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Yellow Fever

Yellow Fever


Yellow fever, which is also known as sylvatic fever and viral hemorrhagic fever or VHF, is a severe infectious disease caused by a type of virus called a flavivirus. This flavivirus can cause outbreaks of epidemic proportions throughout Africa and tropical America.

The first written evidence of such an epidemic occurred in the Yucatan in 1648. Since that time, much has been learned about the interesting transmission patterns of this devastating illness. It is thought that the disease originated in Africa and spread to the Americas in the 17th and 18th centuries through trading ships. The flavivirus that causes yellow fever was first identified in 1928 and the first vaccine against the disease was produced at the Rockefeller Institute in New York in 1937.


In order to understand how yellow fever is passed, several terms need to be defined. The word "host" refers to an animal that can be infected with a particular disease. The term "vector" refers to an organism which can carry a particular disease-causing agent (such as a virus or bacteria) without actually developing the disease. The vector can then pass the virus or bacterium on to a new host.

Many of the common illnesses in the United States (including the common cold, many viral causes of diarrhea, and influenza or "flu") are spread via direct passage of the causative virus between human beings. Yellow fever, however, cannot be passed directly from one infected human being to another. Instead, the virus responsible for yellow fever requires an intermediate vector, a mosquito, which carries the virus from one host to another.


Wilbur Augustus Sawyer was born in Appleton, Wisconsin, on August 7, 1879, to Minnie Edmea (Birge) and Wesley Caleb Sawyer. The Sawyers moved to Oshkosh, Wisconsin and finally to Stockton, California in 1888. Sawyer spent two years at the University of California and then entered Harvard College where he earned his A.B. degree in 1902. In 1906, Sawyer graduated from Harvard Medical School and began a private practice, which lasted until he started his internship at Massachusetts General Hospital. Sawyer returned to California in 1908 in order to obtain a position at the University of California as a medical examiner. He then worked with California State Board of Health from 1910 until 1918. In 1911, Sawyer married Margaret Henderson. The couple had three children.

Sawyer's first publication (1913) dealt with his research of poliomyelitis. His discovery, in 1915, that examination of the individual's stool could lead to detection of the disease was later regarded as very significant. In 1918 and 1919, Sawyer worked to control venereal disease while employed by the Army Medical Corps. In 1926 and 1927, while director of the West African Yellow Fever Commission, Sawyer succeeded in isolating the yellow fever virus. He would ultimately return to the United States, where he and Wray Lloyd would devise an immunization against yellow fever (1931).

In 1944, Sawyer became director of health for the United Nations Relief and Rehabilitation Administration, a position he held for three years. He retired to Berkeley, California where he died on November 12, 1951.

The hosts of yellow fever include both humans and monkeys. The cycle of yellow fever transmission occurs as follows: an infected monkey is bitten by a tree-hole breeding mosquito. This mosquito acquires the virus, and can pass the virus on to any number of other monkeys that it may bite. This form of yellow fever is known as sylvatic yellow fever, and usually affects humans only incidentally. When a human is bitten by an infected mosquito, however, the human may acquire the virus. In the case of South American yellow fever, the infected human may return to the city, where an urban mosquito (Aedes aegypti ) serves as a viral vector, spreading the infection rapidly by biting humans. This form of the disease is known as urban yellow fever or epidemic yellow fever.

Yellow fever epidemics may also occur after flooding caused by earthquakes and other natural disasters. They result from a combination of new habitats available for the vectors of the disease and changes in human behavior (spending more time outdoors and neglecting sanitation precautions).

Cases of yellow fever are uncommon in the United States and Canada as of 2004. The last reported case in an American citizen concerned a man who contracted yellow fever in Brazil in 1996. The last epidemic in the United States occurred in New Orleans in 1905.


Once a mosquito has passed the yellow fever virus to a human, the chance of disease developing is about 5-20%. Infection may be fought off by the host's immune system, or may be so mild that it is never identified.

In human hosts who develop the disease yellow fever, there are five distinct stages through which the infection evolves. These have been termed the periods of incubation, invasion, remission, intoxication, and convalescence.

Yellow fever's incubation period (the amount of time between the introduction of the virus into the host and the development of symptoms) is three to six days. During this time, there are generally no symptoms identifiable to the host.

The period of invasion lasts two to five days, and begins with an abrupt onset of symptoms, including fever and chills, intense headache and lower backache, muscle aches, nausea, and extreme exhaustion. The patient's tongue shows a characteristic white, furry coating in the center, surrounded by a swollen, reddened margin. While most other infections that cause a high fever also cause an increased heart rate, yellow fever results in an unusual finding, called Faget's sign. This is the simultaneous occurrence of a high fever with a slowed heart rate. Throughout the period of invasion, there are still live viruses circulating in the patient's blood stream. Therefore, a mosquito can bite the ill patient, acquire the virus, and continue passing it on to others.

