterised by acute influenza-like illness leading to full recovery. In some patients the illness can progress to a severe form with haemorrhagic manifestations and hepatitis; possible complications include retinitis (inflammation of the retina) and encephalitis (inflammation of the brain).

Vaccination of the animals at risk is the most important way of preventing infection in humans.

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1. Name and nature of infecting organism

Rift Valley fever (RVF) is a disease of domestic ruminants, caused by an arbovirus belonging to the Phlebovirus genus (Bunyaviridae family). The RVF virus was first identified in 1931 during an investigation into an epidemic among sheep on a farm in the Rift Valley in Kenya.

It produces high mortality rates in newborn ruminants, especially sheep and goats, and abortion in pregnant animals. Human infection by Rift Valley fever virus (RVFV) may result from contact with viraemic animals and their body fluids, and with their carcases and organs including offal, during veterinary practices, necropsy, slaughtering and butchering.

Until 1975, RVF was regarded as an African, animal disease. Human cases were rare and with mild clinical manifestations. Severe outbreaks with hemorrhagic fever cases and fatalities in humans were reported in South Africa in 1975, Egypt in 1977 and Mauritania in 1987. One of the most noticeable outbreaks occurred in East Africa in December 1997, when unexplained human deaths were reported in the north-eastern province of Kenya and southern Somalia. This epidemic was considered the most devastating in the region.

In September 2000, RVF was detected for the first time outside the African continent, in Saudi Arabia and Yemen, leading to human deaths and major losses in livestock populations. In 2006–07 an outbreak was declared in Kenya. Tanzania and Somalia were affected later. Madagascar and South Africa were hit in 2007 and 2008.

Up to date, no outbreaks have been reported in Europe.

2. Clinical features

The incubation period varies from two to five days. Beside non-symptomatic infections, uncomplicated human RVF manifests as an acute influenza-like illness with transient fever, rigor, headache, severe muscle and joint pain, photophobia and anorexia. Occasionally, patients present petaechial rash, nausea, vomiting and epistaxis. The course of the disease is 4–7 days leading to full recovery in two weeks.

A severe form of the disease is a haemorrhagic diathesis with hepatitis, characterised by an acute febrile illness of 2–4 days’ duration followed by jaundice and widespread haemorrhages in mucosae and subcutaneous tissues. Bleeding occurs at needle puncture sites, from the gums and nose. Haematemesis and diarrhoea with melena may occur. Patients usually die within another 3–6 days. A few may recover after a long slow convalescence.

The most frequent complication is retinitis, usually bilateral, occurring 1–3 weeks after the primary febrile illness. Fifty per cent of cases suffer permanent loss of central vision; there may be permanent unilateral or bilateral blindness. Encephalitis may develop during the second febrile phase. Patients suffer confusion, hallucinations, vertigo, and choreiform movements sometimes leading to coma. The case fatality rate is generally low but full recovery may be protracted and long-term neurological complications have been reported.

3. Transmission

3.1 Reservoir

The main amplifying hosts are domestic ruminants. Wildlife reservoirs such as rodents, wild ruminants or bats may also contribute to the persistence of the virus during inter-epizootic periods.

3.2 Transmission mode

Several mosquito species are involved in the cycle of transmission of the virus. Vertical transmission of RVF virus in some Aedes mosquitospecies from the Aedimorphus and Neomelaniconion sub-genera referred to as flood-water breeding Aedes has been identified.

The virus may be transmitted to humans by mosquito vectors (mainly Aedes and Culex spp.) but mostly through direct contact with blood, abortion products, or any other infected biological material during the viraemia. Meat can be a source of infection but the virus is rapidly destroyed when the acidity of the meat decreases during maturation. RVF is not considered a nosocomial infection.

3.3 Risk groups

Humans are at serious risk of infection from the foetal tissues and from the fluids of infected animals, which heavily contaminate the perineal area and udder after abortions have occurred in livestock. Laboratory staff handling blood and tissues from suspected RVF carcases have historically experienced most accidental infection by RVF. Post-mortem procedures are a real source of danger to veterinarians from RVF infection. Milk is not considered to be a hazard. The importance of blood and bone or offal meal products as a vehicle for RVF virus has not been evaluated.

