Chikungunya is generally spread through bites from
Aedes aegypti mosquitoes, but the
chikungunya virus strains in the 2005-2006 Reunion Island outbreak contained a mutation that facilitated transmission by
Aedes albopictus (Tiger mosquito). Enhanced
transmission of chikungunya virus by
Aedes albopictus could mean an increased risk for chikungunya outbreaks in other areas where the Asian tiger mosquito is present. A recent epidemic in Italy was likely perpetuated by
Aedes albopictus. Currently, chikungunya fever has been identified in nearly 40 countries (see figure 1).
Figure 1: Worldwide distribution of chikungunya virus in 2010. Both green and orange indicate countries where cases of chikungunya fever have been documented, and orange indicates countries where chikungunya virus has been endemic or epidemic. Figure is modified, with permission from Schwartz O and Albert ML. in Nat Rev Microbiol. 2010 Jul;8(7):491
Period before 2004
Chikungunya likely originated in Africa (see also section History of Chikungunya), where the virus is spread via a sylvatic cycle in which the virus largely resides in other primates in between human outbreaks. In 1952, the first outbreak of chikungunya was reported in the Makonde Plateau. The first significant urban outbreaks of chikungunya were reported in the early 1960s in Bangkok and from 1963 through 1973 in India. The chikungunya virus was detected mainly in the Indian cities Calcutta, Maharashtra and Yellore. Minor outbreaks periodically occurred over the next 30 years, but no major outbreaks were recorded. In 1969, chikungunya was detected in Sri Lanka and in 1975 the disease was reported in Vietnam and Myanmar. Another outbreak was reported in Indonesia in 1982.
Period 2004-2005
In 2004, Kenya experienced two major outbreaks of chikungunya. This outbreak started a four year period in which the virus spread throughout numerous islands of the Indian Ocean, India and parts of Southeast Asia. The first outbreak in Lamu, Kenya resulted in an estimated 13,500 cases, which represents more than 70% of the population of the island. The second outbreak occurred in the city of Mombasa a few months after the first cases in Lamu. By January 2005, an outbreak of chikungunya was detected in the Comoros. Over the next several months, the outbreak on the main island led to around 225,000 infections with chikungunya. Entomological investigations detected that Aedes aegypti mosquitoes were carriers of the chikungunya virus.
Period 2006 (Outbreak in La Reunion)
Movements of people and goods from the main land led to the introduction of chikungunya into La Reunion island, which is part of France. This island in the Indian Ocean has a population of roughly 785,000 inhabitants. The virus was first detected in the spring of 2005 with only a limited number of cases until January 2006, when there was a substantial increase in the number of cases. Strikingly, an estimated 300,000 infections were reported with a peak of over 40,000 new cases weekly. More than 250 people were killed by the chikungunya virus.
Mutation of the virus
The primary mosquito responsible for the transmission of chikungunya virus was Aedes aegypti. However, these mosquitoes were present in only limited numbers on the island of La Reunion due to massive dichlorodiphenyltrichloroethane usage. The Aedes albopictus mosquito was present and this resulted in an ecological pressure. Studies revealed that the chikungunya virus in La Reunion had a single point mutation in the E1 glycoprotein that increased infectivity in Aedes albopictus. There was a replacement of alanine at position 226 with valine (E1-A226V). Within a year, the mutated virus was present in La Reunion Island, and Aedes albopictus apparently vectored the large epidemic infecting one third of the Island’s population. The E1-A226V mutation also enabled an increase in infectivity of Aedes albopictus when compared to its infectivity of Aedes aegypti. Aedes albopictus has become the new preferred and more lethal vector for chikungunya virus.
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Figure 2: Chikungunya and Dengue virus in the Indian Ocean, Status as of 17 March 2006. Dark red indicates countries wth occurence of dengue and/or chikungunya. Light red are affected areas. Source: WHO
Period after 2006
Other outbreaks of chikungunya fever subsequently occurred in other Indian Ocean countries, including Gabon, Madagascar, the Maldives, Mauritius, Mayotte, and the Seychelles (see figure 2). The epidemic also spread to India, where it is estimated that more than 1.5 million people were infected between February and October 2006. During this period, the WHO Regional Office for South-East Asia has reported 151 districts in 8 states/provinces of India affected by chikungunya fever. The affected states are Andhra Pradesh, Andaman and Nicobar Islands, Tamil Nadu, Karnataka, Maharashtra, Gujarat, Madhya Pradesh, Kerala and Delhi. The persistence number of infections in India is probably attributable to a large amount of immunologically naive people, who help sustain viral transmission. Several other countries in South-East Asia were also affected.
From India the virus spread further into Europe and the United States, where it is thought to have been imported by infected travelers returning from areas with high incidence rates. During 2005-2006 twelve cases of chikungunya fever were diagnosed in the United States. Between July and September 2007 the virus caused the first autochthonous epidemic outbreak in the north-east of Italy, with more than 200 human infections. Since 2008, infections were also reported from Singapore, Malaysia, Thailand and Australia.