In the last four years, Malaysia has had three outbreaks of chikungunya virus infection. The first two occurred in Perak in 2006.The third began in Johor in early 2008. The genome of the viruses suggests that on each occasion a different virus was introduced into the population. The first outbreak in Bagan Panchor was due to an Asian genotype virus. The second in the Kinta district of Perak in late 2006 was due to a Central/East African genotype virus. Contact tracing was even able to discover the patient who was the source of the virus from the Indian subcontinent. The third outbreak in Johor was also of a Central/East African strain of virus, but introduced independently. The epidemiology of that outbreak is described in this issue of the MJM.
This is a retrospective cross-sectional study based on the database of clusters of patients with clinical diagnosis of chikungunya (CHIK) that were referred to the National Public Health Laboratory for diagnostic investigations from January 2006 to December 2009. Of the 13,759 referred patients, a total of 6314 (45.9%) patients were laboratory confirmed to have CHIK and 7445 (54.1) patients were considered as clinical cases of CHIK by epidemiological link. Epidemic curves plotted using date of onset of illness for all referred clusters of cases showed that there were three unrelated outbreaks of CHIK in Malaysia from 2006 to 2009. There were two small outbreaks that occurred within the state of Perak in 2006. The cluster of cases in 2008 and 2009 were of related outbreak which started in Johor state and subsequently spread to various parts of Malaysia. The mean age of the patients was 37.0 years old and those patients in the laboratory confirmed group were significantly younger than those in the epidemiological linked group. The main presenting clinical features recorded in this study were fever, arthralgia, myalgia and rashes. Those patients in the laboratory confirmed group had a significant higher incidence of fever, arthralgia and rash than those in the epidemiological linked group.
Many triggering factors for onset of emerging infectious diseases are now recognised, such as: globalisation, demographic increase, population movements, international trade, urbanisation, forest destruction, climate changes, loss in biodiversity, and extreme life conditions such as poverty, famine and war. Epidemic burden is often leading to disasters, in terms of human losses, as well as economic, political or social consequences. These outbreaks may jeopardize within a few weeks or months, industry, trade, or tourism. While dengue and its most severe forms (hemorrhagic and shock syndrome) is spreading all over the tropical world, another arbovirosis, chikungunya disease dramatically spread in Indian Ocean islands where 30 to 75% of population were infected in 2005 and 2006, and then extended its progression towards India, Sri Lanka, Indonesia, Malaysia, Maldives islands with more than a million people infected with the East-African strain, replacing the former Asian strain which was known to prevail more than 30 years ago in India. Patients experience sequelae with disability, work loss, and rarely severe outcome recently identified in La Réunion and Mayotte (French overseas territories). No country, no part of the world may consider itself as protected against such events. However, consequences of emerging or re-emerging diseases are more and more unacceptable when they impact the poorest countries of the world. Viruses, bacteria, as well as wild animals, birds, or arthropods are not stopped by borders. It is time now to promote barriers against infectious diseases, including prevention, anticipation, disease surveillance and research. This is not only for humanitarian reasons, but also for contributing to a sustainable development with equity for worldwide population. This report presents comprehensive actions taken in 2006 for tracing the epidemic and mobilise research, as requested to the task force set up by the Prime Minister by March 20, 2006.
In the last few years, chikungunya has become a major problem in Southeast Asia, with large numbers of cases being reported in Singapore, Malaysia, and Thailand. Much of the current epidemic of chikungunya in Southeast Asia is being driven by the emergence of a strain of chikungunya virus that originated in Africa and spread to islands in the Indian Ocean, as well as to India and Sri Lanka, and then onwards to Southeast Asia. There is currently no specific treatment for chikungunya and no vaccine is available for this disease. This review seeks to provide a short update on the reemergence of chikungunya in Southeast Asia and the prospects for control of this disease.
