Rift Valley Fever

Also Known As: RVF

Caused By: Rift Valley Fever Virus — RVFV

Introduction

Rift Valley Fever (RVF) is a viral zoonotic disease belonging to the family Bunyaviridae in the Phlebovirus genus, possessing a segmented negative sense RNA genome. The disease has an episodic occurrence remerging ever 5-25 years and is seasonal in its occurrence. The occurrence of non immune animal populations every 5-25years combined with the introduction of RVF (due to rainfall) accounts for the explosive cyclical nature of the disease. RVF primarily affects animals but can infect humans and has the capacity to cause severe disease in both.

RVF has a wide economic impact due to livestock loss and trade restrictions as well as public health implications. It is a notifiable disease.

Distribution

RVF virus was first identified in 1831 in the Rift Valley in Kenya during an investigation on a sheep farm and has since spread throughout Sub Saharan Africa emerging into North Africa in the 1970’s. the outbreak in Egypt in 1977-78 is considered to be the largest outbreak with 200,000 human cases reported. In September 2000 it was reported for the first time outside of Africa, in Saudi Arabia and Yemen, probably introduced through infected livestock or mosquitoes. The increase in cases in South Africa may be due to the end of an inter epizootic period. Outbreaks are frequently reported though there is no evidence that it has spread to previously uninfected countries in the last 10 years, though it is hard to monitor changes in disease occurrence due to the cyclical occurrence of epidemics. Most recently RVF was reported in Mauritania in November 2012. A map detailing current outbreaks can be found here

A number of mosquito species (Aedes, Culex, Mansonia, Anopheles) are implicated as vectors of RFV, the most important being Aedes and Culex spp. They are responsible for both maintenance and amplification of RVF.

Mosquitoes can be infected via feeding on infected animals. Vertical transmission can also occur (particularly in Aedes spp); female infected mosquitoes lay virus infected eggs leading to a new generation of infected mosquitoes. Vertical transmission is important in the survival of the virus as the eggs laid by the female can survive for many months in dry conditions, hatching after a period of rain and so increasing spread post rainfall leading to epizootics. Once animal infection has occurred mosquitoes are then responsible for amplifying infection. Aedes mosquito numbers decrease following rain but Culex tend to breed in more permanent water sites, hence the continuation of virus spread.

RVF affects 4 areas:
Dambos (e.g. East Africa) – Shallow depressions, often near rivers, that fill with water during the rainy season. Vertical transmission in mosquitoes occurs here.

Semi-arid (e.g. Senegal, Mauritania) – At temporary water points. It is unknown how the virus persists here, presumably either via vertical transmission or reintroduction of virus through visiting herds.

Irrigated areas (e.g. Nile Delta and Senegal River Valley). Yearlong viral transmission occurs here as the permanent water favours Culex breeding.

Temperate and Mountainous (e.g. Madagascar) – Virus is transmitted by vectors through cattle movement.

No outbreaks have been reported in urban areas.

Zoonotic transmission occurs through direct or indirect contact with infective blood or organs through slaughter, assisting with births and carcass disposal amongst other means. Faecal shedding of virus also occurs, as does spread through nasal and ocular secretions. Aerosol infection has also occurred within laboratory workers. Consuming unpasteurised or uncooked milk has also been associated with infection and seropositivity. Mosquito bites have resulted in infection as well, and blood feeding flies also have the potential to transmit infection. There is no evidence of human to human transmission.

Virus particles are shed in milk but animals have not been infected via suckling or ingestion of milk.

It is currently unknown if there are animal reservoirs of RVF between outbreaks. The namaqua rock rat and bats have been implicated and have been shown to be capable of infection but the potential impact of this is unknown. Low levels of circulation between livestock or wild ruminants and mosquitoes (sylvatic cycle) is also likely to occur.

Outbreaks occur after heavy rain and flooding due to favourable breeding conditions for mosquitoes.

RVF can also be spread by the introduction of infected livestock into previously unaffected areas where mosquitoes are present.

Signalment

Cattle, sheep, goats and humans are important hosts. This is due in part to their presence in huge numbers in epizootic areas and therefore ability to greatly amplify viral presence in a population and transmit to others.

Bos Taurus cattle and other European breed imported into Africa appear highly susceptible to RVF. Indigenous breeds appear to be resistant to disease, as do pigs.

Cats, dogs, rats and other rodents seem to be accidental hosts infected by mosquitoes.

Humans working closely with animals or ingesting raw animal products, e.g. in rituals, are most predisposed.

Clinical Signs

Abortions occurring in huge storms with high mortality in both neonates and adults are characteristic of the disease. Agalactia may also develop.

In milder clinical cases diarrhoea may occur and involve melaena and haematochezia.

Tachycardia, cyanosis, petechiation, haemorrhage and clotting defects are haematological consequences of RVF.

The respiratory disease of RVF is non-specific: Purulent nasal discharge, epistaxis, tachypnoea and dyspnoea.

Fever, lymphadenopathy, depression and lethargy usually accompany infection. Hepatitis may cause consequent photosensitisation.

In young animals, peracute disease causes anorexia, listlessness, collapse and death.

Humans develop malarial-like disease. High risk individuals include farmers, veterinarians and abattoir staff. Mild disease is most common but severe hepatitis, encephalitis and ocular damage can develop. The usual presentation is of sudden onset fever, myalgia, biphasic behaviour and gastrointestinal disease.

Diagnosis

Sudden onset of acute debilitating disease in man and abortion/neonatal death in domestic animals should raise suspicion in the appropriate countries.

Viral isolation can be performed from placenta, foetal liver and other tissues. The virus can also be innoculated into tissue cultures and diagnosed by Fluorescent Antibody Testing (FAT) or immune-peroxidase staining.

Fixed liver samples can be immunostained and sera from aborted animals examined to confirm viral presence and are both simple and sensitive.

IgM ELISA can also be performed on serum. Virus neutralisation is the prescribed test for international trading of animals

On necropsy, in the viraemic stage, widespread petechiae and ecchymoses on serous surfaces and organs will be seen and extravasated blood present in the body cavities.

In older animals, the liver is enlarged and inflamed, with many foci of necrosis which are bronzed and jaundiced. The gall bladder may also be distended and haemorrhagic. Lymph nodes are enlarged and their germinal centres may be necrotic on closer examination. Extensive subcapsular haemorrhage in the spleen is usual. Renal changes include oedema and congestion. Epicardial and endocardial haemorrhages are often present on the heart.

Treatment

No treatment is available.

Control

Modified live and inactivated vaccines are available. Live vaccination is only recommended in non-pregnant animals due to its ability to cause abortion and neurological deficits in lambs. In epizootic situations though, this risk may well be worth taking.

Inactivated vaccines are ineffective during epizootics and therefore less widely used than modified live strains.

Mosquito and larval control is extremely valuable. Slow release larvicides such as methoprene can be applied to well-defined mosquito breeding areas.

Sentinel cattle are used for epidemiological surveillance, and are tested 2-3months after the seasonal rains.

Rift Valley Fever Learning Resources
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References

This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project. The datasheet was accessed on 8 June 2011.

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