Chikungunya is a mosquito-borne viral disease first described during an outbreak in southern Tanzania in 1952. It is an RNA virus that belongs to the alphavirus genus of the family Togaviridae. The name “chikungunya” derives from a word in the Kimakonde language, meaning “to become contorted”, and describes the stooped appearance of sufferers with joint pain (arthralgia).
Signs and symptoms
Chikungunya is characterized by an abrupt onset of fever frequently accompanied by joint pain. Other common signs and symptoms include muscle pain, headache, nausea, fatigue and rash. The joint pain is often very debilitating, but usually lasts for a few days or may be prolonged to weeks. Hence the virus can cause acute, subacute or chronic disease.
Most patients recover fully, but in some cases joint pain may persist for several months, or even years. Occasional cases of eye, neurological and heart complications have been reported, as well as gastrointestinal complaints. Serious complications are not common, but in older people, the disease can contribute to the cause of death. Often symptoms in infected individuals are mild and the infection may go unrecognized, or be misdiagnosed in areas where dengue occurs.
Chikungunya has been identified in over 60 countries in Asia, Africa, Europe and the Americas. The virus is transmitted from human to human by the bites of infected female mosquitoes. Most commonly, the mosquitoes involved are Aedes aegypti and Aedes albopictus, two species which can also transmit other mosquito-borne viruses, including dengue. These mosquitoes can be found biting throughout daylight hours, though there may be peaks of activity in the early morning and late afternoon. Both species are found biting outdoors, but Ae. aegypti will also readily feed indoors. After the bite of an infected mosquito, onset of illness occurs usually between 4 and 8 days but can range from 2 to 12 days.
Several methods can be used for diagnosis. Serological tests, such as enzyme-linked immunosorbent assays (ELISA), may confirm the presence of IgM and IgG anti-chikungunya antibodies. IgM antibody levels are highest 3 to 5 weeks after the onset of illness and persist for about 2 months. Samples collected during the first week after the onset of symptoms should be tested by both serological and virological methods (RT-PCR). The virus may be isolated from the blood during the first few days of infection. Various reverse transcriptase–polymerase chain reaction (RT–PCR) methods are available but are of variable sensitivity. Some are suited to clinical diagnosis. RT–PCR products from clinical samples may also be used for genotyping of the virus, allowing comparisons with virus samples from various geographical sources.
There is no specific antiviral drug treatment for chikungunya. Treatment is directed primarily at relieving the symptoms, including the joint pain using anti-pyretics, optimal analgesics and fluids. There is no commercial chikungunya vaccine.
Prevention and control
The proximity of mosquito vector breeding sites to human habitation is a significant risk factor for chikungunya as well as for other diseases that these species transmit. Prevention and control relies heavily on reducing the number of natural and artificial water-filled container habitats that support breeding of the mosquitoes. This requires mobilization of affected communities. During outbreaks, insecticides may be sprayed to kill flying mosquitoes, applied to surfaces in and around containers where the mosquitoes land, and used to treat water in containers to kill the immature larvae. For protection during outbreaks of chikungunya, clothing which minimizes skin exposure to the day-biting vectors is advised. Repellents can be applied to exposed skin or to clothing in strict accordance with product label instructions. Repellents should contain DEET (N, N-diethyl-3-methylbenzamide), IR3535 (3-[N acetyl N-butyl]-aminopropionic acid ethyl ester) or icaridin (1-piperidinecarboxylic acid, 2-(2-hydroxyethyl)-1 ethylpropylester). For those who sleep during the daytime, particularly young children, or sick or older people, insecticide-treated mosquito nets afford good protection. Mosquito coils or other insecticide vaporizers may also reduce indoor biting. Basic precautions should be taken by people travelling to risk areas and these include use of repellents, wearing long sleeves and pants and ensuring rooms are fitted with screens to prevent mosquitoes from entering.
