Chikungunya, also known as Chicken Guinea, is a rare form of viral infection caused by an alphavirus that is spread by the mosquitoes of genus Aedes i.e. Aedes Aegypti, Aedes Albopicticus (Tiger mosquito). The name of the disease is derived from the word ‘Swahili’, a language spoken in East Africa meaning ‘that which bends up’, reflecting the physique of a person suffering from the disease. Chikungunya virus is highly-infective and disabling. It is possible for a person to have Chikungunya and Dengue fever together at the same time because the infected Aedes mosquito can carry both the viruses.



  • Chikungunya is a viral disease transmitted to humans by infected mosquitoes. It causes fever and severe joint pain. Other symptoms include muscle pain, headache, nausea, fatigue and rash.
  • Joint pain is often debilitating and can vary in duration.
  • The disease shares some clinical signs with dengue, and can be misdiagnosed in areas where dengue is common.
  • There is no cure for the disease. Treatment is focused on relieving the symptoms.
  • The proximity of mosquito breeding sites to human habitation is a significant risk factor for chikungunya.
  • The disease occurs in Africa, Asia and the Indian subcontinent. In recent decades mosquito vectors of chikungunya have spread to Europe and the Americas. In 2007, disease transmission was reported for the first time in a localized outbreak in north-eastern Italy. Outbreaks have since been recorded in France and Croatia.



Chikungunya is an infection in humans caused by the chikungunya virus.

The chikungunya virus is present in Africa, southeast Asia, the Indian subcontinent and Indian Ocean islands, where a number of outbreaks have occurred.

Chikungunya virus is an alpha virus that belongs to the Togaviridae family. It is a single-stranded RNA virus and is approximately 11.8 kb long with a capsid and a phospholipid envelope. Phylogenetic analysis has revealed 3 distinct groups based on partial sequences of NS4 and E1 genes: (1) the West African, (2) the East-Central-South African (ECSA), and (3) the Asian.

Chikungunya virus is transmitted to humans through day-biting mosquitoes that belong to the Aedes genus. Being an arbovirus, the virus is maintained in the environment between humans or other animals and mosquitoes. Humans serve as major reservoirs during epidemics.

During inter-epidemic quiescence in Africa, the virus is thought to be maintained in an epizootic cycle that involves vertebrates such as monkeys, rodents, and birds. In Africa, the virus is maintained in a sylvatic cycle among wild primates, monkeys and, wild Aedes mosquitoes (Aedes furcifer, Aedes taylori, Aedes luteocephalus, Aedes africanus, Aedes neoafricanus). A sylvatic cycle has not yet been identified outside the African continent.

In Asia, the virus is maintained in an urban cycle involving Aedes aegypti mosquitoes and humans. The method of viral maintenance in the environment during the quiescent inter-epidemic periods in Asia remains unknown. Unlike its counterpart, the dengue virus, a transovarian transmission has not yet been reported, supporting the historical theory that the virus first originated in Africa and later spread to other countries in Asia. Historically, Chikungunya outbreaks are known to demonstrate a secular, cyclical, and seasonal trend.




Humans and other primates are the natural hosts for the chikungunya virus. The virus is spread to humans by the bite of an infected female Aedes species mosquito – Aedes aegypti or Aedes albopictus. These are the same tropical and sub-tropical mosquitoes that carry the dengue virus. They breed in or near human habitations and prefer to feed on humans during the daytime in shady areas, but may also bite early in the night.

In Australia, Aedes aegypti currently is found in north Queensland while Aedes albopictus is found in a few locations in the Torres Strait. Infections reported in Australia are from people who have travelled overseas to regions where the chikungunya virus is present.

To date chikungunya virus infection has not been transmitted by mosquitoes in Australia. However, since the mosquitoes capable of transmitting the infection are found in northern Australia there is the potential for this to occur.



Phylogenetic analysis has revealed that the Chikungunya virus genome has remained stable over the years since its first discovery in 1952. Comparison of two Asian Chikungunya virus strains that were isolated 10 years apart showed 99.4% identity. Most of the early strains isolated from the Reunion Island Chikungunya virus outbreak were similar to the ECSA cluster. However, the strains isolated from the 2006-2007 outbreak revealed an alanine to valine amino acid mutation at position 226 in the E1 glycoprotein. The presence of alanine (A226) denotes cholesterol-dependent growth and replication of Chikungunya virus in certain Aedes species.

This particular mutation raised considerable interest in the research field, as it resulted in cholesterol-independent growth and replication of Chikungunya virus and was exclusively seen in Chikungunya virus isolated from Aedes albopictus mosquitoes. This mutation was also associated with enhanced fitness in Chikungunya virus, enabling it to infect A albopictus mosquitoes and other species that normally lack cholesterol. This ability of the Chikungunya virus to adapt to a new species has significant implications with respect to the range of transmission and spread across the globe.

The above findings led experts to speculate that Chikungunya virus would no longer be restricted to the tropical countries but could spread to temperate regions, as A albopictus predominates in temperate zones where A aegypti is scarce (the Americas, Europe, China, Japan).



The exact pathophysiology of Chikungunya virus remains to be investigated. To date, most of the research in this field has been from the Indian subcontinent and other Asian countries.

