亚非暴发基孔肯雅病的流行特点

2006年基孔肯雅病在非洲、亚洲及印度洋的众多岛屿和国家暴发流行。基孔肯雅病是一种由基孔肯雅病毒引起的急性传染病,伊蚊是其主要传播媒介。基孔肯雅病典型的临床表现是双峰热、皮疹和废用性关节痛。据推测,此次的大规模流行,可能的原因有病毒变异、游客增多和人群免疫力缺乏。现就此次暴发流行的流行特点、病原学特点及临床表现等做简要概述。我国大多数地区拥有传播媒介伊蚊,由于缺乏有效的疫苗和特异性的治疗方法,因此应尽快采取应对措施,防止基孔肯雅病的传入及流行。     

基孔肯雅热诊断和治疗方案

基孔肯雅热是由基孔肯雅病毒引起，经伊蚊传播，以发热、皮疹及关节疼痛为主要特征的急性传染病。1952年首次在坦桑尼亚证实了基孔肯雅热流行，1956年分离到病毒。本病主要流行于非洲和东南亚地区，近年在印度洋地区造成了大规模流行。     

一起基孔肯雅热暴发的蚊媒监控及其病毒检测

目的 分析基孔肯雅热流行与诱蚊诱卵指数的关系,调查白纹伊蚊成幼虫感染基孔肯雅病毒状况.方法 基孔肯雅热流行期间,通过诱蚊诱卵器和布雷图指数调查蚊虫密度和采集蚊虫,用实时荧光PCR和细胞分离2种方法对野外捕获的白纹伊蚊体内病毒进行检测.结果 确认基孔肯雅热暴发流行后,启动包括应急灭蚊的综合控制措施1周后,疫情得到有效控制,布雷图指数和诱蚊诱卵指数下降到5以下;采集的蚊样品按照时间和地点分成27份进行病毒检测,成蚊标本都显示病毒阴性,有3份乙醇浸泡处理的蚊幼虫标本为可疑阳性,占总幼虫标本(24份)的12.5％.细胞培养分离病毒均为阴性.该社区共报告病例253例,应急控制在22d结束.结论 基孔肯雅热暴发流行时,诱蚊诱卵器法作为应急灭蚊安全、有效、简便易行的评价方法,尤其在成蚊控制效果评价和捕获成蚊检测带病毒指数上有优势,流行期间白纹伊蚊对基孔肯雅病毒的感染率、传播率有待进一步研究.     

基孔肯雅病毒与基孔肯雅热

基孔肯雅热是一种人兽共患病,是由基孔肯雅病毒（chikungunya virus,CHIKV）引起,以发热、皮疹、关节疼痛和轻度出血为主要特征的急性传染病。这种病毒病主要分布在非洲、南亚、东南亚热带和亚热带地区。近年来在印度洋地区造成大规模流行,并波及我国南方,疫区在不断扩大。埃及伊蚊和白纹伊蚊是主要传播媒介。通过携带病毒的伊蚊叮咬而传播。在实验室内可通过气溶胶传播,目前尚无直接人传人的报道。多数病人能完全痊愈,但有些病人关节疼痛持续较长时间。     

一例输入性基孔肯雅病的实验室诊断

基孔肯雅病（Chikungunya disease）是由基孔肯雅病毒（Chikungunya virus）引起的一种急性传染病，通过伊蚊传播。临床上以发热、关节疼痛、皮疹和轻度出血为特征。基孔肯雅病毒是单股RNA病毒，属于披膜病毒科甲病毒属。基孔肯雅热始发于非洲，1952年，基孔肯雅热被首次报道，主要流行于非洲。到了20世纪60年代以后，基孔肯雅热东移东南亚地区。1965年，印度发生大流行，30万人感染。     

