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Resurgence of chikungunya
Transactions of the Royal Society of Tropical Medicine and Hygiene (2008) 102, 308—309
available at www.sciencedirect.com
journal homepage: www.elsevierhealth.com/journals/trst
MINI-REVIEW
Resurgence of chikungunya Harold Townson a,∗, Michael B. Nathan b a
Vector Group, Liverpool School of Tropical Medicine, Pembroke Place, Liverpool L3 5QA, UK Vector Ecology and Management Team, Department of Control of Neglected Tropical Diseases, World Health Organization, Geneva, Switzerland Available online 21 February 2008
b
KEYWORDS Chikungunya; Aedes aegypti; Aedes albopictus; Arboviruses; Prevention; Control
Summary Chikungunya, an arboviral disease transmitted by Aedes mosquitoes, has recently increased dramatically in incidence and geographic extent. Large outbreaks have affected islands of the Indian Ocean, India and other parts of South and Southeast Asia, Africa and most recently Italy. International travellers have disseminated new strains of the virus, some into regions from which chikungunya has hitherto been absent. In parallel, over the past 30 years international trade has resulted in the spread of A. albopictus from its original range in Asia, to all continents but Antarctica, thereby extending the geographic area over which transmission can occur. © 2007 Royal Society of Tropical Medicine and Hygiene. Published by Elsevier Ltd. All rights reserved.
Chikungunya, a mosquito-borne disease first described from Tanzania in 1952, is caused by an alphavirus of the family Togaviridae. The principal vectors during outbreaks are the day-biting mosquitoes Aedes aegypti and A. albopictus. Chikungunya usually produces a transient illness often confused with dengue; symptoms include fever, headache, polyarthralgia, myalgia and rash. Although serious complications are uncommon, the arthralgia is incapacitating and may persist for months. Not all those infected develop overt illness. Laboratory diagnosis is commonly based on detection of virus-specific antibodies, but RT-PCR to detect viral RNA is more sensitive. In the absence of serological screening, a diagnosis of chikungunya is often missed. There is no vaccine available for public health use. Treatment is symptomatic and supportive: ensuring adequate fluid intake, maintaining electrolyte balance and providing relief from polyarthralgia (Mohan, 2006).
∗
Corresponding author. Tel.: +44 151 705 3124. E-mail address: [email protected] (H. Townson)
Chikungunya circulates throughout much of sub-Saharan Africa in a sylvatic cycle involving primates and, typically, forest-dwelling species of Aedes (McIntosh and Gear, 1981). Since the 1960s, there have been periodic outbreaks in Africa and Asia, involving thousands of people, interspersed by periods of low activity. In February 2005, a major outbreak commenced in islands of the western Indian Ocean. By June 2006 there had been an estimated 266 000 cases in La R´ eunion, roughly one-third of the population. The virus belongs to the East Africa lineage, and A. albopictus appears to have been the sole vector. Shortly after the chikungunya virus reached La R´ eunion, a mutation occurred that is thought to have increased transmission by A. albopictus (Schuffenecker et al., 2006). If this hypothesis were confirmed, it could explain the subsequent rapid spread of chikungunya. Subsequently in 2006, an outbreak developed in India, with over 1.42 million officially reported cases by October 2007 and attack rates up to 45%. The viral strain was of the same lineage as that in the Indian Ocean islands, whereas previous outbreaks in India have involved an Asian genotype (Dash et al., 2007). The outbreak was generally associated
0035-9203/$ — see front matter © 2007 Royal Society of Tropical Medicine and Hygiene. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.trstmh.2007.11.013