Malaysia experienced the first outbreak of chikungunya (CHIK) in Klang in late 1998 due to CHIK virus of Asian genotype. The CHIK virus of Asian genotype reemerged causing outbreak in Bangan Panchor, Perak in March 2006. CHIK virus of Central/East African genotype was first detected from a patient who returned from India in August 2006. In December 2006, CHIK virus of Central/East African genotype was re-introduced into Malaysia from India and caused an outbreak in Kinta district, Perak but was successfully controlled following an early detection and institution of intensive vector control measures. In late April 2008, CHIK virus of Central/East African genotype was laboratory confirmed as the cause of CHIK outbreak in Johore which spread to other parts of Malaysia by August 2008. Phylogenetic analysis based on the 254-bp fragment of the virus envelope protein gene as the genetic marker showed that three different strains of CHIK virus of Central/East African genotype were introduced into Malaysia on three separate occasions from 2006 to 2008. The strain that was introduced into Johor state was responsible for its subsequent spread to other parts of Malaysia, inclusive of Sarawak.
In 2008, an outbreak of chikungunya infection occurred in Johor. We performed a retrospective review of all laboratory confirmed adult chikungunya cases admitted to Hospital Sultanah Aminah, Johor Bahru from April to August 2008, looking into clinical and laboratory features. A total of 18 laboratory confirmed cases of chikungunya were identified with patients presenting with fever, joint pain, rash and vomiting. Haemorrhagic signs were not seen. Lymphopenia, neutropenia, thrombocytopenia, raised liver enzymes and deranged coagulation profile were the prominent laboratory findings. We hope this study can help guide physician making a diagnosis of chikungunya against other arborviruses infection.
In 2006, an outbreak of Chikungunya virus (CHIKV) of the Asian genotype affected over 200 people in Bagan Panchor village in Malaysia. One year later, a post-outbreak survey was performed to determine attack rate, asymptomatic rate, and post-infection sequelae. Findings were compared with recent CHIKV outbreaks of the Central/East African genotype. A total of 180 residents were interviewed for acute symptoms and post-infection physical quality of life and depressive symptoms. Sera from 72 residents were tested for CHIKV neutralizing antibodies. The estimated attack rate was 55.6%, and 17.5% of infected residents were asymptomatic. Arthralgia was reported up to 3 months after infection, but there were no reports of long-term functional dependence or depression. Symptomatic and seropositive residents were significantly more likely to live in the area with the most dense housing and commercial activities. CHIKV had a high attack rate and considerable clinical impact during the Bagan Panchor outbreak.
An adult Malaysian woman returned to Japan from Kuala Lumpur and had onset of dengue fever-like symptoms including high fever, malaise and arthritis in early January 2009. Serum obtained on the following day was tested at the National Institute of Infectious Diseases in Tokyo, where it was determined to be positive for chikungunya virus (CHIKV) RNA. IgM antibody against CHIKV was negative on January 6 and sero-converted to be positive on January 14, confirming a recent CHIKV infection. Except for arthralgia, all her symptoms resolved uneventfully within 10 days.
An outbreak of Chikugunya (CHIK) fever occurred among the fishing community in Bagan Pancor, Perak. The outbreak was laboratory confirmed within 48 hours after the receipt of the specimens. Fifty-three patients' serum samples were submitted for laboratory investigation and 47 (88.7%) were confirmed to be positive for CHIK infection by RT-PCR, and/or virus isolation, and/or in-house immunoflourescent test. RT-PCR and virus isolation were the tests of choice for patients with illness of four days or less and detection of CHIK specific IgM for those with more than four days of fever. The nucleic acid sequence based on the 354- and 294-bp of the nsP1 and E1 genes of the CHIK virus detected from pools of adults Aedes aegypti mosquitoes were identical to those CHIKV virus isolated from humans in the same locality. Phylogenetic analysis of the CHIK virus based on the 257 nts partial E1 gene indicates that Bagan Panchor's strain was closely related to the first CHIK virus isolated during the outbreak in Klang in 1998.
