Weaver S C, Salas R, Rico-Hesse R, Ludwig G V, Oberste M S, Boshell J, Tesh R B
Center for Tropical Diseases, University of Texas Medical Branch, Galveston 77555-0605, USA.
Lancet. 1996 Aug 17;348(9025):436-40. doi: 10.1016/s0140-6736(96)02275-1.
Venezuelan equine encephalomyelitis (VEE) virus has caused periodic epidemics among human beings and equines in Latin America from the 1920s to the early 1970s. The first major outbreak since 1973 occurred in Venezuela and Colombia during 1995, and involved an estimated 75,000 to 100,000 people. We report an epidemiological and virological investigation of this epidemic.
Virus isolates were made in cell culture from human serum, human throat swabs, and brain tissue from aborted and stillborn human fetuses, as well as from horse brain tissue and pooled mosquito collections. Human sera were also tested for VEE-specific antibodies. The serotypes of VEE isolates were identified by antigen assays, and viruses were characterised genetically by sequencing PCR products generated from the E3 and E2 genes. Phylogenetic analyses were done to determine evolutionary relations with respect to previous epidemic/epizootic and enzootic VEE virus isolates. Mosquito collections were made to identify possible vectors, and clinical findings were determined by direct observation of patients visiting hospitals and clinics in affected regions, and by inspecting patient records. Equine vaccination and vector control were used in an attempt to halt the spread of the outbreak.
Most affected people had an acute, self-limited febrile illness of 3 to 4 days duration. However, convulsions were often seen in children, and abortions and fetal deaths occurred in pregnant women infected with VEE virus. Antigenic characterisation of 12 virus isolates spanning the temporal and spatial range of the outbreak indicated that all are VEE serotype IC. Phylogenetic analysis revealed that all of the 1995 viruses were closely related to serotype IC viruses isolated during a large VEE outbreak that occurred in the same regions of Colombia and Venezuela from 1962-1964. A 1983 mosquito isolate from north central Venezuela was also closely related to the 1995 isolates.
This outbreak was remarkably similar to one that occurred in same regions of Venezuela and Colombia during 1962-1964. Symptoms of infected patients, estimated mortality rates, meteorological conditions preceding the epidemic, and seasonal patterns of transmission were all very similar to those reported in the previous outbreak. In addition, viruses isolated during 1995 were antigenically and genetically nearly identifical to those obtained during 1962-1964. These findings suggest that the epidemic resulted from the re-emergence of an epizootic serotype IC VEE virus. Identification of a similar virus isolate in mosquitoes in Venezuela in 1983, 10 years after epidemic/epizootic VEE activity ceased, raises the possibility of a serotype IC enzootic transmission cycle in northern Venezuela.
从20世纪20年代到70年代初，委内瑞拉马脑炎（VEE）病毒在拉丁美洲的人类和马匹中引发了周期性疫情。1995年，自1973年以来的首次重大疫情在委内瑞拉和哥伦比亚爆发，估计涉及75000至100000人。我们报告了对此次疫情的流行病学和病毒学调查。
从人血清、人咽拭子、流产和死产人类胎儿的脑组织以及马脑组织和收集的混合蚊子样本中进行细胞培养分离病毒。还对人血清进行了VEE特异性抗体检测。通过抗原检测鉴定VEE分离株的血清型，并通过对从E3和E2基因产生的PCR产物进行测序对病毒进行基因特征分析。进行系统发育分析以确定与先前疫情/动物疫情和地方流行性VEE病毒分离株的进化关系。收集蚊子样本以确定可能的传播媒介，并通过直接观察受影响地区医院和诊所的患者以及检查患者记录来确定临床发现。使用马疫苗接种和媒介控制措施试图阻止疫情的传播。
大多数受影响的人患有持续3至4天的急性自限性发热疾病。然而，儿童中经常出现惊厥，感染VEE病毒的孕妇会出现流产和胎儿死亡。对跨越疫情时间和空间范围的12株病毒分离株进行抗原特征分析表明，所有分离株均为VEE血清型IC。系统发育分析显示，所有1995年的病毒与1962 - 1964年在哥伦比亚和委内瑞拉相同地区发生的一次大规模VEE疫情期间分离的血清型IC病毒密切相关。1983年从委内瑞拉中北部分离的一株蚊子病毒也与1995年的分离株密切相关。
此次疫情与1962 - 1964年在委内瑞拉和哥伦比亚相同地区发生的疫情非常相似。感染患者的症状、估计死亡率、疫情前的气象条件以及传播的季节性模式都与先前疫情报告的情况非常相似。此外，1995年分离的病毒在抗原性和基因上与1962 - 1964年获得的病毒几乎相同。这些发现表明，此次疫情是由动物疫情血清型IC VEE病毒的再次出现引起的。1983年在疫情/动物疫情VEE活动停止10年后在委内瑞拉的蚊子中鉴定出类似的病毒分离株，增加了在委内瑞拉北部存在血清型IC地方流行传播循环的可能性。