一起登革热和一起基孔肯雅热暴发疫情的对比分析

目的 了解登革热和基孔肯雅热这两种伊蚊传播疾病的流行病学特征和临床特征异同点,为预防控制这两种疾病提供依据.方法 采用问卷调查和查阅患者就诊资料的方法,搜集东莞市2010年发生的一起登革热和一起基孔肯雅热社区暴发疫情的流行病学特征和临床特征资料并进行对比分析.结果 两起疫情共同点为:输入性疫情;发生在夏秋季节;具有一定的家庭聚集性;发生疫情的社区蚊媒密度高;采取以杀灭成蚊和清除伊蚊孳生地为主的综合性防控措施可有效控制疫情;登革热和基孔肯雅热临床表现类似,以发热、疼痛为主.两起疫情的不同点:与登革热暴发疫情相比,基孔肯雅热暴发疫情强度更大、扩散范围更广、家庭聚集性更强,但疫情持续时间短;在临床表现方面,基孔肯雅热患者关节痛、皮疹、肌肉痛的发生率高于登革热患者,而登革热患者头痛、白细胞减少、血小板减少的发生率高于基孔肯雅热患者.结论 登革热和基孔肯雅热的流行病学和临床特征类似.但与登革热相比,基孔肯雅热传播能力更强;病人更常见关节痛、皮疹,而白细胞、血小板则多正常.     

全国口岸首例输入性基孔肯雅热合并登革热病例调查及处置报告

正基孔肯雅热(chikungunya fever)是由伊蚊叮咬传播,以发热、皮疹及关节疼痛为主要特征的急性传染病。1953年首次由Ross Gordona在坦桑尼亚地区分离获得基孔肯雅病毒(chikungunya virus,CHIKV),同时也从伊蚊中分离到该病毒[1,2]。该病主要流行于夏、秋季节,主要分布于非洲、南亚和东南亚地区,2005—2007年在印度洋岛屿、印度和东南亚地     

云南省景洪市蚊虫分布特点及与虫媒病毒的关系

的：掌握蚊虫分布特点及其在虫媒病毒传播中的作用。方法：捕获蚊虫，分离病毒。结果：１９８１、１９８２、１９８６和１９８８年在景洪市采获成年雌性蚊虫３１种２２８２３只。白天在野外竹林采获蚊虫１７种，优势蚊种为圆斑伊蚊、刺扰伊蚊和白纹伊蚊；夜间在农村畜圈及其周围采获蚊虫１９种，优势蚊种为棕头库蚊、三带喙库蚊、迷走按蚊。从采获的７种蚊虫体内分离到流行性乙型脑炎病毒１０株，基孔肯雅病毒３株，登革热病毒１株。其中从白纹伊蚊分离到３株病毒（２株基孔肯雅病毒、１株登革热病毒），从三带喙库蚊分离到５株病毒（４株流行性乙型脑炎病毒，１株基孔肯雅病毒）。结论：白纹伊蚊是当地基孔肯雅和登革热病毒的主要传播媒介，三带喙库蚊是流行性乙型脑炎病毒的主要传播媒介     

卫生部办公厅关于印发《基孔肯雅热诊断和治疗方案》的通知

卫办医发[2008]99号各省、自治区、直辖市卫生厅局,新疆生产建设兵团卫生局:基孔肯雅热是由基孔肯雅病毒引起、经伊蚊传播、以发热、皮疹及关节疼痛为主要特征的急性传染病。为保证人民群众的身体健康和生命安全,在借鉴其他国家和地区基孔肯雅热防治经验的基础上,我部委托中华医学会组织相关领域专家编写了《基孔肯雅热诊断和治疗方案》。现印发给你们,以指导各地基孔肯雅热的诊断和治疗工作。     

基孔肯雅热的流行现况及其研究进展

基孔肯雅病毒(chikungunya virus,CHIKV)是1种动物源性、昆虫媒介传播的病原体,自20世纪50年代被发现以来导致了大规模的基孔肯雅热的暴发.掌握该病流行特点,防止该病在我国广泛流行是当前面临盏的重要任务.现就基孔肯雅热全球流行情况以及临床学、媒介生物学和基孔肯雅病毒的分子流行病学等方面的研究进展作一...     