Emerging and re-emerging infectious diseases have become a major global problem. Malaysia appears to be an epicenter for such infections and in recent years, several outbreaks have occurred resulting in loss of lives and economic hardships. In this paper, we discussed the outbreaks of leptospirosis, enterovirus 71 encephalitis, chikungunya polyarthritis and Nipah encephalitis and how a developing country such as Malaysia managed the situation with the help of international agencies and organisations. Many valuable lessons were learned and by sharing our experience, it is hoped that we will be in a better position to handle future outbreaks and prevent their spread to countries in the region.
The resurgence of Chikungunya virus (CHIKV) in the southern, northeastern and northern parts of Thailand, inflicting approximately 46,000 reported cases since October 2008 until December 2009, has raised public health concerns. In the present study, we characterized nearly complete genome sequences of four CHIKV isolates obtained from 2008 to 2009 outbreaks in Thailand. Phylogenetic analysis was performed to determine the relationships of the study viruses with previously reported isolates. Results showed that 2008-2009 Thailand isolates belonged to the East, Central and South African genotype and were most closely related to isolates detected in Malaysia and Singapore in 2008. This was in contrast to isolates from all previous outbreaks in Thailand which were caused by an Asian genotype. We describe several novel mutations in Thailand isolates that warrants further investigation on characterization of CHIKV from different parts of the country to better understand the molecular epidemiology of Chikungunya fever outbreaks in Thailand.
Chikungunya is a re-emerging mosquito-borne viral infection that has spread from East Africa to Indian Ocean islands and re-emerged in India since 2004. In Malaysia, chikungunya re-emerged after a hiatus of seven years, causing a localised outbreak in a north-western coastal town in 2006 and subsequently widespread outbreaks in 2008. Since the first local outbreak of chikungunya in Singapore in January 2008, chikungunya infections have been increasingly reported in Singapore. In this case series, five patients aged 37-62 years, with chikungunya infection confirmed in August 2008, were reported. Three of the five were male, and only one had medical comorbidities. Two had a travel history to Johor, Malaysia, where local outbreaks of chikungunya had been reported. Fever, arthralgia and rash were the most common symptoms. Fever lasted four to five days while viraemia lasted four to 11 days, persisting two to three days after defervescence in three patients. A biphasic pattern of fever was observed in two patients. Leucopenia was noted in all patients, while mild thrombocytopenia and transaminitis occurred in three of five patients. Two patients had persistent polyarthralgia at two to three weeks after the onset of symptoms. Fever, arthralgia and rash should prompt consideration of acute chikungunya in Singapore. While taking the travel history, doctors should be mindful that indigenous chikungunya cases can occur.
Chikungunya infection has become a public health threat in Malaysia since the 2008 nationwide outbreaks. Aedes albopictus Skuse has been identified as the chikungunya vector in Johor State during the outbreaks. In 2009, several outbreaks had been reported in the State of Kelantan. Entomological studies were conducted in Kelantan in four districts, namely Jeli, Tumpat, Pasir Mas and Tanah Merah to identify the vector responsible for the virus transmission.
Chikungunya virus infection recently reemerged in Malaysia after 7 years of nondetection. Genomic sequences of recovered isolates were highly similar to those of Malaysian isolates from the 1998 outbreak. The reemergence of the infection is not part of the epidemics in other Indian Ocean countries but raises the possibility that chikungunya virus is endemic in Malaysia.
Malaysia experienced its first outbreak of chikungunya virus (CHIKV) infection in late 1998 in Klang District in Selangor; six years later the virus re-emerged in the state of Perak. All the CHIKV isolates in 1988 and 2006 shared high sequence similarities and belonged to the Asian genotype. In 2007 and 2008 CHIKV infection again reemerged but the genotype was the Central/East African genotype. This strain was found to be similar to the strains causing outbreaks in the India Ocean. In 2009, the strains circulating in Malaysia, including the state of Kelantan, based on the partial E1 gene, also belong to the Central/East African genotype.