The next phase is called the period of remission. The fever falls, and symptoms decrease in severity for several hours to several days. In some patients, this signals the end of the disease; in other patients, this proves only to be the calm before the storm.

The period of intoxication represents the most severe and potentially fatal phase of the illness. During this time, lasting three to nine days, a type of degeneration of the internal organs (specifically the kidneys, liver, and heart) occurs. This fatty degeneration results in what is considered the classic triad of yellow fever symptoms: jaundice, black vomit, and the dumping of protein into the urine. Jaundice causes the whites of the patient's eyes and the patient's skin to take on a distinctive yellow color. This is due to liver damage, and the accumulation of a substance called bilirubin, which is normally processed by a healthy liver. The liver damage also results in a tendency toward bleeding; the patient's vomit appears black due to the presence of blood. Protein, which is normally kept out of the urine by healthy, intact kidneys, appears in the urine due to disruption of the kidney's healthy functioning.

Patients who survive the period of intoxication enter into a relatively short period of convalescence. They recover with no long term effects related to the yellow fever infection. Further, infection with the yellow fever virus results in lifelong immunity against repeated infection with the virus.

The course of yellow fever is complicated in some patients by secondary bacterial infections.


Diagnosis of yellow fever depends on the examination of blood by various techniques in order to demonstrate either yellow fever viral antigens (the part of the virus that stimulates the patient's immune system to respond) or specific antibodies (specific cells produced by the patient's immune system which are directed against the yellow fever virus). The most rapid method of diagnosis as of 2004 is capture enzyme immunoassay. The diagnosis can be strongly suspected when Faget's sign is present. When the classic triad of symptoms is noted yellow fever is strongly suspected.


There are no antiviral treatments available as of 2004 to combat the yellow fever virus, although researchers at the University of Texas are studying ribavirin (Virazole, Rebetol), a drug that is given by mouth to treat hepatitis C, as a potential treatment for liver damage caused by yellow fever. The only treatments for yellow fever are given to relieve its symptoms. Fevers and pain should be relieved with acetaminophen, not aspirin or ibuprofen, both of which could increase the already-present risk of bleeding. Dehydration (due to fluid loss both from fever and bleeding) needs to be carefully avoided. This can be accomplished by increasing fluids. The risk of bleeding into the stomach can be decreased through the administration of antacids and other medications. Hemorrhage may require blood transfusions. Kidney failure may require dialysis (a process that allows the work of the kidneys in clearing the blood of potentially toxic substances to be taken over by a machine, outside of the body).


Five to ten percent of all diagnosed cases of yellow fever are fatal. Jaundice occurring during a yellow fever infection is an extremely grave predictor. Twenty to fifty percent of these patients die of the infection. Death may occur due to massive bleeding (hemorrhage), often following a lapse into a comatose state.


A very safe and very effective yellow fever vaccine exists. The Arilvax vaccine is made from a live attenuated form of the yellow fever virus, strain 17D. In the United States, the vaccine is given only at Yellow Fever Vaccination Centers authorized by the U.S. Public Health Service. About 95% of vaccine recipients acquire long-term immunity to the yellow fever virus. Careful measures to decrease mosquito populations in both urban areas and jungle areas in which humans are working, along with programs to vaccinate all people living in such areas, are necessary to avoid massive yellow fever outbreaks.

Persons planning to travel to countries where yellow fever in endemic may obtain up-to-date information on yellow fever vaccination from the Centers for Disease Control and Prevention by telephone (404-332-4559) or fax (404-332-4265).


Epidemic A situation in which a particular disease spreads rapidly through a population of people in a relatively short period of time.

Faget's sign The simultaneous occurrence of a high fever with a slowed heart rate.

Host The organism (such as a monkey or human) in which another organism (such as a virus or bacteria) is living.

Sylvatic Pertaining to or living in the woods or forested areas. The form of yellow fever transmitted by mosquitoes to rainforest monkeys is called sylvatic yellow fever.

Vector A carrier organism (such as a fly or mosquito) which serves to deliver a virus (or other agent of infection) to a host.



Beers, Mark H., MD, and Robert Berkow, MD., editors. "Viral Diseases." Section 13, Chapter 162 In The Merck Manual of Diagnosis and Therapy. Whitehouse Station, NJ: Merck Research Laboratories, 2002.


Barrett, A. D. "Current Status of the Arilvax Yellow Fever Vaccine." Expert Review of Vaccines 3 (August 2004): 413-420.

Lo Re, V., III, and S. J. Gluckman. "Travel Immunizations." American Family Physician 70 (July 1, 2004): 89-99.