Chikungunya virus infection has a clinical presentation that overlaps with that of Ross River virus infection (fever, rash, polyarthritis) and dengue fever virus transmitted by the same mosquitoes. Evaluation of the T-cell– and B-cell–mediated immunity has shed light on some possible mechanisms.

Using a murine model, Lum et al have shown that anti–Chikungunya virus antibodies were elicited early in the course of the illness and were directed against the C-terminus of the viral E2 glycoprotein. They showed that both natural and Chikungunya virus infection–induced specific antibodies were essential for controlling Chikungunya virus infections.

Waquier et al conducted a large ex vivo multiplex study of T-cell immunity and 50 cytokine, chemokine, and growth factor plasma profiles in 69 acutely infected patients from the Gabonese outbreak in 2007. They concluded that Chikungunya virus infection elicited strong innate immunity with an abundant production of proinflammatory markers and cytokines, including high levels of alpha interferon, interleukin (IL)–4, IL10, and gamma interferon. By flow cytometric analysis, the authors also demonstrated that humans show a CD8+ lymphocytic response in the early stages and a CD4+ predominant response in the later stages. Most importantly, the authors described a CD95-based apoptosis of CD4+ lymphocytes that could partially explain the lymphopenia in these patients. Hence, severe or chronic infections could be attributed to an absence or deregulation of one of these pathways.

The exact mechanism of entry of the virus into mammalian cells is under investigation.  Bernard et al evaluated this mechanism and found that Chikungunya virus enters mammalian epithelial cells via a clathrin-independent, Esp-15–dependent, dynamin 2–dependent route and requires an endocytic pathway in combination with other unknown pathways. The authors speculate that Chikungunya virus is capable of undergoing genetic drifts and could acquire alternate entry mechanisms.

Several murine models with Chikungunya virus–related joint and neurological diseases are being investigated. Other state-of-the-art in vivo imaging techniques using bioluminescence imaging with luciferase-tagged pathogens and intravital 2-photon imaging systems are being evaluated for study of Chikungunya infection’s chronic phase. Further research in this field would undoubtedly provide a better understanding of the in vivo interactions between Chikungunya virus and immune cells and shed light on the immunopathogenesis.



Numerous Chikungunya epidemics have been reported in several countries in Southern and South East Asia. Distinct strains of Chikungunya virus within varying transmission cycles have been reported from different locations. The African variant has managed to persist over the years with frequent outbreaks due to a sylvatic cycle maintained between monkeys and wild mosquitoes. Conversely, the Asian variant causes epidemics that are maintained by an urban cycle, characterized by long inter-epidemic quiescence for more than 10 years or so.

The first Asian epidemic was reported in Bangkok, Thailand, in 1958, continued until 1964, and reappeared after a hiatus in the mid-1970s and declined again in 1976. Major outbreaks were also reported from northwestern and southern parts of India, Sri Lanka, Myanmar, and Thailand in the early 1960s. The cases then declined before sporadic outbreaks were later reported in the Philippines and Indonesia in 1980s and Malaysia in the 1990s.

The next major outbreak occurred in 2001 on islands in the Indian Ocean (Mauritius, Mayotte, Madagascar, Reunion Island). The most severe Chikungunya fever outbreak was reported in 2006 on Reunion Island, where one-third of the population was infected, resulting in 237 deaths. Around the same time, an historical outbreak on the Indian subcontinent involved 1.42 million people, with high morbidity rates.

By 2007, the disease was no longer considered a tropical illness, as it had spread to several nontropical and temperate areas, including Singapore.

According to figures from 2013-2014 from the Centers for Disease Control and Prevention (CDC), European Center for Disease Prevention and Control (ECDC), and the Pan American Health Organization (PAHO), several imported cases of travel-related Chikungunya fever have been reported in the United States, Caribbean islands, Britain, France, Germany, Sweden, Portugal, Canary Islands, and the archipelagos off the coast of Western Africa.


CDC update

Many travel-related cases of Chikungunya infection have been imported into the United States since 2006. As of December 2014, a total of 1,938 travel-associated cases from 47 states and 2 US territories (Puerto Rico, Virgin Islands) have been reported.

The first case of local transmission to a person who had not traveled outside the United States was reported in July 2014, which was the first documented case of mosquitoes in the United States spreading the illness to a nontraveler. As of December 2014, a total of 11 locally transmitted cases have been reported in the United States, all in Florida.

In addition, 3402 locally mosquito-transmitted cases in Puerto Rico and 86 cases in the Virgin Islands have been reported. However, a recent study by the Puerto Rico Department of Health (PRDH) and the CDC shows that cases are underreported in Puerto Rico. From June 20 to August 19, 2014, The PRDH and CDC collected passive surveillance data in 250 participants, 70 (28%) of whom tested positive for past or current chikungunya virus infection. Only two of 25 participants (8%) with chikungunya infection who sought care had been reported to health authorities.

These cases illustrate the magnitude of the global spread of Chikungunya infection. They also emphasize the need to maintain efficient surveillance networks and implementation of adequate prevention measures, both at the personal and community level, to contain the infection and to prevent outbreaks.



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.



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.



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-methylpropylester). 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 reportedto 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.

The decreasing trend continues in 2016, with about 31 000 cases reported to PAHO as of 18 March 2016, representing a 5-fold decrease compared to the same period in 2015. Despite this trend, chikungunya remains a threat for the region with Argentina recently reporting its first chikungunya outbreak.