Resurgence of chikungunya with high densities of A. aegypti, but in Kerala A. albopictus was identified as the primary vector. There were outbreaks elsewhere in South Asia in 2006, including Sri Lanka, and Indonesia reported 15 207 cases between 2001 and 2007. Aedes albopictus was first found in Gabon in late 2006, followed by a large outbreak of chikungunya. By June 2007, 17 618 cases had been reported, with 808 people hospitalized. The virus was isolated from A. albopictus but not from A. aegypti. Associated with the Indian Ocean islands outbreak, there were over 800 imported cases of chikungunya in Europe and nine in the Caribbean, mostly among returning tourists. In the United States there were 37 confirmed cases with onset in 2006, mainly in travellers returning from India. Large areas of the Americas are potentially vulnerable to chikungunya, owing to the abundance of both A. albopictus and A. aegypti. In August 2007, the first indigenous transmission of chikungunya in Europe was reported from a rural area in Emilia-Romagna, Italy. The presumed index case returned from Kerala in mid-June. By the end of September 2007, 292 suspected cases had been identified and the virus was isolated from local A. albopictus, a mosquito that is now widespread in Italy following its accidental importation as eggs in used tyres (European Centre for Disease Prevention and Control, 2007). Whereas A. aegypti is confined to the tropics and subtropics, A. albopictus also occurs extensively in temperate regions, thereby extending the geographical range over which chikungunya transmission may occur. Both species have drought-resistant eggs that remain viable over many weeks. A key factor in the increasing range and prevalence of chikungunya is the spread of A. albopictus resulting from the globalization of trade, particularly the transportation of used tyres. Both species are competent vectors of other arboviruses, including dengue. In areas at high risk of the introduction of A. albopictus, good vector surveillance is required to ensure that new foci are eliminated before they become well established. Aedes albopictus exploits a wider range of larval habitats, both natural and artificial, than does A. aegypti, explaining its abundance in rural areas as well as parks and suburbs. Aedes aegypti is more closely associated with human habitation, breeding indoors and outdoors in artificial habitats. To prevent chikungunya, a reduction in the number of water-filled containers in and around the home is an important public-
309 health priority. Used-tyre dumps enable large-scale breeding of Aedes, and recycling programmes for tyres should be encouraged. Once outbreaks occur, communities should be mobilized to eliminate breeding sites. Effective vector control also requires the application of insecticides as space sprays, as residual applications on surfaces in and around container habitats where mosquitoes alight, including tyre dumps, and as larvicides to kill the immature stages. Viraemic patients should be nursed in screened wards or under mosquito nets in hospital or at home. The potential risks of transmission through donation of blood or organs must also be considered. For individual protection, clothing that minimizes skin exposure to the day-biting vectors is advised, as are repellents that can be applied to exposed skin or to clothing. Insecticide-treated mosquito nets afford good protection for those who sleep during the day, particularly young children. Funding: None. Conflicts of interest: None declared. Ethical approval: Not required.
References Dash, P.K., Parida, M.M., Santhosh, S.R., Verma, S.K., Tripathi, N.K., Ambuj, Saxena, P., Gupta, N., Chaudhary, M., Pradeep Babu, J., 2007. East Central South African genotype as the causative agent in reemergence of chikungunya outbreak in India. Vector Borne Zoonotic Dis. 7, 519—528. European Centre for Disease Prevention and Control, 2007. Mission Report. Chikungunya in Italy: Joint ECDC/WHO visit for a European risk assessment; 17—21 September 2007. http://www.ecdc.eu.int/Publications/Technicalreports.html [accessed November 2007]. McIntosh, B.M., Gear, J.H.S., 1981. Arboviral zoonoses in southern Africa: Chikungunya fever, in: Steele, J.H., Beran, G.W. (Eds), Section B: Viral Zoonoses. CRC Handbook Series in Zoonoses. CRC Press, Boca Raton, FL, pp. 217—220. Mohan, A., 2006. Chikungunya fever: clinical manifestations and management. Indian J. Med. Res. 124, 471—474. Schuffenecker, I., Iteman, I., Michault, A., Murri, S., Frangeul, L., Vaney, M.-C., Lavenir, R., Pardigon, N., Reynes, J.-M., Pettinelli, F., 2006. Genome microevolution of chikungunya viruses causing the Indian Ocean outbreak. PLoS Med. 3, e263.