Reeder, G. David, MD, and Theodore E. Woodward, MD. "Yellow Fever." eMedicine February 25, 2002.

Sbrana, E., S. Y. Xiao, H. Guzman, et al. "Efficacy of Post-Exposure Treatment of Yellow Fever with Ribavirin in a Hamster Model of the Disease." American Journal of Tropical Medicine and Hygiene 71 (September 2004): 306-312.


Centers for Disease Control and Prevention (CDC). 1600 Clifton Rd., NE, Atlanta, GA 30333. (800) 311-3435, (404) 639-3311.

Infectious Diseases Society of America (IDSA). 66 Canal Center Plaza, Suite 600, Alexandria, VA 22314. (703) 299-0200. Fax: (703) 299-0204.

World Health Organization (WHO).


World Health Organization Fact Sheet. "Flooding and Communicable Diseases Fact Sheet: Risk Assessment and Preventive Measures." December 2004.

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Yellow Fever and Malaria

Yellow Fever and Malaria


Dreaded Diseases . Yellow fever and malaria, two of the most feared diseases of the period, were often confused. Their symptomschills, aches, and high feverare similar, and they tended to appear in hot weather. Neither is contagiousone person cannot catch it directly from another personand both are transmitted by mosquitoes. In the late eighteenth century no one knew what caused these diseases; some thought there was a connection with swamp air or with summer heat. Yellow fever attacks the liver, producing the jaundice that makes the skin turn yellow, while with malaria, parasites build up rapidly in the liver, and the overworked spleen becomes enlarged as it tries to filter the parasites out. In severe cases blood vessels to the brain are blocked, causing delirium, coma, and death. The two diseases were apt to strike differently: yellow fever broke out in frightening epidemics, sometimes as far north as Philadelphia and New York City; malaria was a constant menace in hot, swampy areas of the Southeast, especially South Carolina and Georgia.

Philadelphia . The worst outbreak of yellow fever in America occurred in Philadelphia during the summer and fall of 1793. There were an estimated five thousand fatalities out of a population of forty-five thousand. A victims first symptoms were high fever and headache, followed a day or two later by severe vomiting of blood as the internal organs degenerated. Death often occurred within four days to a week after contracting the disease. People were so afraid of catching the disease that they avoided contact even with their friends and stopped shaking hands. Relatives were afraid to bury the victims, and a familiar sight was the death cart passing by and the cry of the grave diggers: Bring out your dead!

Causes. Even experienced doctors who recognized the symptoms were ignorant of the cause, although there were plenty of theories. The best-known physician of the day, Benjamin Rush, believed that the contagion may have resulted from a shipment of coffee that was rotting on a Philadelphia wharf. It was also thought possible that the air itself carried the disease. Crews on ships in the harbor were advised to burn tobacco in the hope that its smoke would cleanse the air somehow. Others, convinced it was God punishing a sinful population, noted with some satisfaction that many of the victims were from the poor sections of town, and of course the poor were more wicked than the rich. And while it was true that the poor were afflicted more than the wealthy, it was because of unsanitary conditions in their neighborhoodsstagnant water and open sewage that drew mosquitoesand not the wrath of God. But the disease attacked the rich as well, especially those brave enough to stay in the city rather than flee to the countryside. As the rich fled, there were other kinds of victims: shops and businesses had to close, leaving thousands out of work.

Prevention and Cure . Once the epidemic had struck, health officials tried to keep the contagion from getting worse by burning tobacco to clean the air and by recommending public prayer and fasting. People tried mud baths or garlic to prevent the disease from striking. Doctors would try anything to save their patients. The most common cure was to administer mercury pills and extract large volumes of blood. Bleeding was the fashionable theory of the day: if enough blood were removed, it was believed, the disease would have nothing to attack. One can only imagine how many lives would have been saved if the patient had simply been left alone. Although emergency hospitals were set up, it was difficult to find people brave enough to staff them, and in any case victims had no desire to go to a hospital to die.

Government Shutdown . Philadelphias municipal government practically disintegrated during the epidemic. Only the work of an unofficial committee of public-spirited citizens, acting as a combined government and board of health, prevented total chaos. The U.S. capital was then at Philadelphia. It was common practice at the time to partially shut down the government during the hot summer months, so it was not unusual that President George Washington left for Mount Vernon. Secretary of State Thomas Jefferson, remaining calm in the midst of all the panic, tried to stay on, but found that his staff had evacuated the city, so he too went home to Virginia. Secretary of the Treasury Alexander Hamilton also went home, but not before contracting a mild case. As the time approached for the government officials to return, many feared for their lives. Washington decided to move the capital to Germantown, which became the temporary seat of government until November. By December the crisis had passed, and Congress was able to reconvene in Philadelphia.

