Updated 27 November 2015
Chikungunya is a viral disease transmitted by Aedes mosquitoes to humans. The word ‘chikungunya’ means 'that which bends up', an allusion to the posture of the suffering patients. The most common clinical form associates fever, arthralgia and rash. Recovery is the usual outcome but chronic arthritis is not rare. Diagnostic tests are available but there is no antiviral treatment or licensed vaccine. The disease is notifiable at EU level.
Chikungunya has caused numerous epidemics in Africa and Asia. In 2005-2006 a major outbreak occurred in the Indian Ocean. Imported cases were found in Asia, Australia, USA, Canada and continental Europe. In 2007, an outbreak of autochthonous chikungunya virus infections took place for the first time in Europe (Italy). In 2010 and 2014, autochthonous cases were reported in France. In December 2013, chikungunya emerged in the Caribbean and quickly spread in the Americas. Now the virus has spread to the whole (sub) tropical regions of America, Africa and Asia.
The risk of chikungunya spreading in EU is high due to importation through infected travellers, presence of competent vectors in many countries (particularly around the Mediterranean coast) and population susceptibility.
- The virus was first identified in Tanzania in 1953.
- Humans are the major source, or reservoir, of chikungunya virus. However, in Africa natural hosts of chikungunya virus are wild primates bitten by forest-dwelling Aedes mosquitoes.
- The virus is a single-stranded positive-sense RNA enveloped virus from the Togaviridae family, genus Alphavirus. The virus is a member of the Semliki Forest Virus serogroup that includes Ross River virus (Australia and Pacific), Mayaro (South America) and O’nyong-nyong virus (Africa).
- There are three major genetically distinct lineages of chikungunya virus. They were reflecting the geographical distribution (West Africa, East-Central-South Africa and Asia) until the spread of the East- Central-South African serotype to Asia in 2006 and the spread of the Asian type in to the Americas in 2013.
- The main vectors of the chikungunya virus are Ae. aegypti and Ae. albopictus mosquito species. During the 2005-2006 outbreak in La Reunion island an amino-acid change (A226V) in the E1 glycoprotein of East-Central-South Africa genotype chikungunya virus has been identified. This change induced a gain of fitness for dissemination by Ae. albopictus mosquitoes. Further mutations in E1 and E2 glycoproteins also modify mosquito infectivity.
Clinical features and sequelae
- A broad range of asymptomatic infection rates are seen, varying from 17% in La Réunion (2005-2006), 39% in Saint-Martin (2014) to more than 40% in Asia.
- The incubation period ranges from 1 to 12 days, with an average of 3–7 days.
- The disease is characterized by a sudden onset of fever, chills, headache, myalgia, nausea, photophobia, incapacitating joint pain and petechial or maculopapular rash.
- The acute phase lasts for about 10 days. The typical clinical sign of the diseases is arthralgia, usually symmetric, but neurological, haemorrhagic and ocular manifestations have also been described.
- The chronic phase of the disease, characterized by recurrent joint pain, affects a variable proportion (mainly 30-40%) of those infected. It can last for years in some cases.
- General complications are rare and include myocarditis, hepatitis and ocular and neurological disorders.
- Risk factors for more severe disease are: last weeks of pregnancy for the neonates exposed intrapartum, older age (> 65 years) and co-morbidities. In the elderly, arthralgia can evolve to a chronic rheumatoid arthritis syndrome. Meningoencephalitis affects primarily neonates.
- Despite it being considered as a non-fatal disease, deaths have been partly attributed to the virus. During the 2005-2006 outbreak in La Réunion the case fatality rate (CFR) potentially associated with chikungunya virus infection was 0,1% and increased markedly with age. Most of the deaths occurred in cases with underlying medical conditions. As of 13 February 2015, according to the Pan American Health Organization, at least 182 deaths out of nearly 1.2 million cases have been attributed to chikungunya virus in the Caribbean and other regions of the Americas (overall case fatality rate 0,02%).
- Chikungunya is spread by the bite of Aedes mosquitoes, primarily Aedes aegypti and also Aedes albopictus, two species which can also transmit other mosquito-borne viruses, including dengue virus. These mosquitoes are active during the day. Both species are found biting outdoors, but Aedes aegypti will also readily feed indoors.
- Ae. aegypti is not able to undergo winter diapause as eggs, and this therefore limits to some extent their ability to exploit more northerly temperate regions. However it may establish in regions of Europe showing a humid subtropical climate (parts of Mediterranean and Black Sea countries).
- The distribution of Ae. albopictus has expanded recently and this expansion is still ongoing. Native to Southeast Asia, it has colonised both tropical and temperate regions. Currently, it is established in at least 11 European countries, primarily along the Mediterranean coast (see updated information on the distribution of Aedes aegypti and Aedes albopictus in Europe).
- Given the chikungunya epidemics and the distribution of the vectors Ae. aegypti and Ae. albopictus, the risk of importation of the virus into new areas by infected travellers needs to be considered.
- The transmission usually occurs during or just after the hot rainy season, even though it may also occur during another period of the year.