available at www.sciencedirect.com
journal homepage: www.elsevierhealth.com/journals/trst
MINI-REVIEW
Resurgence of chikungunya Harold Townson a,∗, Michael B. Nathan b a
Vector Group, Liverpool School of Tropical Medicine, Pembroke Place, Liverpool L3 5QA, UK Vector Ecology and Management Team, Department of Control of Neglected Tropical Diseases, World Health Organization, Geneva, Switzerland Available online 21 February 2008
b
KEYWORDS Chikungunya; Aedes aegypti; Aedes albopictus; Arboviruses; Prevention; Control
Summary Chikungunya, an arboviral disease transmitted by Aedes mosquitoes, has recently increased dramatically in incidence and geographic extent. Large outbreaks have affected islands of the Indian Ocean, India and other parts of South and Southeast Asia, Africa and most recently Italy. International travellers have disseminated new strains of the virus, some into regions from which chikungunya has hitherto been absent. In parallel, over the past 30 years international trade has resulted in the spread of A. albopictus from its original range in Asia, to all continents but Antarctica, thereby extending the geographic area over which transmission can occur. © 2007 Royal Society of Tropical Medicine and Hygiene. Published by Elsevier Ltd. All rights reserved.
Chikungunya, a mosquito-borne disease first described from Tanzania in 1952, is caused by an alphavirus of the family Togaviridae. The principal vectors during outbreaks are the day-biting mosquitoes Aedes aegypti and A. albopictus. Chikungunya usually produces a transient illness often confused with dengue; symptoms include fever, headache, polyarthralgia, myalgia and rash. Although serious complications are uncommon, the arthralgia is incapacitating and may persist for months. Not all those infected develop overt illness. Laboratory diagnosis is commonly based on detection of virus-specific antibodies, but RT-PCR to detect viral RNA is more sensitive. In the absence of serological screening, a diagnosis of chikungunya is often missed. There is no vaccine available for public health use. Treatment is symptomatic and supportive: ensuring adequate fluid intake, maintaining electrolyte balance and providing relief from polyarthralgia (Mohan, 2006).
∗
Corresponding author. Tel.: +44 151 705 3124. E-mail address: [email protected] (H. Townson)
Chikungunya circulates throughout much of sub-Saharan Africa in a sylvatic cycle involving primates and, typically, forest-dwelling species of Aedes (McIntosh and Gear, 1981). Since the 1960s, there have been periodic outbreaks in Africa and Asia, involving thousands of people, interspersed by periods of low activity. In February 2005, a major outbreak commenced in islands of the western Indian Ocean. By June 2006 there had been an estimated 266 000 cases in La R´ eunion, roughly one-third of the population. The virus belongs to the East Africa lineage, and A. albopictus appears to have been the sole vector. Shortly after the chikungunya virus reached La R´ eunion, a mutation occurred that is thought to have increased transmission by A. albopictus (Schuffenecker et al., 2006). If this hypothesis were confirmed, it could explain the subsequent rapid spread of chikungunya. Subsequently in 2006, an outbreak developed in India, with over 1.42 million officially reported cases by October 2007 and attack rates up to 45%. The viral strain was of the same lineage as that in the Indian Ocean islands, whereas previous outbreaks in India have involved an Asian genotype (Dash et al., 2007). The outbreak was generally associated
0035-9203/$ — see front matter © 2007 Royal Society of Tropical Medicine and Hygiene. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.trstmh.2007.11.013