Lessons Learned . Since there was no fundamental understanding of the cause of yellow fever, not many lessons emerged, although Benjamin Rushs critics now had more examples of the ill effects of his practice of excessive bleeding. When the disease struck Philadelphia again, mildly in 1795 and 1796 and violently in 1797, the same inadequate measures were taken. Dr. Rush did, however, correctly point out that poor sanitation appeared to be a contributing factor, and his efforts to clean up Philadelphia finally resulted in the development of a public water system. It would be years before people trusted the public health conditions in Philadelphia, and more than a century before Walter Reed would prove that the female Aedes aegypti mosquito was the carrier.

Malaria . While yellow fever also reached epidemic levels in southern cities, it was malaria that was the most prevalent killer in the South. Malaria the word comes from mala aria, an Italian phrase for bad airhad been a problem in the warm, wet Southeast coastal regions of America since early colonial days. Many early settlers from Europe, with no defenses against malaria, suffered and died from what they called fever and ague. South Carolinians were particularly susceptible to malaria because rice plants, for which large tracts of land had been cleared, grew best in shallow pools of standing water, which also formed breeding grounds for mosquitoes. Of course, at the time the mosquito was considered merely a pest, not a carrier of deadly disease.

Remedies . Although malarias cause was unknown, it was often treated differently from yellow fever. First of all, malaria was not always life threatening, so measures such as bleeding were not considered necessary. Fevers were intermittent, and chronic fatigue was often the most debilitating effect. Second, it had been recognized from early colonial times that cinchona bark (from a South American tree) was effective in reducing the symptoms of malaria. We now know that it worked because it contains a substance similar to quinine.

Rich Versus Poor . Unlike yellow fever, which was likely to strike in the crowded cities, malaria was prevalent in the low-lying countryside (it was often called country fever). The wealthy landowners simply left during the hot season; in fact, some of South Carolinas richest families spent the summer in Newport, Rhode Island. That left the poor and slaves to labor in the intensely hot and mosquito-infested rice fields. It was generally believed that African slaves were not only better able than whites to endure the intense heat of southern summers, but were also resistant to malaria. Medical studies have since proved that black Africans were, in fact, partially immune, having come from areas where malaria was prevalent, and having built up antibodies, which were not genetic, but passed from mother to child during pregnancy. This immunity is curiously tied to sickle-cell anemia, a condition that causes blood circulation problems in black children, yet helps ward off malaria. The tragic social consequence was the belief in a natural law that blacks immunity to malaria justified their slavery to work the plantations of the South while the white owners spent the hot months in safer regions. Like yellow fever, malaria was eventually reduced through improved public sanitation, quarantine of ships coming from infected regions, and (after 1900) control of mosquitoes.


Dumas Malone, Jefferson and the Ordeal of Liberty (Boston: Little, Brown, 1962);

Page Smith, The Shaping of America (New York: McGraw-Hill, 1980);

Peter H. Wood, Black Majority (New York: Norton, 1974).

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Yellow Fever

Yellow fever

Yellow fever is the name given to a disease that is caused by the yellow fever virus. The virus is a member of the flavivirus group. The name of the disease is derived from the appearance of those infected, who usually present a jaundiced appearance (yellow-tinted skin).

The agent of infection of yellow fever is the mosquito. The agent was first identified in 1900 when the United States Army Yellow Fever Commission (also referred to as the Reed Commission after its leader, Walter Reed) proved that the mosquito species Aedes aegypti was responsible for spreading the disease. Until then, yellow fever was regarded as requiring direct person-to-person contact or contact with a contaminated object.

The disease has caused large outbreaks involving many people in North America, South America, and Africa, stretching back at least to the 1700s. At that time the disease was often fatal. The availability of a vaccine reduced the incidence and mortality of the disease considerably in the latter part of the twentieth century. However, since 1980 the number of cases of the disease has begun to rise again.

There are now about 200,000 estimated cases of yellow fever in the world each year. Of these, some 30,000 people die. Most researchers and health officials regard these numbers as underestimates, due to underreporting and because in the initial stages yellow fever can be misdiagnosed.

The yellow fever virus infects humans and monkeysno other hosts are known. Humans become infected when the virus is transmitted from monkeys to humans by mosquitoes. This is referred to as horizontal transmission. Several different species of mosquito are capable of transmitting the virus. Mosquitoes can also pass the virus to their own offspring via infected eggs. This form of transmission is called vertical transmission. When the offspring hatch they are already infected and can transmit the virus to humans when they have a blood meal. Vertical transmission can be particularly insidious as the eggs are very hardy and can resist dry conditions, hatching when the next rainy season occurs. Thus the infection can be continued from one year to the next even when there is no active infection occurring in a region.

