Rift Valley Fever

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Spread of Rift Valley fever according to data from the CDC:
  • Countries with endemic occurrence and relevant disease outbreaks: Gambia , Senegal , Mauritania , Namibia , South Africa , Mozambique , Zimbabwe , Zambia , Kenya , Sudan , Egypt , Madagascar , Saudi Arabia , Yemen
  • Countries with few cases of disease, sporadic isolation of the pathogen or serological evidence for the infection: Botswana , Angola , Democratic Republic of the Congo , Republic of the Congo , Gabon , Cameroon , Nigeria , Central African Republic , Chad , Niger , Burkina Faso , Mali , Guinea , Tanzania , Malawi , Uganda , Ethiopia , Somalia
  • Classification according to ICD-10
    A92.4 Rift Valley Fever
    ICD-10 online (WHO version 2019)

    The Rift Valley fever ( English Rift valley fever , RVF) is a by phleboviruses ( Family Phenuiviridae ) evoked haemorrhagic fever in ruminants . The illness can cause a flu-like illness in humans , which can rarely be fatal. The Rift Valley fever is therefore a zoonosis . It is notifiable.

    Occurrence

    Rift valley fever was first described as a disease in the valley of the same name ( Rift Valley ) in Kenya in 1913. 1931 there was a first major epidemic and since then the disease has throughout Africa south of the Sahara spread. When it first appeared on the Arabian Peninsula in 2000, more than 160 people died.

    The disease has not yet been observed in Europe.

    The World Health Organization provides information on current cases .

    Pathogen

    Rift Valley Fever Virus
    Rift Valley fever tissue.jpg

    Rift valley fever viruses under the electron microscope (source: CDC )

    Systematics
    Classification : Viruses
    Area : Riboviria
    Empire : Orthornavirae
    Phylum : Negarnaviricota
    Subphylum : Polyploviricotina
    Class : Ellioviricetes
    Order : Bunyavirales
    Family : Phenuiviridae
    Genre : Phlebovirus
    Type : Rift Valley Fever Virus
    Taxonomic characteristics
    Genome : (-) ss RNA segmented
    Baltimore : Group 5
    Symmetry : helical
    Cover : available
    Scientific name
    Rift Valley fever phlebovirus
    Short name
    RVFV
    Left
    Rift Valley fever viruses in the tissue (detail enlargement)

    The causative agents of Rift Valley fever are viruses of the species Rift Valley fever phlebovirus (RVFV, Rift Valley Fever Virus ) from the genus Phlebovirus of the family Phenuiviridae in the order Bunyavirales . These are single-stranded RNA - viruses . Your genome is segmented into three parts (tripartite). While it is commonly referred to as negative polarity classified Indeed, the situation is complicated, however: The L and M segment have both negative polarity ( English negative-sense ), but the S-segment (and thus the entire genome) is ambisense . The three genome segments code for 6 main proteins :

    As with all bunyaviruses, the virus particles ( virions ) of RVFV have an outer lipid envelope (with the two glycoproteins - G (N) and G (C)). These are required for entry into the host cell, because they fuse the virus envelope with its endosomal membrane and thus bring the viral genome into the host cell.

    The G (C) protein has a structure like the class II membrane fusion proteins of the flaviviruses and alphaviruses . This structural similarity suggests a possible common ancestry.

    The virus originally caused a ruminant disease ( sheep , goats , cattle , camels , antelopes ), but it can also be transmitted to humans by various mosquitoes (especially Culex and Aedes species).

    Clinical picture in ruminants

    In young animals the disease is mostly dramatic with high fever , anorexia , weakness and ends in 70% of the animals fatal. Occasionally, nasal discharge and bloody diarrhea also occur. Adult animals show less pronounced courses. In pregnant animals, it usually comes to miscarriage . The disease is milder in cattle than in sheep.

    Severe necrosis of the liver is typical of the disease.

    Clinic in humans

    Infections in humans mostly occur in connection with animal epidemics. The virus can be transmitted both through the air and through direct contact with infected animals, for example when slaughtered. The incubation period is between three and 12 days; Serological determination of the virus is possible from the fourth day of illness .

    Symptoms of the disease include high fever , headache and muscle pain, and rarely hepatitis . About 1% of patients develop a pronounced hemorrhagic fever with hepatitis and often fatal outcome after a few days . After the fever has subsided, some patients develop a usually fatal inflammation of the meninges (meningitis) or inflammation of the retina (retinitis), which can lead to blindness .

    A curative treatment option for Rift Valley fever does not yet exist (possibly ribavirin , which is effective in animal studies), so preventive protection ( exposure prophylaxis ) against insect bites in endemic areas is urgently recommended. Effective and well-tolerated vaccines are available for both humans and animals. However, they are not yet approved in Germany.

    Combat

    According to the IfSG , illnesses and deaths from Rift Valley fever must be reported. According to the ordinance on notifiable animal diseases (TierSeuchAnzV), a disease in animals is a notifiable animal disease .

    Web links

    Individual evidence

    1. Arabian Peninsula Primed for Rift Valley Fever NASA Earthobservatory (English)
    2. ^ WHO: Global Alert and Response - Rift Valley fever
    3. ICTV Master Species List 2018b v1 MSL # 34, Feb. 2019
    4. a b ICTV: ICTV Taxonomy history: Akabane orthobunyavirus , EC 51, Berlin, Germany, July 2019; Email ratification March 2020 (MSL # 35)
    5. a b ViralZone: Phlebovirus . Retrieved September 14, 2016.
    6. ^ Dessau M, Modis Y: Crystal structure of glycoprotein C from Rift Valley fever virus . In: Proceedings of the National Academy of Sciences of the United States of America . 110, No. 5, January 2013, pp. 1696-701. bibcode : 2013PNAS..110.1696D . doi : 10.1073 / pnas.1217780110 . PMID 23319635 . PMC 3562824 (free full text).
    7. Robert Koch Institute: Epidemiological Bulletin No. 3/2007 of January 19, 2007, p. 19