Resurgence of chikungunya with high densities of A. aegypti, but in Kerala A. albopictus was identified as the primary vector. There were outbreaks elsewhere in South Asia in 2006, including Sri Lanka, and Indonesia reported 15 207 cases between 2001 and 2007. Aedes albopictus was first found in Gabon in late 2006, followed by a large outbreak of chikungunya. By June 2007, 17 618 cases had been reported, with 808 people hospitalized. The virus was isolated from A. albopictus but not from A. aegypti. Associated with the Indian Ocean islands outbreak, there were over 800 imported cases of chikungunya in Europe and nine in the Caribbean, mostly among returning tourists. In the United States there were 37 confirmed cases with onset in 2006, mainly in travellers returning from India. Large areas of the Americas are potentially vulnerable to chikungunya, owing to the abundance of both A. albopictus and A. aegypti. In August 2007, the first indigenous transmission of chikungunya in Europe was reported from a rural area in Emilia-Romagna, Italy. The presumed index case returned from Kerala in mid-June. By the end of September 2007, 292 suspected cases had been identified and the virus was isolated from local A. albopictus, a mosquito that is now widespread in Italy following its accidental importation as eggs in used tyres (European Centre for Disease Prevention and Control, 2007). Whereas A. aegypti is confined to the tropics and subtropics, A. albopictus also occurs extensively in temperate regions, thereby extending the geographical range over which chikungunya transmission may occur. Both species have drought-resistant eggs that remain viable over many weeks. A key factor in the increasing range and prevalence of chikungunya is the spread of A. albopictus resulting from the globalization of trade, particularly the transportation of used tyres. Both species are competent vectors of other arboviruses, including dengue. In areas at high risk of the introduction of A. albopictus, good vector surveillance is required to ensure that new foci are eliminated before they become well established. Aedes albopictus exploits a wider range of larval habitats, both natural and artificial, than does A. aegypti, explaining its abundance in rural areas as well as parks and suburbs. Aedes aegypti is more closely associated with human habitation, breeding indoors and outdoors in artificial habitats. To prevent chikungunya, a reduction in the number of water-filled containers in and around the home is an important public-
309 health priority. Used-tyre dumps enable large-scale breeding of Aedes, and recycling programmes for tyres should be encouraged. Once outbreaks occur, communities should be mobilized to eliminate breeding sites. Effective vector control also requires the application of insecticides as space sprays, as residual applications on surfaces in and around container habitats where mosquitoes alight, including tyre dumps, and as larvicides to kill the immature stages. Viraemic patients should be nursed in screened wards or under mosquito nets in hospital or at home. The potential risks of transmission through donation of blood or organs must also be considered. For individual protection, clothing that minimizes skin exposure to the day-biting vectors is advised, as are repellents that can be applied to exposed skin or to clothing. Insecticide-treated mosquito nets afford good protection for those who sleep during the day, particularly young children. Funding: None. Conflicts of interest: None declared. Ethical approval: Not required.
References Dash, P.K., Parida, M.M., Santhosh, S.R., Verma, S.K., Tripathi, N.K., Ambuj, Saxena, P., Gupta, N., Chaudhary, M., Pradeep Babu, J., 2007. East Central South African genotype as the causative agent in reemergence of chikungunya outbreak in India. Vector Borne Zoonotic Dis. 7, 519—528. European Centre for Disease Prevention and Control, 2007. Mission Report. Chikungunya in Italy: Joint ECDC/WHO visit for a European risk assessment; 17—21 September 2007. http://www.ecdc.eu.int/Publications/Technicalreports.html [accessed November 2007]. McIntosh, B.M., Gear, J.H.S., 1981. Arboviral zoonoses in southern Africa: Chikungunya fever, in: Steele, J.H., Beran, G.W. (Eds), Section B: Viral Zoonoses. CRC Handbook Series in Zoonoses. CRC Press, Boca Raton, FL, pp. 217—220. Mohan, A., 2006. Chikungunya fever: clinical manifestations and management. Indian J. Med. Res. 124, 471—474. Schuffenecker, I., Iteman, I., Michault, A., Murri, S., Frangeul, L., Vaney, M.-C., Lavenir, R., Pardigon, N., Reynes, J.-M., Pettinelli, F., 2006. Genome microevolution of chikungunya viruses causing the Indian Ocean outbreak. PLoS Med. 3, e263.