The different habitats of the mosquitoes ensures a wide distribution of the yellow fever virus. Some of the mosquito species breed in urban areas while others are confined to rural regions. The latter types were associated with the outbreak of yellow fever that struck workers during the construction of the Panama Canal in Central America in the nineteenth century. In South America a concerted campaign to control mosquito populations up until the 1970s greatly reduced the number of cases of yellow fever. However, since that time the control programs have lapsed and yellow fever has increased as the mosquito populations have increased.

Infection with the yellow fever virus sometimes produced no symptoms whatsoever. However, in many people, so-called acute (rapid-onset, intense) symptoms appear about three to six days after infection. The symptoms include fever, muscle pain (particularly in the back), headache, chills, nausea, and vomiting. In this early stage the disease is easily confused with a number of other diseases, including malaria , typhoid fever , hemorrhagic fevers such as Lassa fever, and viral hepatitis . Diagnosis requires the detection of an antibody to the virus in the blood. Such diagnosis is not always possible in underdeveloped regions or in rural areas that are distant from medical facilities and trained laboratory personnel.

In many people the acute symptoms last only a few days and recovery is complete. However, in about 15% of those infected, the disease enters what is termed the toxic phase: a fever reappears and several regions of the body become infected as the virus disseminates from the point of the mosquito bite. Disruption of liver function produces jaundice. Kidney function can also be damaged and even totally shut down. Recovery from this more serious phase of the infection can be complete; although half of those who are afflicted die.

Yellow fever appears in human populations in different ways. One pattern of appearance is called sylvatic (or jungle) yellow fever. As the name implies, this form is restricted to regions that are largely uninhabited by humans. The virus cycles between the indigenous monkey population and the mosquitoes that bite them. Humans that enter the region, such as loggers, can become infected.

Another cycle of infection is referred to as intermediate yellow fever. This infection is found in semi-urban areas, such as where villages are separated by intervening areas of farmland or more natural areas. Infections can spring up in several areas simultaneously. Migration of people from the infected areas to larger population centers can spread the infection. This is the most common pattern of yellow fever occurring in present day Africa.

The final pattern of yellow fever is that which occurs in fully urban settings. The large population base can produce a large epidemic. The infection is spread exclusively by mosquitoes feeding on one person then on another. Control of these epidemics concentrates on eradicating the mosquito populations.

Treatment for yellow fever consists primarily of keeping the patient hydrated and comfortable. Prevention of the infection, via vaccination , is the most prudent course of action. The current vaccine (which consists of living but weakened virus) is safe and provides long-lasting immunity . While side effects are possible, the risks of not vaccinating far outweigh the risk of the adverse vaccine reactions. For a vaccination campaign to be effective, over 80% of the people in a suspect region need to be vaccinated. Unfortunately few countries in Africa have achieved this level of coverage. Another course of action is the control of mosquito populations, typically by spraying with a compound that is toxic to mosquito larvae during breeding season. Once again, this coverage must be extensive to be successful. Breeding areas missed during spraying ensure the re-emergence of mosquitoes and, hence, of the yellow fever virus.

See also Transmission of pathogens; Zoonoses

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Yellow Fever


Yellow fever, a member of the genus Flavivirus, is an arboviral infection found throughout Africa and South America. It is transmitted primarily by the bite of the Aedes aegypti mosquito and also by Haemogogus mosquitoes in South America.

Though yellow fever caused epidemics in the United States and Europe in earlier centuries, today it exists only in Africa and Central and South America.

There are two main cycles of transmission of yellow fever: the sylvatic, or jungle, cycle; and the urban cycle. In the sylvatic cycle, the infection is maintained between monkeys and mosquitoes. A human entering the jungle environment (e.g., loggers, hunters) is at risk if bitten by an infected mosquito. Urban yellow fever occurs when the virus is introduced into urban centers, for example by migrant laborers arriving from rural regions. The domestic mosquito, A. aegypti, then carries the infection from person to person. In contrast to jungle yellow fever, where only small numbers of individuals are at risk, urban yellow fever epidemics may be quite extensive.

An intermediate cycle has also been described in Africa in areas where there is increased contact between humans, monkeys, and mosquitoes, such as at the edges of forested areas; this is a likely source of larger urban outbreaks.

Following the bite of an infective mosquito, the incubation period is three to six days. Although some cases may be asymptomatic or very mild, most cases are characterized by sudden onset of fever, chills, myalgias, backache, headache, nausea, and vomiting. Relative bradycardia (Faget's sign) is common, as are leukopenia and proteinuria. This early stage lasts three to five days, at which point the majority of patients will recover. Approximately 15 percent will relapse within twenty-four hours and develop a stage of "intoxication" characterized by a reocurrence and worsening of the above symptoms. Jaundice appears (hence the name "yellow fever"), and patients develop a bleeding tendency marked by blood in the vomit and stool, bruising, and bleeding from mucous membranes. Kidney failure is common. The mortality rate for this stage is over 50 percent. Treatment is supportive as there is no specific antiviral agent available.