Update: chikungunya fever diagnosed among international travelers--United States, 2006

Chikungunya virus (CHIKV) is a mosquitoborne alphavirus indigenous to tropical Africa and Asia, where it causes endemic and epidemic chikungunya (CHIK) fever, an acute illness characterized by fever, arthralgias, and sometimes arthritis, commonly accompanied by conjunctivitis and rash. Although symptoms of CHIKV infection usually last days to weeks, joint symptoms and signs usually last for months and occasionally for 1 year or longer; deaths from CHIKV infection are rare. No specific antiviral treatment exists for CHIKV infection; treatment consists of supportive care, including analgesics and anti-inflammatory medication for joint symptoms. During 2005-2006, an epidemic of CHIK fever occurred on islands in the Indian Ocean and in India, resulting in millions of clinically suspected cases, mainly in southern India. In the United States, CHIK fever has been diagnosed in travelers from abroad. CDC previously reported 12 imported cases of CHIK fever diagnosed in the United States from 2005 through late September 2006, including 11 with illness onset in 2006. This report of 26 additional imported cases with onset in 2006 underscores the importance of recognizing such cases among travelers. Health-care providers are encouraged to suspect CHIKV infection in travelers with fever and arthralgias who have recently returned from areas with CHIKV transmission. Acute- and convalescent-phase serum specimens can be submitted to CDC for testing through state health departments. Public health officials and health-care providers are encouraged to be vigilant for the possibility of indigenous CHIKV transmission in areas of the United States where CHIKV mosquito vectors are prevalent.     

Regulatory considerations in development of vaccines to prevent disease caused by Chikungunya virus

Chikungunya virus (CHIKV) is a mosquito-transmitted alphavirus. Chikungunya disease (CHIK) in humans is characterized by sudden onset of high fever, cutaneous rash, myalgia and debilitating polyarthralgia. Until recently the virus was considered endemic to only Africa and Asia, but since 2004 CHIK has spread to previously non-endemic regions, including Europe and the Americas, thereby emerging as a global health threat. Although a variety of CHIKV vaccine candidates have been tested in animals, and a few have advanced to human clinical trials, no licensed vaccine is currently available for prevention of disease. In this article, we review recent efforts in CHIKV vaccine development and discuss regulatory considerations for CHIKV vaccine licensure under U.S. FDA regulations. Several licensure pathways are available, and the most appropriate licensure pathway for a CHIK vaccine will depend on the type of evidence that can be generated to demonstrate the vaccine’s effectiveness. If “traditional approval” following demonstration of direct benefit in adequate and well-controlled clinical disease endpoint studies is not possible, the Accelerated Approval and Animal Rule pathways are potential alternatives. In terms of vaccine safety, the potential for vaccine associated arthralgia and antibody-dependent enhancement of infectivity and disease severity are important issues that should be addressed in both pre-clinical and clinical studies. CHIK vaccine developers are encouraged to communicate with the FDA during all stages of vaccine development.     

Seroprevalence of Antibodies against Chikungunya,Dengue, and Rift Valley Fever Viruses after Febrile Illness Outbreak,Madagascar

In October 2009, two–3 months after an outbreak of a febrile disease with joint pain on the eastern coast of Madagascar, we assessed serologic markers for chikungunya virus (CHIKV), dengue virus (DENV), and Rift Valley fever virus (RVFV) in 1,244 pregnant women at 6 locations. In 2 eastern coast towns, IgG seroprevalence against CHIKV was 45% and 23%; IgM seroprevalence was 28% and 5%. IgG seroprevalence against DENV was 17% and 11%. No anti-DENV IgM was detected. At 4 locations, 450–1,300 m high, IgG seroprevalence against CHIKV was 0%–3%, suggesting CHIKV had not spread to higher inland-altitudes. Four women had IgG against RVFV, probably antibodies from a 2008 epidemic. Most (78%) women from coastal locations with CHIKV-specific IgG reported joint pain and stiffness; 21% reported no symptoms. CHIKV infection was significantly associated with high bodyweight. The outbreak was an isolated CHIKV epidemic without relevant DENV co-transmission.     

