Yellow Fever


Yellow fever is an acute infection characterized in its most severe form by fever, jaundice, proteinuria, and hemorrhage. The virus is mosquito-borne and occurs in epidemic or endemic form in South America and Africa. Seasonal epidemics occurred in cities located in temperate areas of Europe and the Americas until 1900, and epidemics continue in West, Central, and East Africa.

Etiology

Yellow fever is the prototype of the Flavivirus genus of the family Flaviviridae, which are enveloped single-stranded RNA viruses 35-50 nm in diameter.

Yellow fever circulates zoonotically as five genotypes: type IA in West Central Africa, type IB in South America, type II in West Africa, type III in East Central Africa, and type IV in East Africa. Types IA and IB virus are capable of urban transmission between human beings by Aedes aegypti. Sometime in the 1600s, yellow fever virus was brought to the American tropics through the African slave trade. Subsequently, yellow fever caused enormous coastal and riverine epidemics in the Atlantic and Caribbean basins until the 20th century, when the virus and its urban and sylvan mosquito cycles were identified, mosquito control methods were perfected, and a vaccine was developed. The East and East/Central African genotypes have not fully entered the urban cycle and have not spread to the East Coast of Africa or to the countries of Asia.

Epidemiology

Human and nonhuman primate hosts acquire the yellow fever infection by the bite of infected mosquitoes. After an incubation period of 3-6 days, virus appears in the blood and may serve as a source of infection for other mosquitoes. The virus must replicate in the gut of the mosquito and pass to the salivary gland before the mosquito can transmit the virus. Yellow fever virus is transmitted in an urban cycle—human to A. aegypti to human—and a jungle cycle—monkey to jungle mosquitoes to monkey. Classic yellow fever epidemics in the United States, South America, the Caribbean, and parts of Europe were of the urban variety. Since 2000, West Africa has experienced five urban epidemics, including in the capital cities of Abidjan (Cote d'Ivoire), Conakry (Guinea), and Dakar (Senegal). In 2012-2013, large outbreaks of East and East/Central yellow fever occurred across a large, predominantly rural area of war-ravaged Darfur in southwestern Sudan and in adjacent areas of northern Uganda. Beginning in 2015 and continuing to mid-2016, there were sharp outbreaks of yellow fever in and around Rwanda, Angola, and the bordering Democratic Republic of Congo, where there were 7,000 reported cases and 500 deaths. Eleven cases were imported into China by workers in Angola. In South America, all of the approximately 200 cases reported each year are jungle yellow fever. In late 2016 and continuing through 2018, a widespread zoonosis resulted in an estimated 2,000 yellow fever cases in Brazil. In colonial times, urban yellow fever attack rates in white adults were very high, suggesting that subclinical infections are uncommon in this age-group. Yellow fever may be less severe in children, with subclinical infection:clinical case ratios ≥ 2:1. In areas where outbreaks of urban yellow fever are common, most cases involve children because many adults are immune. Transmission in West Africa is highest during the rainy season, from July to November.

In tropical forests, yellow fever virus is maintained in a transmission cycle involving monkeys and tree hole–breeding mosquitoes ( Haemagogus in Central and South America; the Aedes africanus complex in Africa). In the Americas, most cases involve tourists, campers, those who work in forested areas, and vacationers exposed to infected mosquitoes. In Africa, enzootic virus is prevalent in moist savanna and savanna transition areas, where other tree hole–breeding Aedes vectors transmit the virus between monkeys and humans and between humans.

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