As the clinical presentation of yellow fever is similar to that of other viral hemorrhagic fevers, the diagnosis should be confirmed in a laboratory. Diagnosis can be made by culture of the virus or by finding viral antigen in blood or liver tissue. It is also possible to identify virus-specific antibodies in blood.

A live, attenuated vaccine against yellow fever is over 95 percent effective and confers protection for ten years. As it is a live vaccine, it is contraindicated in infants under the age of six months, in pregnant women, and in immunocompromised individuals. It should be used with caution in anyone with a history of egg allergy.

The best method for control of yellow fever is mass vaccination of susceptible populations. Although the World Health Organization advocates including the yellow fever vaccine in the Expanded Programme of Immunization (EPI) for children, most countries use the vaccine only in outbreak situations, a strategy that has not proven to be very effective in controlling the disease.

Martha Fulford

Jay Keystone

(see also: Communicable Disease Control; Epidemics; Vector-Borne Diseases )


Desowitz, R. (1997). Who Gave Pinta to the Santa Maria? Torrid Diseases in a Temperate World. New York: W. W. Norton & Company.

Halstead, S. (1998). "Emergence Mechanisms in Yellow Fever and Dengue." Emerging Infections 2, eds. W. M. Scheld, W. A. Craig, and J. M. Hughes. Washington, DC: ASM Press.

Robertson, S. E.; Hull, B. P.; Tomori, O.; et al. (1998). "Yellow Fever: A Decade of Re-emergence." Journal of the American Medical Association 276:11571162.

Tomori, O. (1999). "Impact of Yellow Fever on the Developing World." Advances in Virus Research 53:534.

World Health Organization (1998). "Yellow Fever." Bulletin of the World Health Organization 76 (Supp. 2):158159.

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Yellow Fever


YELLOW FEVER. The first reference to yellow fever in America is found in that indispensable sourcebook The History of New England (1647) by John Winthrop, governor of Massachusetts. The effort of the colonial court to exclude from Massachusetts the crew and the cargo of the ship that had brought the fever ("Barbados distemper") from the West Indies to America was the colonies' initial enforcement of quarantine. Later, in 1694, British ships that had sailed from Boston in an unsuccessful effort to capture Martinique brought back an epidemic of yellow fever, and subsequently, despite its endemic focus on the African coast, yellow fever emerged as a peculiarly American disease ("the American plague"). It spread through America as the African slave trade increased. With the single exception of smallpox, the most dreaded verdict on the lips of a colonial physician was "yellow fever."

The worst American epidemic of yellow fever occurred in 1793 and doomed the supremacy of Philadelphia among U.S. cities. Approximately 10 percent of the city's population died from the disease. Forty years later, the combined effects of yellow fever and cholera killed about 20 percent of the population of New Orleans. The last epidemic of yellow fever in the United States occurred in New Orleans in 1905.

Recurring epidemics of yellow fever and cholera led to the formation of municipal health boards in most major U.S. cities by mid-nineteenth century. But for much of that century, these agencies had few powers. Their lack

of authority was, in part, due to distrust of the medical profession—a distrust fed by the inability of physicians to satisfactorily explain epidemic diseases. One camp of physicians argued that yellow fever was transmitted by touch and called for strict quarantines. Other physicians supported the "miasm" theory and argued that yellow fever was carried through the air by poisonous gases (miasm) emitted by rotting vegetation or dead animals. They called for swamp drainage and thorough cleaning of streets and abandoned buildings.

In 1900 the U.S. Army Yellow Fever Commission, with Walter Reed, James Carroll, Jesse W. Lazear, and Aristides Agramonte, was sent to track the pestilence in Cuba. The group, working with the aid of Carlos J. Finlay, demonstrated Finlay's theory that the infection is not a contagion but is transmitted by the bite of the female Aëdes aegypti mosquito. William Crawford Gorgas, chief sanitary officer of the Panama Canal Commission from 1904 until 1913, eliminated the mosquito in the region of the canal and made possible the building of the Panama Canal. Vaccines against the disease were developed in the early 1940s and today are required of anyone traveling to a hazardous area.


Carrigan, Jo Ann. The Saffron Scourge: A History of Yellow Fever in Louisiana, 1796–1905. Lafayette: University of Southwestern Louisiana, Center for Louisiana Studies, 1994.

Ellis, John H. Yellow Fever and Public Health in the New South. Lexington: University Press of Kentucky, 1992.

Foster, Kenneth R., Mary F. Jenkins, and Anna Coxe Toogood. "The Philadelphia Yellow Fever Epidemic of 1792." Scientific American 279, no. 2 (August 1998): 88.

