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yellow fever,acute infectious disease endemic in tropical Africa and many areas of South and Central America. Yellow fever is caused by a virus transmitted by the bite of the female Aedes aegypti mosquito, which breeds in stagnant water near human habitations. A form of the disease called sylvan or jungle yellow fever is transmitted in tropical jungles by other species of mosquitoes that live in trees. Other primates are susceptible to the disease and function as a reservoir of the virus. Although the disease still occurs, typically in sporadic outbreaks, its incidence has been greatly reduced by vaccination and mosquito-control measures. The disease may be carried by travelers coming from endemic regions, and epidemics have extended into subtropical and temperate regions during warm seasons.
Yellow fever begins suddenly after an incubation period of three to five days. In mild cases only fever and headache may be present. The severe form of the disease commences with fever, chills, bleeding into the skin, rapid heartbeat, headache, back pains, and extreme prostration. Nausea, vomiting, and constipation are common. Jaundice usually appears on the second or third day. After the third day the symptoms recede, only to return with increased severity in the final stage, during which there is a marked tendency to hemorrhage internally; the characteristic "coffee ground" vomitus contains blood. The patient then lapses into delirium and coma, often followed by death. During epidemics the fatality rate was often as high as 85%.
The disease was highly prevalent in the Caribbean at the end of the 19th cent., and a way of controlling it had to be found before construction of the Panama CanalPanama Canal,
waterway across the Isthmus of Panama, connecting the Atlantic (by way of the Caribbean Sea) and Pacific oceans, built by the United States (1904–14, on territory leased from the republic of Panama) and expanded by Pamana (2007–16).
..... Click the link for more information. could be undertaken. In 1900 an American commission headed by Walter ReedReed, Walter,
1851–1902, American army surgeon, b. Gloucester co., Va. In 1900 he was sent to Havana as head of an army commission to investigate an outbreak of yellow fever among American soldiers. Following the earlier suggestion by C. J.
..... Click the link for more information. and including James CarrollCarroll, James,
1854–1907, American bacteriologist and army surgeon, b. Woolwich, England, M.D. Univ. of Maryland, 1891. He went to Canada at 15 and later joined the U.S. army.
..... Click the link for more information. , Jesse Lazear, and Arístides AgramonteAgramonte, Arístides
, 1869–1931, Cuban physician and pathologist, M.D. Columbia, 1892. A member of the medical corps of the U.S. army, he was appointed pathologist on the Commission on Yellow Fever in Havana, with Walter Reed and James Carroll, in 1900.
..... Click the link for more information. gathered in the U.S. Army's Camp Columbia in Cuba. Through their experiments—one of which severely sickened Carroll and killed Lazear—they proved the theory of C. J. FinlayFinlay, Carlos Juan
, or Charles John Finlay
, 1833–1915, Cuban physician of Scottish and French descent; studied in France; M.D. Jefferson Medical College, Philadelphia, 1855.
..... Click the link for more information. that yellow fever was a mosquito-borne infection. Within the next few years, W. C. GorgasGorgas, William Crawford,
1854–1920, American disease and sanitation expert, surgeon general of the United States, b. Mobile, Ala., grad. Bellevue Hospital Medical College, 1879. He served with the U.S. army medical corps after 1880.
..... Click the link for more information. , an army physician and sanitation expert, succeeded in controlling the disease in the Panama Canal Zone and other areas in that part of the world by mosquito-eradication measures. The last epidemic in the United States occurred in New Orleans in 1905; a severe outbreak in the Mississippi Valley in 1878 killed about 20,000. The development in 1936 of an immunizing vaccine (work on which won Max TheilerTheiler, Max
, 1899–1972, South African–American research physician, b. Pretoria, educated at the Univ. of Cape Town, St. Thomas's Hospital (London), and the London School of Tropical Medicine.
..... Click the link for more information. a Nobel Prize) and strict quarantine measures against ships, planes, and passengers coming from known or suspected yellow-fever areas further aided control of the disease.
