Sudia W D, Newhouse V F, Beadle I D, Miller D L, Johnston J G, Young R, Calisher C H, Maness K
Am J Epidemiol. 1975 Jan;101(1):17-35. doi: 10.1093/oxfordjournals.aje.a112068.
A major epidemic of Venezuelan equine encephalitis occurred in south Texas in the summer of 1971. More than 1500 equines died of VEE in Texas, and 110 human cases with no deaths were reported. Vector studies in south Texas and northern Tamaulipas revealed that the overall mosquito infection rates during the peak of the epidemic were about 1:100, one of the highest rates observed for a major epidemic. Mosquito infection rates of this magnitude could easily explain the intensity of VEE outbreaks in both equines and man. A total of 943 VEE virus isolations were made from mosquitoes. Eight of the 12 mosquito species found infected were implicated in the epidemic cycle of VEE for the first time. Sufficient laboratory and field evidence is available to prove that Psorophora confinnis was one of the primary vectors of VEE. The lack of laboratory evidence necessitates the use of the term "probable" primary vectors for other species apparently equally as involved on the basis of field infections; these include Aedes sollicitans, Aedes thelcter and Psorophora discolor. Eight other species from which less than 10 VEE virus isolations were made were considered auxiliary vectors. Mosquitoes of some species were tested individually; such tests showed 2-4% of the probable primary vectors to be infected. The first isolation of VEE virus of the epidemic was made from P. confinnis on June 28, 1971. Highest mosquito infection rates occurred during the week of July 5. Mosquito infection rates declined precipitously in the last 3 weeks of July 1971, signaling the end of the epidemic in the study area. One explanation for the decline was that equines, the principal epidemic hosts, were eliminated as a source of virus by death or by acquisition of natural or induced immunity. Mosquito control appeared to be effective in reducing the infected mosquito population while the immunization of equines with TC 83 VEE vaccine was accomplished. Quarantines appeared to be effective in restricting the VEE virus activity to south Texas. Undoubtedly all of the control measures contributed to stopping the epidemic. Continued VEE surveillance by various government and other agencies failed to reveal any further epidemic VEE activity in the US in 1972. Other arboviruses isolated during the VEE studies in south Texas included St. Louis encephalitis virus, and San Angelo subtype of the California Group. A virus of the Bunyamwera Group was also isolated from Palo Blanco, Tamaulipas.
1971年夏天，德克萨斯州南部爆发了一场大规模的委内瑞拉马脑炎疫情。在德克萨斯州，超过1500匹马死于委内瑞拉马脑炎，报告了110例人类病例，但无人死亡。对德克萨斯州南部和塔毛利帕斯州北部的病媒研究表明，疫情高峰期蚊子的总体感染率约为1:100，这是主要疫情中观察到的最高感染率之一。如此高的蚊子感染率很容易解释委内瑞拉马脑炎在马匹和人类中爆发的强度。从蚊子中总共分离出943株委内瑞拉马脑炎病毒。发现受感染的12种蚊子中有8种首次被牵涉到委内瑞拉马脑炎的传播循环中。有足够的实验室和现场证据证明康氏按蚊是委内瑞拉马脑炎的主要病媒之一。由于缺乏实验室证据，对于其他显然同样因野外感染而牵涉其中的物种，必须使用“可能的”主要病媒这一术语；这些物种包括骚扰伊蚊、特氏伊蚊和变色按蚊。从其他物种中分离出的委内瑞拉马脑炎病毒少于10株的另外8个物种被视为辅助病媒。对某些物种的蚊子进行了单独检测；此类检测表明，约2 - 4%的可能主要病媒受到感染。该疫情的第一株委内瑞拉马脑炎病毒于1971年6月28日从康氏按蚊中分离出来。蚊子感染率在7月5日那周达到最高。1971年7月的最后3周，蚊子感染率急剧下降，这表明研究区域内疫情结束。感染率下降的一个原因是，作为主要疫情宿主的马匹因死亡或获得天然或诱导免疫力而不再是病毒来源。在对马匹接种TC 83委内瑞拉马脑炎疫苗的同时，蚊虫控制似乎有效地减少了受感染蚊子的数量。检疫措施似乎有效地将委内瑞拉马脑炎病毒的活动限制在了德克萨斯州南部。毫无疑问，所有这些控制措施都有助于阻止疫情。1972年，各政府机构和其他机构持续进行的委内瑞拉马脑炎监测未发现美国境内有任何进一步的委内瑞拉马脑炎疫情活动。在德克萨斯州南部进行委内瑞拉马脑炎研究期间分离出的其他虫媒病毒包括圣路易斯脑炎病毒以及加利福尼亚血清群的圣安吉洛亚型。还从塔毛利帕斯州的帕洛布兰科分离出了一种本扬韦拉血清群病毒。