Humphreys, Margaret. Yellow Fever and the South. New Brunswick, N.J.: Rutgers University Press, 1992.

VictorRobinson/c. p.

See alsoEpidemics and Public Health ; Medicine, Military .

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yellow fever

yellow fever, acute infectious disease endemic in tropical Africa and many areas of South America. Epidemics have extended into subtropical and temperate regions during warm seasons. In 1878 a severe outbreak in the Mississippi Valley killed about 20,000; the last epidemic in the United States occurred in New Orleans in 1905. 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.

At the end of the 19th cent., yellow fever was highly prevalent in the Caribbean, and a way of controlling it had to be found before construction of the Panama Canal could be undertaken. In 1900 an American commission headed by Walter Reed and including James Carroll, Jesse Lazear, and Arístides Agramonte 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. Finlay that yellow fever was a mosquito-borne infection. Within the next few years, W. C. Gorgas, 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 later development of an immunizing vaccine (work on which won Max Theiler 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.

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%. Although the disease still occurs, it is usually confined to sporadic outbreaks.

See study by M. C. Crosby (2006).

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Yellow Fever

Yellow Fever

What Is Yellow Fever?

Are There Different Kinds of Yellow Fever?

How Do People Know They Have Yellow Fever?

How Do Doctors Diagnose and Treat Yellow Fever?

How Can Yellow Fever Be Prevented?


Yellow fever is an infectious disease caused by a virus that is transmitted to humans by mosquitoes.


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Aedes aegypti mosquito



Mosquito-borne disease

Viral hemorrhagic fevers

What Is Yellow Fever?

Yellow fever is a disease caused by yellow fever virus, a member of the flavivirus (FLAY-vih-vy-rus) group of viruses. The disease gets its name because it often causes jaundice*, which tints the skin yellow, and a high fever. Yellow fever also can cause kidney failure and uncontrolled bleeding, or hemorrhaging (HEM-rij-ing). Many cases produce only mild illness, but severe cases of yellow fever can be fatal. Once someone has survived the disease, the person will have lifetime immunity* against it.

(JON-dis) is a yellowing of the skin, and sometimes the whites of the eyes, caused by a buildup in the body of bilirubin, a chemical produced in and released by the liver. An increase in bilirubin may indicate disease of the liver or certain blood disorders.
(ih-MYOON-uh-tee) is the condition of being protected against an infectious disease. Immunity often develops after a germ is introduced to the body. One type of immunity occurs when the body makes special protein molecules called antibodies to fight the disease-causing germ. The next time that germ enters the body, the antibodies quickly attack it, usually preventing the germ from causing disease.

Yellow fever afflicts both humans and monkeys and has been known since at least the 1600s. The disease is not spread by person-to-person contact. It is transmitted by several different species of mosquitoes; a person can contract yellow fever only from the bite of a mosquito that has bitten an infected person or monkey.

The disease once caused epidemics in the Americas, Europe, and the Caribbean, but at the beginning of the twenty-first century the disease occurs almost exclusively in South America and Africa. Each year, outbreaks lead to an estimated 200,000 cases and 30,000 deaths worldwide. Vaccines against the virus were developed in 1928 and 1937, and mosquito-eradication programs have made great progress in controlling the disease. The last recorded outbreak of yellow fever in the United States was in New Orleans in 1905. However, lapses in prevention programs in Africa and South America have allowed yellow fever to once again become a serious public health issue on those continents.

Are There Different Kinds of Yellow Fever?

Yellow fever occurs as three subtypes: epidemic (urban), intermediate, and jungle-acquired. Epidemic yellow fever spreads in densely populated areas of Africa and South America via the bite of Aedes aegypti (a-E-deez eh-JIP-tie) mosquitoes. Intermediate yellow fever occurs in Africa as the result of mosquitoes breeding in humid flat grasslands (savannahs) during rainy seasons, then infecting both monkeys and humans. In dry seasons, the virus can remain alive in unhatched mosquito eggs that are resistant to the heat.

Jungle-acquired yellow fever occurs mainly in South America when mosquitoes pick up the virus from infected forest monkeys and then transmit the disease to humans in jungles and rainforests. People who are regional settlers, soldiers, or agricultural or forestry workers are at greatest risk for this less common form of the disease.

How Do People Know They Have Yellow Fever?

After an incubation* period of 3 to 6 days, the yellow fever virus begins to produce symptoms. An early phase of disease occurs, which includes fever, headache, muscle aches, and vomiting. The infected person may have a slower heartbeat than that expected with a high fever. After a few days, most of the symptoms disappear. Many people recover from yellow fever at this point without complications. However, about 15 percent of patients develop a second, toxic phase of the disease, in which fever reappears and the disease becomes more severe. Inflammation of the liver occurs, along with jaundice, stomach pains, and vomiting. The mouth, nose, eyes, and stomach can bleed uncontrollably, with blood present in vomited material and bowel movements. The kidneys may begin to fail, and patients may go into a coma (an unconscious state in which a person cannot be awakened).