4. Prevention measures

A human inactivated vaccine was used in the USA to protect laboratory and military staff (RVF is considered as a possible biological weapon). Its production was stopped because of logistical constraints.

Because the initial epidemiological cycle involves domestic ruminants, and humans mostly become infected after contact with viraemic animals, vaccination of ruminants is the favoured method of preventing human disease. Both live and inactivated vaccines are available for livestock. The Smithburn vaccine is a modified live virus vaccine. It is immunogenic for sheep, goats and cattle, and it protects against abortion caused by a wild virus strain. However, it has a residual pathogenic effect in humans (flu-like syndrome) and ruminants (abortion, congenital malformation).

The inactivated RVF vaccine provides a lower level of protection and its production is more expensive. Moreover, it requires at least two inoculations to induce the desired level of protection.

Candidate vaccines have been developed; some of them are in the evaluation phase (e.g. clone 13 for ruminants).

Other recommended measures include a ban on slaughtering and butchering ruminants during epizootics, the use of insect repellents and bed nets during outbreaks, the implementation of information campaigns for people at risk (farmers, veterinarians, slaughterhouse employees, butchers, etc.), and the appropriate disposal of dead animals.

5. Diagnosis

The virus can be detected in blood specimens up to day 4–5 post onset of the disease by RT-PCR, antigen-capture and/or viral isolation, then specific IgM antibodies from day 5–6 and afterwards specific IgG. Due to unrecognised cross reactions with other phleboviruses, confirmation of serological results by neutralisation assay may be needed.

A few commercial diagnostic tests are available for humans and animals. However, their performances remain to be tested in a European context.

6. Management and treatment

There is no specific treatment for either humans or animals.

7. Key areas of uncertainty

The intensification of international trade, ecological alterations, global warming, and extreme climatic events could lead to a geographical expansion from tropical to sub-tropical — or even temperate — areas. Field performance and cost-effectiveness assessments of available diagnostic tests and animal vaccines should be carried out.

The use of vaccines for at-risk human populations and vulnerable people (farmers, veterinarians, etc.) in the case of animal outbreaks should be studied on the basis of sociological and epidemiological surveys.

8. References

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CDC. Rift Valley fever outbreak – Kenya, Nov 2006-Jan 2007. MMWR. 2007;56(4):73-76.
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Davies FG, Martin V. Recognizing Rift Valley fever. Vet Ital. 2006;42(1):31-53.
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EFSA. The risk of Rift Valley fever incursion and its persistence within the Community. In: EFSA Journal 2005, EFSA. p. 1-128.

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Muller R, Saluzzo JF, Lopez N, Dreier T, Turell M, Smith J, Bouloy M. Characterization of clone 13, a naturally attenuated avirulent isolate of Rift Valley fever virus, which is altered in the small segment. Am J Trop Med Hyg 1995;53(4):405-411.

Paweska JT, Van Muren PJ, Kemp A, Buss P, Bengis RG, Gayuka F et al. Recombinant nucleocapsid-based ELISA for detection of IgG antibody to Rift Valley fever in African buffalo. Vet Microbiol 2007;Aug 17.

Peters C, Meegan J. Rift Valley fever. In: Beran GW, Editor. Viral zoonoses, section B. Florida: CRC press; 1981.

Swanepoel R. Contributions to epidemiology and biostatistics: Rift Valley fever (Klingberg MA, ed.), Vol 3. Basel, 1981, 91p.

Wallace DB, Ellis CE, Espach A, Smith SJ, Greyling RR, Viljoen GJ. Protective immune responses induced by different recombinant vaccine regimes to Rift Valley fever. Vaccine 2006;24:7181-7189.

WHO. Rift valley fever in Sudan – Update 4. Geneva: WHO; 2007.