Chikungunya epidemic-related mortality

Port Blair, the capital city of the Union Territory of Andaman and Nicobar Islands in the republic of India, witnessed an outbreak of chikungunya (CHIK) fever in 2006. Although no deaths attributable to CHIK fever were registered, thousands of people were affected. In view of evidence from other parts of the world indicating that CHIK fever does cause death we studied the mortality trend in Port Blair from 2002 to 2008 in order to verify if there was increased mortality during the CHIK fever epidemic. The expected number of monthly deaths in 2006 was calculated by multiplying the average monthly mortality rate from 2002 to 2008 (with the exception of 2006) with the monthly population in 2006. The results indicated that there was a significant increase in expected deaths during some months of 2006, which coincided with the peak in the CHIK fever epidemic in Port Blair.     

Rapid spread of chikungunya virus following its resurgence during 2006 in West Bengal, India

Re-emergence of chikungunya virus (CHIKV) in West Bengal was detected after almost 40 years when an outbreak of fever occurred in Baduria village (West Bengal, India) in October 2006. The symptoms of CHIKV infection are similar to those of dengue virus (DENV) infection. Serum samples were tested for detection of IgM antibody to CHIKV and DENV and the aetiological agent was detected as CHIKV. RT-PCR was carried out for confirmation of CHIKV infection. By 2009, CHIKV had spread rapidly within ten districts of West Bengal. Middle-aged women (age group 31-40 years) were predominantly affected. Here we report the analysis of 2134 serum samples collected during 2006-2009 from the different districts of West Bengal, among which IgM antibody to CHIKV and DENV was detected in 403 and 199 samples, respectively. This report highlights the gradual dominating activity of CHIKV with dengue-like clinical features in dengue-endemic regions such as West Bengal.     

Yellow fever infection after recent convalescence from chikungunya fever: report of a fatal case

An epidemic of chikungunya fever occurred in Luanda, Angola, at the end of 1970, being followed by, and partly concurrent with, an epidemic of yellow fever. In March 1971, a 16-year-old white boy, who had chikungunya fever 3 weeks before, was admitted to hospital with yellow fever. He had a severe illness ending in death on the 8th day. Serum taken on admission yielded YF virus designated as strain 47FA; it is essentially identical to YF (Asibi strain) virus. This serum had HI antibody only to CHIK virus, of 11 arbovirus antigens tested. A positive CF test for CHIK antibody in this serum confirmed the earlier infection with CHIK virus. The authors speculate that persons convalescent from chikungunya fever may be less resistant to infection with YF virus.     

Chikungunya virus adaptation to a mosquito vector correlates with only few point mutations in the viral envelope glycoprotein

Like most arthropod-borne viruses (arboviruses), chikungunya virus (CHIKV) is a RNA virus maintained in nature in an alternating cycle of replication between invertebrate and vertebrate hosts. It has been assumed that host alternation restricts arbovirus genome evolution and imposes fitness trade-offs. Despite their slower rates of evolution, arboviruses still have the capacity to produce variants capable to exploit new environments.To test whether the evolution of the newly emerged epidemic variant of CHIKV (E1-226V) is constrained by host alternation, the virus was alternately-passaged in hamster-derived BHK-21 cells and Aedes aegypti-derived Aag-2 cells. It was also serially-passaged in BHK-21 or Aag-2 cells to promote adaptation to one cell type and presumably, fitness cost in the bypassed cell type. After 30 passages, obtained CHIKV strains were genetically and phenotypically characterized using in vitro and in vivo systems.Serially- and alternately-passaged strains can be distinguished by amino-acid substitutions in the E2 glycoprotein, responsible for receptor binding. Two substitutions at positions E2-64 and E2-208 only lower the dissemination of the variant E1-226V in Ae. aegypti. These amino-acid changes in the E2 glycoprotein might affect viral infectivity by altering the interaction between CHIKV E1-226V and the cellular receptor on the midgut epithelial cells in Ae. aegypti but not in Aedes albopictus.