(ing-kyoo-BAY-shun) is the period of time between infection by a germ and when symptoms first appear. Depending on the germ, this period can be from hours to months.

How Do Doctors Diagnose and Treat Yellow Fever?

Early stages of yellow fever can be easily confused with other diseases such as malaria*, typhoid fever*, and other hemorrhagic (heh-muh-RAH-jik) fevers and types of viral hepatitis*. Blood tests can detect whether a patients body has produced yellow fever antibodies* to fight the infection. Doctors also will take a travel history to see if a patient recently has visited a country where yellow fever occurs.

(mah-LAIR-e-uh) is a disease spread to humans by the bite of an infected mosquito.
*typhoid fever
(TIE-foyd FEE-ver) is an infection with the bacterium Salmonella typhi that causes fever, headache, confusion, and muscle aches.
(heh-puh-TIE-tis) is an inflammation of the liver. Hepatitis can be caused by viruses, bacteria, and a number of other noninfectious medical conditions.
(AN-tih-bah-deez) are protein molecules produced by the bodys immune system to help fight specific infections caused by microorganisms, such as bacteria and viruses.

No specific treatment exists for yellow fever. Care is geared toward treating complications of the disease. In serious cases, intensive care in the hospital usually is needed. Patients may be given fluids to prevent dehydration*, and blood transfusions* may be necessary if bleeding is severe.

(dee-hi-DRAY-shun) is a condition in which the body is depleted of water, usually caused by excessive and unre-placed loss of body fluids, such as through sweating, vomiting, or diarrhea.
(trans-FYOO-zhunz) are procedures in which blood or certain parts of blood, such as specific cells, are given to a person who needs them because of illness or blood loss.

Most people who contract yellow fever recover from the early phase of the disease within a week; those who progress to the toxic phase may take several weeks or longer to recover. About half of those who develop toxic phase symptoms die within 2 weeks; the other half may recover without significant long-term problems.

How Can Yellow Fever Be Prevented?

Vaccination against yellow fever is the single most important prevention measure, and it is a must for people traveling to countries where the disease is common. Most countries in which yellow fever occurs require a certificate proving that travelers have been vaccinated before they are allowed into the country. One dose of vaccine provides at least 10 years of immunity.

Doctors recommend that infants under 6 months of age, pregnant women, people allergic to eggs (eggs are used in producing the vaccine), and people with weakened immune systems (such as people who have AIDS* or certain cancers) not receive the vaccine; these people are advised to delay visits to countries where yellow fever is endemic*.

or acquired immunodeficiency (ih-myoo-no-dih-FIH-shen-see) syndrome, is an infection that severely weakens the immune system; it is caused by the human immunodeficiency virus (HIV).
(en-DEH-mik) describes a disease or condition that is present in a population or geographic area at all times.

Avoiding mosquito bites when traveling abroad reduces the risk of contracting yellow fever. To help prevent infection, experts suggest that travelers:

  • wear long sleeves and pants
  • avoid going outside when mosquitoes are activeat dawn, dusk, and early evening
  • use mosquito repellent
  • sleep beneath a mosquito net

See also

Dengue Fever

Hepatitis, Infectious


West Nile Fever



U.S. Centers for Disease Control and Prevention (CDC), 1600 Clifton Road, Atlanta, GA 30333. The CDC is the U.S. government authority for information about infectious and other diseases, including yellow fever.

Telephone 800-311-3435

World Health Organization (WHO), Avenue Appia 20, 1211 Geneva 27, Switzerland. WHO provides information about yellow fever at its website.

Telephone 011-41-22-791-2111

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yellow fever

yellow fever (yel-oh) n. an infectious disease, caused by an arbovirus, occurring in tropical Africa and South America. It is transmitted by mosquitoes, principally Aëdes aegypti. The virus causes degeneration of the tissues of the liver and kidneys. Symptoms include chill, headache, pains in the back and limbs, fever, vomiting, constipation, a reduced flow of urine (which contains high levels of albumin), and jaundice. Yellow fever often proves fatal.

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yellow fever

yellow fever Acute, infectious disease marked by sudden onset of headaches, fever, muscle and joint pain, jaundice and vomiting; the kidneys and heart may also be affected. It is caused by a virus transmitted by mosquitoes in tropical and subtropical regions. It may be prevented by vaccination.

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yellow fever

yel·low fe·ver • n. a tropical viral disease affecting the liver and kidneys, causing fever and jaundice and often fatal. It is transmitted by mosquitoes.

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