See study by M. C. Crosby (2006).
An acute, febrile, mosquito-borne viral disease characterized in severe cases by jaundice, albuminuria, and hemorrhage. Inapparent infections also occur.
The agent is a flavivirus, an arbovirus of group B. The virus multiplies in mosquitoes, which remain infectious for life. After the mosquito ingests a virus-containing blood meal, an interval of 12–18 days (called the extrinsic incubation period) is required for it to become infectious. See Animal virus, Arboviral encephalitides
The virus enters the body through a mosquito bite and multiplies in lymph nodes, circulates in the blood, and localizes in the liver, spleen, kidney, bone marrow, and lymph glands. The severity of the disease and the major signs and symptoms which appear depend upon where the virus localizes and how much cell destruction occurs. The incubation period is 3–6 days. At the onset, the individual has fever, chills, headache, and backache, followed by nausea and vomiting. A short period of remission often follows. On about the fourth day, the period of intoxication begins with a slow pulse relative to a high fever and moderate jaundice. In severe cases, there are high levels of protein in the urine, and manifestations of bleeding appear; the vomit may be black with altered blood; and there is an abnormally low number of lymphocytes in the blood. When the disease progresses to the severe stage (black vomit and jaundice), the mortality rate is high. However, the infection may be mild and go unrecognized. Diagnosis is made by isolation of the virus from the serum obtained from an individual as early as possible in the disease, or by the rise in serum antibody. See Antibody, Complement-fixation test, Neutralization reaction (immunology)
There are two major epidemiological cycles of yellow fever: classical or urban epidemic yellow fever, and sylvan or jungle yellow fever. Urban yellow fever involves person-to-person transmission by Aedes aegypti mosquitoes in the Western Hemisphere and West Africa. This mosquito breeds in the accumulations of water that accompany human settlement. Jungle yellow fever is primarily a disease of monkeys. In South America and Africa, it is transmitted from monkey to monkey by arboreal mosquitoes (Haemagogus and Aedes species) that inhabit the moist forest canopy. The infection in animals ranges from severe to inapparent. Persons who come in contact with these mosquitoes in the forest can become infected. Jungle yellow fever may also occur when an infected monkey visits a human habitation and is bitten by A. aegypti, which then transmits the virus to a human.
Vigorous mosquito abatement programs have virtually eliminated urban yellow fever. However, with the speed of modern air travel, the threat of a yellow fever outbreak exists where A. aegypti is present. An excellent attenuated live-virus vaccine is available. See Vaccination
an acute infectious disease, caused by a virus, and accompanied by fever, intoxication, jaundice, and hemorrhages. Yellow fever is prevalent in Central and South America and in west and central Africa; it does not occur in the USSR. Reservoirs of the virus in nature include apes, rodents, and marsupials. In nature the carriers of the disease are mosquitoes of the genus Haemogagus and in population centers, mosquitoes of the genus Aëdes.
Two types of yellow fever may be distinguished: urban yellow fever, in which the mosquitoes become infected from a diseased person and transmit the infection to healthy persons, and jungle yellow fever, in which the mosquitoes become infected from sick monkeys and transmit the infection to healthy persons or monkeys. In humans, after an incubation period of three-six days body temperature rises to 39°-41°C, accompanied by headache, muscle pains, jaundice, and hemorrhage. Persons who recover have a lifelong immunity. Treatment is symptomatic, and preventive measures include mosquito control, the protection of humans from their bite, and vaccination.
REFERENCESGapochko, K. G., N. S. Garin, and V. A. Lebedinskii. “Zheltaia likhoradka.” In Klinika i epidemiologiia nekotorykh maloizvestnykh infektsii. Moscow, 1957.
Teiler, M. “Zheltaia likhoradka.” In Virusnye i rikketsioznye infektsii cheloveka. Edited by M. P. Chumakov. Moscow, 1955. (Translated from English.)
I. I. ELKIN