Chapter 262 Yellow Fever Scott B. Halstead 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 3 genotypes: type I in Central Africa, type IIA in West Africa, and type IIB in South America. Type IIA virus is capable of urban transmission between human beings by Aedes aegypti. Sometime in the 1600s this virus was brought to the American tropics through the African slave trade. Subsequently, yellow fever caused enormous coastal and riverine epidemics 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 Central African genotype of yellow fever has not fully entered the urban cycle and has never 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 USA, South America, the Caribbean, and parts of Europe were of the urban variety. Since 2000, West Africa has experienced 5 urban epidemics, including in the capital cities of Abidjan (Cote d’Ivoire), Conakry (Guinea), and Dakar (Senegal). Most of the approximately 200 cases reported each year in South America are jungle yellow fever. In colonial times, 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. The migration of nonimmune laborers into endemic regions is a significant factor in some outbreaks. 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, Aedes africanus in Africa). In the Americas, most cases involve men who work in forested areas and are exposed to infected mosquitoes. In Africa, the 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. Pathogenesis Pathologic changes seen in the liver include (1) coagulative necrosis of hepatocytes in the midzone of the liver lobule, with sparing of cells around the portal areas and central veins; (2) eosinophilic degeneration of hepatocytes (Councilman bodies); (3) microvacuolar fatty change; and (4) minimal inflammation. The kidneys show acute tubular necrosis. In the heart, myocardial fiber degeneration and fatty infiltration are seen. The brain may show edema and petechial hemorrhages. Direct viral injury to the liver results in impaired ability to perform functions of biosynthesis and detoxification; this is the central pathogenic event of yellow fever. Hemorrhage is postulated to result from decreased synthesis of vitamin K–dependent clotting factors and, in some cases, disseminated intravascular clotting. However, because the pathogenesis of shock in patients with yellow fever appears similar to that described for dengue shock syndrome and the other viral hemorrhagic fevers, viral damage to platelets and endothelial cells resulting in release of prohemorrhagic factors may be the central mechanism of hemorrhage in yellow fever. Only gold members can continue reading. Log In or Register to continue Share this: Share on X (Opens in new window) X Share on Facebook (Opens in new window) Facebook Related Related posts: Rumination, Pica, and Elimination (Enuresis, Encopresis) Disorders Adolescent Pregnancy Neisseria gonorrhoeae (Gonococcus) Blastomycosis (Blastomyces dermatitidis) Stay updated, free articles. Join our Telegram channel Join Tags: Nelson Textbook of Pediatrics Expert Consult Jun 18, 2016 | Posted by admin in PEDIATRICS | Comments Off on Yellow Fever Full access? Get Clinical Tree
Chapter 262 Yellow Fever Scott B. Halstead 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 3 genotypes: type I in Central Africa, type IIA in West Africa, and type IIB in South America. Type IIA virus is capable of urban transmission between human beings by Aedes aegypti. Sometime in the 1600s this virus was brought to the American tropics through the African slave trade. Subsequently, yellow fever caused enormous coastal and riverine epidemics 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 Central African genotype of yellow fever has not fully entered the urban cycle and has never 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 USA, South America, the Caribbean, and parts of Europe were of the urban variety. Since 2000, West Africa has experienced 5 urban epidemics, including in the capital cities of Abidjan (Cote d’Ivoire), Conakry (Guinea), and Dakar (Senegal). Most of the approximately 200 cases reported each year in South America are jungle yellow fever. In colonial times, 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. The migration of nonimmune laborers into endemic regions is a significant factor in some outbreaks. 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, Aedes africanus in Africa). In the Americas, most cases involve men who work in forested areas and are exposed to infected mosquitoes. In Africa, the 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. Pathogenesis Pathologic changes seen in the liver include (1) coagulative necrosis of hepatocytes in the midzone of the liver lobule, with sparing of cells around the portal areas and central veins; (2) eosinophilic degeneration of hepatocytes (Councilman bodies); (3) microvacuolar fatty change; and (4) minimal inflammation. The kidneys show acute tubular necrosis. In the heart, myocardial fiber degeneration and fatty infiltration are seen. The brain may show edema and petechial hemorrhages. Direct viral injury to the liver results in impaired ability to perform functions of biosynthesis and detoxification; this is the central pathogenic event of yellow fever. Hemorrhage is postulated to result from decreased synthesis of vitamin K–dependent clotting factors and, in some cases, disseminated intravascular clotting. However, because the pathogenesis of shock in patients with yellow fever appears similar to that described for dengue shock syndrome and the other viral hemorrhagic fevers, viral damage to platelets and endothelial cells resulting in release of prohemorrhagic factors may be the central mechanism of hemorrhage in yellow fever. Only gold members can continue reading. Log In or Register to continue Share this: Share on X (Opens in new window) X Share on Facebook (Opens in new window) Facebook Related Related posts: Rumination, Pica, and Elimination (Enuresis, Encopresis) Disorders Adolescent Pregnancy Neisseria gonorrhoeae (Gonococcus) Blastomycosis (Blastomyces dermatitidis) Stay updated, free articles. Join our Telegram channel Join Tags: Nelson Textbook of Pediatrics Expert Consult Jun 18, 2016 | Posted by admin in PEDIATRICS | Comments Off on Yellow Fever Full access? Get Clinical Tree
