PubMed1999
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