Digoutte J P
Institut Pasteur, Dakar, Sénégal.
Bull Soc Pathol Exot. 1999 Dec;92(5):343-8.
In the early 20th century, when it was discovered that the yellow fever virus was transmitted in its urban cycle by Aedes aegypti, measures of control were introduced leading to its disappearance. Progressive neglect of the disease, however, led to a new outbreak in 1927 during which the etiological agent was isolated; some years later a vaccine was discovered and yellow fever disappeared again. In the 1960s, rare cases of encephalitis were observed in young children after vaccination and the administration of the vaccine was forbidden for children under 10 years. Five years later, a new outbreak of yellow fever in Diourbel, Senegal, was linked to the presence of Aedes aegypti. In the late 1970s, the idea of a selvatic cycle for yellow fever arose. Thanks to new investigative techniques in Senegal and Côte d'Ivoire, the yellow fever virus was isolated from the reservoir of virus and vectors. The isolated virus was identified in monkeys and several vectors: Aedes furcifer, Aedes taylori, Aedes luteocephalus. Most importantly, the virus was isolated in male mosquitoes. Until recently, the only known cycle had been that of Haddow in East Africa. The virus circulate in the canopea between monkeys and Aedes africanus. These monkeys infect Aedes bromeliae when they come to eat in banana plantations. This cycle does not occur in West Africa. Vertical transmission is the main method of maintenance of the virus through the dry season. "Reservoirs of virus" are often mentioned in medical literature, monkeys having a short viremia whereas mosquitoes remain infected throughout their life cycle. In such a selvatic cycle, circulation can reach very high levels and no child would be able to escape an infecting bite and yet no clinical cases of yellow fever have been reported. The virulence--as it affects man--of the yellow fever virus in its wild cycle is very low. In areas where the virus can circulate in epidemic form, two types of circulation can be distinguished. Intermediate yellow fever--a term coined to define epidemia which do not correspond exactly to urban yellow fever. The cycle involves men and monkeys through wild vectors as Aedes furcifer but also through Aedes aegypti and the mortality rate is much lower than for urban epidemics. In urban yellow fever, man is the only vertebrate host involved in the circulation of the virus, the vector being generally Aedes aegypti. This vector maintains a selective pressure, increasing the transmission of virus capable of producing high viremia in man. In the selvatic cycles, two cycles can be distinguished: one of maintenance which does not increase the quantity of virus in circulation and one of amplification which does increase this quantity. As we shall see, it develops into an epizootic form but also in an epidemic form in man. When the decrease in yellow fevers across Africa is considered, it appears that all major epidemics occur in West Africa inspite of the presence of wild cycles of the yellow fever virus in Central and East Africa. For the rare epidemics that have occurred there, the vector has never been Aedes aegypti. In a recent outbreak in Kenya, the vector was Aedes bromeliae. The examination of part of the gene encoding for envelope protein showed the presence of two geographical types corresponding to West-Africa and Central East-Africa. Clinically speaking, yellow fever is an haemorrhagic fever with hepatitis similar to other haemorrhagic fevers such as Rift Valley fever. When, in 1987, an outbreak of haemorrhagic fever occurred in southern Mauritania, for several days it was thought to be yellow fever. Four days later, the diagnosis was corrected by isolating and identifying the virus as that of Rift Valley fever (RVFV). RVFV causes several pathogenic syndromes in human beings: acute febrile illness, haemorrhagic fever, haemorrhagic fever with hepatitis, nervous syndromes or ocular disease. Mortality rate was high for haemorrhagic fever with hepatitis, reaching 36%. (ABST
20世纪初,当发现黄热病病毒在城市传播周期中由埃及伊蚊传播时,便采取了控制措施,导致其消失。然而,对该疾病的逐渐忽视导致1927年出现了新的疫情,在此期间分离出了病原体;几年后发现了一种疫苗,黄热病再次消失。20世纪60年代,在幼儿接种疫苗后观察到罕见的脑炎病例,10岁以下儿童被禁止接种该疫苗。五年后,塞内加尔迪乌尔贝勒出现了新的黄热病疫情,与埃及伊蚊的存在有关。20世纪70年代末,出现了黄热病存在野生传播周期的观点。由于塞内加尔和科特迪瓦采用了新的调查技术,从病毒宿主和媒介中分离出了黄热病病毒。在猴子和几种媒介中鉴定出了分离出的病毒:叉尾伊蚊、泰勒伊蚊、黄头伊蚊。最重要的是,在雄蚊中分离出了病毒。直到最近,唯一已知的传播周期是东非的哈多传播周期。病毒在树冠层的猴子和非洲伊蚊之间传播。这些猴子在香蕉种植园觅食时感染凤梨伊蚊。这种传播周期在西非不会发生。垂直传播是病毒在旱季维持的主要方式。医学文献中经常提到“病毒宿主”,猴子的病毒血症期较短,而蚊子在其整个生命周期中都保持感染状态。在这样的野生传播周期中,病毒传播水平可以非常高,没有儿童能够逃脱感染叮咬,但却没有黄热病临床病例的报告。黄热病病毒在其自然传播周期中对人类的毒力非常低。在病毒能够以流行形式传播的地区,可以区分两种传播类型。中间型黄热病——这个术语是为定义不完全符合城市黄热病的流行病而创造的。传播周期涉及人类和猴子,通过叉尾伊蚊等野生媒介,也通过埃及伊蚊,死亡率远低于城市疫情。在城市黄热病中,人类是病毒传播中唯一涉及的脊椎动物宿主,媒介通常是埃及伊蚊。这种媒介保持着一种选择压力,增加了能够在人类中产生高病毒血症的病毒的传播。在野生传播周期中,可以区分出两种周期:一种是维持周期,不会增加传播中的病毒数量;另一种是扩增周期,会增加病毒数量。正如我们将看到的,它会发展成动物流行病形式,也会在人类中发展成流行病形式。当考虑到非洲黄热病发病率的下降时,尽管在中非和东非存在黄热病病毒的野生传播周期,但所有主要疫情似乎都发生在西非。在那里发生的罕见疫情中,媒介从未是埃及伊蚊。在肯尼亚最近的一次疫情中,媒介是凤梨伊蚊。对包膜蛋白编码基因的部分检测显示存在对应于西非和中非-东非的两种地理类型。从临床角度来看,黄热病是一种伴有肝炎的出血热,与其他出血热如裂谷热相似。1987年,毛里塔尼亚南部发生出血热疫情时,有几天被认为是黄热病。四天后,通过分离和鉴定病毒为裂谷热病毒(RVFV)纠正了诊断。RVFV在人类中会引发几种致病综合征:急性发热性疾病、出血热、伴有肝炎的出血热、神经综合征或眼部疾病。伴有肝炎的出血热死亡率很高,达到36%。(摘要)