- In humans, the viral load in the blood can be very high at the beginning of the illness and lasts 5-6 days (up to 10 days), allowing mosquitoes to feed and disseminate the virus.
- Mother-to-child transmission has also been reported in women who developed the disease within the final week prior to delivery. There are rare reports of spontaneous abortions following maternal chikungunya virus infection. There is no evidence that the virus is transmitted through breast milk.
- Once a person has recovered from chikungunya infection, he or she is likely to have a life-long immunity against subsequent chikungunya virus infections.
- Transmission of chikungunya virus through transfusion and transplantation has not been reported, although animal models using intravenous inoculation are able to transmit chikungunya virus. Limited data suggests that clinical manifestations may correlate with the dose of chikungunya virus in the inoculum.
- Chikungunya virus can be identified using nucleic acid/genomic amplification techniques or viral isolation during the first week of illness. Serological diagnosis can be performed by detection of specific IgM antibodies in serum specimen from day 4–5 after the onset of illness. Specific IgM can persist for many months, in particular in patients with long-lasting arthralgia.
- Serological cross-reactions between closely related alphaviruses have been reported.
Case Management and treatment
- Due to the absence of specific antiviral drugs, the treatment is symptomatic including non-salicylate analgesics and non-steroid anti-inflammatory therapy.
- The chikungunya virus is endemic in Africa, Southeast Asia, the Indian subcontinent, Pacific Region and most probably in the (sub) tropical regions of the Americas.
- Globally, large scaled outbreaks were reported in 2004-2007 from Kenya, Comoros islands, La Reunion, Mauritius, and then spread to various Indian states and South East Asia.
- Autochthonous transmission has occurred in Europe and the United States, where chikungunya virus is thought to have been imported by infected travellers returning from affected areas. However, in 2007 the first autochthonous outbreak occurred in Italy, with 217 laboratory-confirmed cases. This was the first outbreak reported in a non-tropical region where a competent vector for the chikungunya virus was present. In France, autochthonous cases linked to imported cases were detected in 2010 (two cases) and 2014 (11 cases).
- In December 2013, chikungunya emerged on the island of Saint Martin in the Caribbean and then quickly spread in the Americas. This was the first documented autochthonous transmission of chikungunya virus in the Americas.
- As of 13 February 2015, nearly 1.2 million suspected and confirmed cases of chikungunya virus infection have been reported in the Caribbean and other regions of the Americas. After the chikungunya outbreaks in the Indian Ocean in 2005–2006 and in Italy in 2007, ECDC established a network for arthropod vector surveillance for human public health in order to improve the surveillance of competent vectors for infectious diseases, and published guidelines for the surveillance of invasive mosquito species and areas at risk for chikungunya outbreaks, based on the current distribution of Aedes albopictus in mainland Europe and Ae. aegypti in Madeira.
PUBLIC HEALTH CONTROL MEASURES
- No vaccine or prophylactic drug is available.
- Integrated vector management program aiming to reduce mosquito vector density in a sustainable manner is of primary importance. Intersectoral collaboration and efficient public communication strategy to ensure community participation are required for sustainable vector control program.
- Activities supporting the reduction of mosquito breeding sites in outdoor/indoor areas by draining or discarding sources of standing water at the community level include:
- removal of all open containers with stagnant water in and surrounding houses on a regular basis (flower plates and pots, used tyres, tree-holes and rock pools), or, if that is not possible, treatment with larvicides),
- tight coverage of water containers, barrels, wells and water storage tanks,
- wide use of window/door screens by the population.
- Measures aiming to control larvae and adult mosquito vector population can be applied in an outbreak situation.
- In affected outbreak areas, elimination of adult mosquitoes through aerial spraying with insecticides can be considered.
- More information on mosquitoes can be found here: Aedes albopictus and Aedes aegypti.
INFECTION CONTROL, PERSONAL PROTECTION AND PREVENTION
- Prevention is also based on protection against mosquito bites. Aedes mosquitoes have diurnal biting activities in both indoor and outdoor environments. Therefore personal protection measures should be applied all day long and especially during the hours of highest mosquito activity (mid-morning, late afternoon to twilight).
- Personal protection measures to avoid mosquito bites should be applied when staying in risk areas by:
- using repellents and wearing long-sleeved shirts and long pants especially during the hours of highest mosquito activity,
- using long-lasting insecticidal treated mosquito bed nets which are essential in providing protection from mosquitos bites if the accommodations are not adequately screened or air conditioned,
- removing mosquito breeding sites in close outdoor/indoor premises.
- Repellent use must be strictly done in accordance with the instructions indicated on the product label. For newborn children under three months of age, repellents are not recommended.
- Travellers, especially children, pregnant women, and people with immune disorders or severe chronic illnesses, should consult their doctor or seek advice from a travel clinic to receive personalised recommendations on use of repellents and protection before travelling;
- Similar protective measures apply to a symptomatic patient in order to prevent transmitting the disease to non-infected mosquitoes.
- More information on mosquitoes can be found here: Aedes albopictus and Aedes aegypti.
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