Chikungunya occurs in Africa, Asia and the Indian subcontinent. Human infections in Africa have been at relatively low levels for a number of years, but in 1999–2000 there was a large outbreak in the Democratic Republic of the Congo, and in 2007 there was an outbreak in Gabon. Starting in February 2005, a major outbreak of chikungunya occurred in islands of the Indian Ocean. A large number of imported cases in Europe were associated with this outbreak, mostly in 2006 when the Indian Ocean epidemic was at its peak. A large outbreak of chikungunya in India occurred in 2006 and 2007. Several other countries in South-East Asia were also affected. Since 2005, India, Indonesia, Maldives, Myanmar and Thailand have reported over 1.9 million cases. In 2007 transmission was reported for the first time in Europe, in a localized outbreak in north-eastern Italy. There were 197 cases recorded during this outbreak and it confirmed that mosquito-borne outbreaks by Ae. Albopictus are plausible in Europe. In December 2013, France reported 2 laboratory-confirmed autochthonous cases in the French part of the Caribbean island of St Martin. Since then, local transmission has been confirmed in over 43 countries and territories in the WHO Region of the Americas. This is the first documented outbreak of chikungunya with autochthonous transmission in the Americas. As of April 2015, over 1 379 788 suspected cases of Chikungunya have been recorded in the Caribbean islands, Latin American countries, and the United States of America. 191 deaths have also been attributed to this disease during the same period. Canada, Mexico and USA have also recorded imported cases. On 21 October 2014, France confirmed 4 cases of locally-acquired chikungunya infection in Montpellier, France. In late 2014, outbreaks were reported in the Pacific islands. Currently chikungunya outbreak is ongoing in Cook Islands and Marshall Islands, while the number of cases in American Samoa, French Polynesia, Kiribati and Samoa has reduced. WHO responded to small outbreaks of chikungunya in late 2015 in the city of Dakar, Senegal, and the state of Punjab, India. In the Americas in 2015, 693 489 suspected cases and 37480 confirmed cases of chikungunya were reported to the Pan American Health Organization (PAHO) regional office, of which Colombia bore the biggest burden with 356 079 suspected cases. This was less than in 2014 when more than 1 million suspected cases were reported in the same region. In 2016 there was a total of 349 936 suspected and 146 914 laboratory confirmed cases reported to the PAHO regional office, half the burden compared to the previous year. Countries reporting most cases were Brazil (265 000 suspected cases), Bolivia and Colombia (19 000 suspected cases, respectively). 2016 is the first time that autochthonous transmission of chikungunya was reported in Argentina following an outbreak of more than 1 000 suspected cases. In the African region, Kenya reported an outbreak of chikungunya resulting in more than 1700 suspected cases. In 2017, Pakistan continues to respond to an outbreak which started in 2016.
More about disease vectors
Both Ae. aegypti and Ae. albopictus have been implicated in large outbreaks of chikungunya. Whereas Ae. aegypti is confined within the tropics and sub-tropics, Ae. albopictus also occurs in temperate and even cold temperate regions. In recent decades Ae. albopictus has spread from Asia to become established in areas of Africa, Europe and the Americas. The species Ae. albopictus thrives in a wider range of water-filled breeding sites than Ae. aegypti, including coconut husks, cocoa pods, bamboo stumps, tree holes and rock pools, in addition to artificial containers such as vehicle tyres and saucers beneath plant pots. This diversity of habitats explains the abundance of Ae. albopictus in rural as well as peri-urban areas and shady city parks. Ae. aegypti is more closely associated with human habitation and uses indoor breeding sites, including flower vases, water storage vessels and concrete water tanks in bathrooms, as well as the same artificial outdoor habitats as Ae. albopictus. In Africa several other mosquito vectors have been implicated in disease transmission, including species of the A. furcifer-taylori group and A. luteocephalus. There is evidence that some animals, including non-primates, rodents, birds and small mammals, may act as reservoirs.