Monath T P, Craven R B, Adjukiewicz A, Germain M, Francy D B, Ferrara L, Samba E M, N'Jie H, Cham K, Fitzgerald S A, Crippen P H, Simpson D I, Bowen E T, Fabiyi A, Salaun J J
Am J Trop Med Hyg. 1980 Sep;29(5):912-28. doi: 10.4269/ajtmh.1980.29.912.
An epidemic of yellow fever (YF) occurred in the Gambia between May 1978 and January 1979. Retrospective case-finding methods and active surveillance led to the identification of 271 clinically suspected cases. A confirmatory or presumptive laboratory diagnosis was established in 94 cases. The earliest serologically documented case occurred in June 1978, at the extreme east of the Gambia. Small numbers of cases occurred in August and September. The epidemic peaked in October, and cases continued to occur at a diminishing rate through January, when a mass vaccination campaign was completed. The outbreak was largely confined to the eastern half of the country (MacCarthy Island and Upper River Divisions). In nine survey villages in this area (total population 1,531) the attack rate was 2.6--4.4%, with a mortality rate of 0.8%, and a case fatality rate of 19.4%. If these villages are representative of the total affected region, there may have been as many as 8,400 cases and 1,600 deaths during the outbreak. The disease incidence was highest in the 0- to 9-year age group (6.7%) and decreased with advancing age to 1.7% in persons over 40 years. Overall, 32.6% of survey village inhabitants had YF complement-fixing (CF) antibodies. The prevalence of antibody patterns indicating primary YF infection decreased with age, in concert with disease incidence. The overall inapparent:apparent infection ratio was 12:1. In persons with serological responses indicating flaviviral superinfection, the inapparent:apparent infection ratio was 10 times higher than in persons with primary YF infection. Sylvatic vectors of YF virus, principally Aedes furcifer-taylori and Ae. luteocephalus are believed to have been responsible for transmission, at least at the beginning of the outbreak. Eighty-four percent of wild monkeys shot in January 1979 had YF neutralizing antibodies, and 32% had CF antibodies. Domestic Aedes aegypti were absent or present at very low indices in many severely affected villages (see companion paper). In January, however, aegypti-borne YF 2.5 months into the dry season was documented by isolation of YF virus from a sick man and from this vector species in the absence of sylvatic vectors. Thus, in villages where the classical urban vector was abundant, interhuman transmission by Ae. aegypti occurred and continued into the dry season. A mass vaccination campaign, begun in December, was completed on 25 January, with over 95% coverage of the Gambian population. A seroconversion rate of 93% was determined in a group of vaccinees. This outbreak emphasizes the continuing public health importance of YF in West Africa and points out the need for inclusion of 17D YF vaccination in future programs of multiple immunication.
1978年5月至1979年1月期间，冈比亚爆发了黄热病疫情。通过回顾性病例发现方法和主动监测，共识别出271例临床疑似病例。其中94例病例得到了确诊或推定的实验室诊断。血清学记录最早的病例发生在1978年6月，位于冈比亚最东部地区。8月和9月出现了少量病例。疫情在10月达到高峰，此后病例数持续下降，直至1月大规模疫苗接种运动结束。此次疫情主要局限于该国东部地区（麦卡锡岛和上河区）。在该地区的9个调查村庄（总人口1531人）中，发病率为2.6% - 4.4%，死亡率为0.8%，病死率为19.4%。如果这些村庄能代表整个受影响地区，那么疫情期间可能多达8400例病例和1600例死亡。疾病发病率在0至9岁年龄组最高（6.7%），并随着年龄增长而下降，40岁以上人群的发病率为1.7%。总体而言，32.6%的调查村庄居民具有黄热病补体结合（CF）抗体。表明原发性黄热病感染的抗体模式患病率随年龄下降，与疾病发病率一致。总体隐性感染与显性感染比例为12:1。在血清学反应表明有黄病毒重叠感染的人群中，隐性感染与显性感染比例比原发性黄热病感染人群高10倍。黄热病病毒的丛林型传播媒介主要是非洲伊蚊和黄头伊蚊，至少在疫情初期被认为是传播的原因。1979年1月射杀的野生猴子中，84%具有黄热病中和抗体，32%具有CF抗体。在许多受严重影响的村庄，埃及伊蚊不存在或数量极少（见配套论文）。然而，在1月，即在旱季开始2.5个月后，从一名患者和该媒介物种中分离出黄热病病毒，证实了埃及伊蚊传播黄热病的情况，此时不存在丛林型传播媒介。因此，在传统城市传播媒介大量存在的村庄，埃及伊蚊在人际间传播并持续到旱季。12月开始的大规模疫苗接种运动于1月25日完成，冈比亚人口接种覆盖率超过95%。一组接种者的血清转化率为93%。此次疫情凸显了黄热病在西非对公共卫生的持续重要性，并指出在未来的联合免疫计划中需要纳入17D黄热病疫苗接种。
