Rift valley fever

Rift valley fever (RVF)

Changed on: 25.10.2021
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Animal disease categories: A D E

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Rift valley fever is caused by a virus that mainly infects livestock such as sheep, cows, goats and camels and leads to abortions or high mortality in newborns, but also to increased mortality in adult animals. Rift valley fever is a viral zoonosis transmitted by vectors (mosquitoes) and also causes disease in humans.

Occurrence

Africa (from South Africa to Egypt), since 2000 also on the Arabian Peninsula (outbreaks in Saudi Arabia and Yemen)

Host animals

Farm animals (sheep, cattle, goats and camels); wild animals e.g. African buffalo, giraffe or roan antelope.

Mode of Transmission

Transmission by mosquitoes, no direct animal-to-animal transmission. Humans are also infected by mosquitoes or by direct or indirect contact with the blood or organs of infected animals.

Incubation period

12 to 36 hours

Symptoms

Fever up to 41°C, loss of appetite, general apathy and reluctance to move, swollen lymph nodes, abdominal pain and bloody diarrhoea. Liver necrosis, occasionally slightly enlarged spleen. The mortality rate varies between 10 and 100 % depending on the age of the animal and the species.

Therapy

There is no therapy against rift valley fever.

Prevention

In endemic areas, both inactivated and live vaccines are used.

Situation in Austria

Rift valley fever has not yet occurred in Austria.

Prfessional information

The first outbreak of Rift Valley fever was first described in 1930 on a farm near Lake Naivasha in the Rift Valley in Kenya. This resulted in increased mortality and abortions in adult sheep and very high mortality in newborn lambs. Within a few weeks, thousands of animals died on this farm. At that time, it was already suspected that the disease was transmitted by mosquitoes, as the outbreak occurred after heavy rains with increased mosquito activity. In addition, almost all sheep herders reported non-specific symptoms such as fever and severe pain during this outbreak.

Rift Valley fever virus is a phlebovirus with a segmented, single-stranded RNA genome with negative polarity. There is only one serotype and there is very limited diversity between isolates with approximately 2% difference in amino acid sequence between isolates. After surviving infection, animals develop neutralizing antibodies within the first week after infection. Sheep and cattle exposed to re-infection are completely immune and have not shown clinical disease.

Mosquitoes are the only important vectors of Rift Valley fever virus, which has been successfully isolated from over 50 different mosquito species. It has also been shown that at least two mosquito species found in Europe(Culex pipiens and Aedes albopictus) are suitable vectors for rift valley fever virus. In endemic areas, Aedes mosquitoes ingest the virus with their blood meal from infected animals and thus pass the virus vertically to their offspring. From these eggs, new generations of infected mosquitoes hatch again. In this way, the virus persists in nature over prolonged dry periods of several years. If livestock are already infected, a number of different mosquito species as well as other vectors, such as ticks or sandflies, can pick up the virus, act as mechanical vectors and ensure further spread of the rift valley fever virus. After periods of heavy rainfall, mosquito populations increase sharply, often leading to rift valley fever outbreaks with high numbers of infected livestock.

Symptomatology

Many different animal species are susceptible to rift valley fever virus, with disease ranging from subclinical illness to sudden death. The severity of the disease depends on the species and age of the animals, with young animals being more severely affected than adults. Sheep are most severely affected followed by goats, cattle and camels. Antibodies to Rift Valley fever virus have also been detected in many wild animals. Neutralizing antibodies have been detected in African buffalo, giraffe, black rhinoceros, impala and African elephant.

As in humans, the liver is the major site of viral replication in the various animal species. Lesions occur with elevated levels of liver enzymes. In severe courses, there is also a reduction in leukocytes. While hepatocytes and monocytes are the main target cells for rift valley fever virus, the virus is also distributed through the blood to other tissues.

Sheep are the most susceptible to the virus among livestock. The incubation period is 24 to 36 hours, followed by the following signs of illness: Fever, loss of appetite, reluctance to move, abdominal pain, and bloody diarrhea. Post-mortem analyses show multifocal liver necrosis and sometimes an enlarged spleen. After experimental infection, 20 to 30% of all adults die, whereas mortality in newborn lambs may reach 95 to 10 0%. Acutely infected pregnant animals abort with almost 100% probability.

Goats are also susceptible and undergo a similar disease course as sheep, although it may be more variable. Blood viral loads are less in experimental infection compared to sheep. In addition, goats often do not show fever.

In cattle, infection can often be asymptomatic in adults, but acute courses can occur with mortality ranging from 0 to 5%. Calves are more susceptible and the mortality rate is 10%.

Camels have been shown to play a role in rift valley fever epidemics in East Africa, Egypt and Mauritania. Adult camels are often subclinically infected, but sudden deaths, abortions and increased neonatal mortality have also been observed in association with Rift Valley fever virus infections.The following two live vaccines are available:

  1. Smithburn RVF vaccine: Based on a mosquito isolate (Uganda, 1948) and passaged over 200 times in mouse brains and subsequently propagated on baby hamster kidney (BHK) cells. Should not be used in pregnant animals.
  2. The so-called clone-13, which is based on a human isolate (1974) attenuated by a natural deletion of the NSs gene, is propagated in cell culture on Vero cells. This vaccine is currently being used in South Africa in sheep and cows (administered as a single dose).

There is also an inactivated vaccine that is based on field isolates from South Africa and Egypt and is produced in cell culture on BHK cells. Inactivation is achieved chemically by formalin, and aluminium hydroxide is used as an adjuvant. This vaccine requires a booster 3 to 6 months after the first vaccination and annual boosters thereafter.

Diagnostic

Direct virus detection by PCR or virus isolation:

  • In blood (spiked with anticoagulants) from live animals during the febrile phase of the disease.
  • In post-mortem tissue samples of approximately 1 mm3 from the liver, spleen or brain of affected animals or from abortions.

Virus detection by histopathological methods in combination with immunofluorescence staining in appropriate organs, such as liverDetection of antibodies.

  • ELISA
  • Serum neutralisation test (SNT)

Differential diagnosis: Infections with other pathogens leading to abortions (e.g. brucella, chlamydia, coxiella, leptospires) or other viral diseases such as bluetongue, plague of small ruminants and Schmallenberg virus. In endemic areas in Africa, outbreaks often occur together with Wesselsbron's disease.

Contact, Forms

Institute for Veterinary Investigations Mödling (National Reference Laboratory)Robert Koch-Gasse 172340 MödlingTel: +43 50 555-38112Fax: +43 50 555-38529E-Mail: vetmed.moedlingno@Spam@agesno.Spam.at

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