Many countries neighboring Malaysia have reported human infections by chikungunya virus, a mosquito-borne togavirus belonging to the genus Alphavirus. However, although there is serological evidence of its presence in Malaysia, chikungunya virus has not been known to be associated with clinical illness in the country. An outbreak of chikungunya virus occurred in Klang, Malaysia, between December 1998 and February 1999. The majority of the cases were in adults and the clinical presentation was similar to classical chikungunya infections. Malaysia is heavily dependent on migrant workers from countries where chikungunya is endemic. It is speculated that the virus has been re-introduced into the country through the movement of these workers.
BACKGROUND: Chikungunya virus (CHIKV) of the Central/East African genotype has caused large outbreaks worldwide in recent years. In Malaysia, limited CHIKV outbreaks of the endemic Asian and imported Central/East African genotypes were reported in 1998 and 2006. Since April 2008, an unprecedented nationwide outbreak has affected Malaysia.
OBJECTIVE: To study the molecular epidemiology of the current Malaysian CHIKV outbreak, and to evaluate cross-neutralisation activity of serum from infected patients against isolates of Asian and Central/East African genotypes.
STUDY DESIGN: Serum samples were collected from 83 patients presenting in 2008, and tested with PCR for the E1 gene, virus isolation, and for IgM. Phylogenetic analysis was performed on partial E1 gene sequences of 837bp length. Convalescent serum from the current outbreak and Bagan Panchor outbreak (Asian genotype, 2006) were tested for cross-neutralising activity against representative strains from each outbreak.
RESULTS: CHIKV was confirmed in 34 patients (41.0%). The current outbreak strain has the A226V mutation in the E1 structural protein, and grouped with Central/East African isolates from recent global outbreaks. Serum cross-neutralisation activity against both Central/East African and Asian genotypes was observed at titres from 40 to 1280.
CONCLUSIONS: The CHIKV strain causing the largest Malaysian outbreak is of the Central/East African genotype. The presence of the A226V mutation, which enhances transmissibility of CHIKV by Aedes albopictus, may explain the extensive spread especially in rural areas. Serum cross-neutralisation of different genotypes may aid potential vaccines and limit the effect of future outbreaks.
Chikungunya is an acute febrile illness caused by an alphavirus which is transmitted by infective Aedes mosquitoes. Two previous outbreaks of chikungunya in Malaysia were due to chikungunya virus of Asian genotype. The present outbreak involved two adjoining areas in the suburb of Ipoh city within the Kinta district of Perak, a state in the northern part of Peninsular Malaysia. Thirty seven residents in the main outbreak area and two patients in the secondary area were laboratory confirmed to be infected with the virus. The index case was a 44-year Indian man who visited Paramakudi, Tamil Naidu, India on 21st November 2006 and returned home on 30th of November 2006, and subsequently developed high fever and joint pain on the 3rd of December 2006. A number of chikungunya virus isolates were isolated from both patients and Aedes albopictus mosquitoes in the affected areas. Molecular study showed that the chikungunya virus causing the Kinta outbreak was of the Central/East African genotype which occurred for the first time in Malaysia.
Chikungunya virus (CHIKV) and dengue virus (DENV) co-circulate in areas endemic with the Aedes mosquito vectors. Both viruses cause similar illnesses which may be difficult to distinguish clinically. CHIKV is also associated with persistent arthralgia.
In 1998, Malaysia experienced its first chikungunya virus (CHIKV) outbreak in the suburban areas followed by another two in 2006 (rural areas) and 2008 (urban areas), respectively. Nevertheless, there is still a lack of documented data regarding the magnitude of CHIKV exposure in the Malaysian population. The aim of this study was to determine the extent of chikungunya virus infection in healthy Malaysian adults residing in outbreak-free locations.