Rift valley feverA92.4

The Rift Valley Fever virus was first isolated in 1931 by Daubney et al. as the causative agent of an animal disease from sheep in the Rift Valley in Kenya. Since then, numerous epizootics (epidemics in animals; subclinically infected camels) have occurred in Africa and countries in the Middle East, in which human infections occurred simultaneously.

Highly feverish, mostly flu-like or dengue-like viral infection of sheep, goats, camels and cattle, transmitted by arthropods but also by contact with infectious material, as a result of en- or epizootic biocycles (arbovirosis).

• Rift Valley Virus, genus Phlebovirus, family Bunyaviridae.
• There are 2 strains known: the classic Rift Valley Virus and the antigenically related, less virulent Zingavirus.

Vectors: Vectors of the Rifttal fever virus (RVF virus - RVFV - Bunyaviridae: Phlebovirus), are various Culex and Aedes mosquitoes. Rifttal fever epidemics often occur after rainfall or floods, which is explained by the hatching of infected eggs and a multiplication of the mosquitoes. During outbreaks, the virus circulates between mosquito and vertebrate host. Although the virus can infect different animal species, farm animals such as sheep, goats or cattle are the main hosts. An outbreak usually first manifests itself in the animals (enzootic hepatitis). Humans are infected either by mosquitoes or through contact with infected animals (i.e. blood and other body fluids), e.g. during slaughter or the disposal of dead animals. During the recent outbreaks in South Africa, mosquitoes played a minor role in transmission to humans. In South Africa, the main victims were farmers, farm workers and veterinarians with direct contact to animals. There is no reliable evidence of horizontal human-to-human transmission.

In animals: transmission by Culex, Mansonia and Aedes mosquitoes.

In humans: direct contact with organs and blood of sick animals or via aerosols from sick or dead sheep and cattle (farmers, butchers, veterinarians, etc. are at risk). Transmission by vectors such as mosquitoes and tabanids.

Direct damage to liver and endothelial cells (necroses of hepatocytes, toxic changes in renal tubules and spleen).

Genetic influence is discussed.

Changing severity due to virulence of certain strains and co-infection with schistosomiasis.

• Incubation period 3-7 days.
• Biphasic fever, severe course of disease: chills, retroorbital headache, joint and muscle pain, nausea, pharyngitis, conjunctivitis.
• Severe course:
• Haemorrhagic clinical picture: petechial haemorrhages, sclerenicterus, hepatitis, hyptonia, oliguria, severe gastrointestinal haemorrhages.
• Encephalitis: up to 12 days after fever drop meningism, motor failure, confusion, unconsciousness
• Ocular involvement: 1-3 weeks after the febrile illness, temporary blindness or blurred vision, loss of visual field, retinal vasculitis, bleeding, infiltrates, edema with retinal detachment.

Thrombocytopenia, elevated transaminases and elevated creatinine as signs of liver or kidney involvement.

Note: Viremia is highest in the first days of illness. The viral load is about 1000 times higher in lethal cases than in non-lethal cases and decreases only slightly before death.

If the prognosis is favourable, the virus titre drops rapidly and is below the detection limit of the PCR after 1-3 weeks. In mild cases, the viraemia may also be too low for PCR detection in the acute phase.

IgM and IgG antibodies occur very early - often within the first week - and are therefore particularly suitable for the acute diagnosis of mild courses. IgM antibodies persist for only a few months. In lethal courses of disease, antibodies are not always detectable. In endemic regions there is a high prevalence of IgG antibody carriers.

• During the fever phase: virus isolation from blood and pharyngeal fluid (cultivation)
• Virus detection by PCR
• Serology (immunofluorescence, haemagglutination inhibition tests).

• Recovery around day 10, slow convalescence. Passive immunity protects for several months. Immunity for many years.
• In hemorrhagic fever: 25% lethality.
• With ocular involvement: 50% permanent eye damage, sometimes total blindness.

• Inactivated vaccine after formalin inactivation (so far only for laboratory personnel, military and for epidemics): produced in USA, South Africa and Egypt, vaccination: 0, week 6-8 and month 6.
• Protection against aerosols and direct contact with infectious material.
• Mosquito control.

The last case of an infection with Rifttal fever diagnosed in Germany affected a 71-year-old woman at the beginning of 2009.

One of the patients referred by the RKI is a 50-year-old woman who was travelling in the coastal region of the Republic of South Africa from 17 March 2010 to 8 April 2010 as a member of a travel group and fell ill on 7 April 2010, one day before returning to Germany.

Starting from Port Elizabeth in the Eastern Cape Province, the group had travelled in rural areas along the coast of South Africa (Eastern Cape, Western Cape Provinces), visiting game reserves and mountain regions. During this time the travellers also encountered farm animals such as goats and cows. The group stayed exclusively in hotels or guesthouses (lodges). Towards the end of the trip the group also spent a few days in the centre of Cape Town (no excursions). According to the woman interviewed, all travellers were bitten by mosquitoes.

Warnings of the so-called Rift Valley Fever were not known to the group. So they did not protect themselves with long-sleeved clothing or long trousers, not even with chemical means to prevent mosquito bites. The patient had also not consulted a doctor before her trip about preventive measures for South Africa trips or received advice from one.

The acute disease of the woman was accompanied by fever (up to 39 °C), severe headache, extensive non-itching erythema on the upper and lower body, a pronounced conjunctivitis, bds. inguinal lymphadenitis and a papulo-vesiculous exanthema in the abdominal area.

Laboratory: Mild thrombocytopenia. Complications like meningitis or retinitis did not occur. An inpatient treatment was not necessary.

Detection of Rifttal fever virus specific IgM and IgG antibodies .

The disease was treated symptomatically and gradually disappeared within the next 3 weeks. However, the patient continued to complain of fatigue symptoms for several weeks.

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7. RKI (2010) Epidemiological Bulletin. No. 17