eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease
Yellow Fever
Updated: Sep 15, 2009
Introduction
Background
Yellow fever (YF) is a mosquito-borne viral infection endemic to Africa and South America. It is characterized by variable symptoms ranging from a minimal flulike illness to one that may be complicated by a toxic phase characterized by hemorrhage, hepatic failure, proteinuria, renal failure, and death. Supportive care is the only treatment. The mortality rate is 20-50%. Prevention using the live, attenuated 17D vaccine is highly efficacious. Yellow fever virus, an arbovirus, is the type species for the family Flaviviridae and is a single, positive-stranded, enveloped RNA virus. The envelope consists of a lipid bilayer containing an envelope glycoprotein and a matrix protein. The single RNA is complexed with a capsid protein.
Immediately report all suspected or confirmed cases of yellow fever to local and state health departments, which then report immediately to the Division of Global Migration and Quarantine (1-404-498-1600) or Division of Vector-Borne Infectious Diseases (1-970-221-6400), Centers for Disease Control and Prevention (CDC). If local or state health departments cannot be reached, contact the CDC directly.
All travelers going to destinations in the tropics or developing countries should at least see a health provider who is familiar with traveler's health recommendations from public health agencies. One source of such recommendations is the Traveler's Health page of the CDC.
History and Epidemiology
Diseases described in texts as old as 400 years match yellow fever. Major 18th-century and 19th-century epidemics occurred in Africa, the Caribbean, Central America, Europe, North America, and South America. In 1793, an epidemic in Philadelphia resulted in the death of approximately 10% of the city's population. In 1881, Carlos Finlay proposed the mosquito-borne transmission of yellow fever. In 1900, Walter Reed and colleagues observed that the infectious agent, a filterable virus, was transmitted by means of a mosquito bite. General Gorgas acted on this information, rapidly eliminating yellow fever from Havana with a mosquito-eradication program. In 1905, the last major yellow fever outbreak occurred in New Orleans, Louisiana. In 1927, yellow fever virus from a viremic man from Ghana was isolated in Rhesus monkeys. Viral strains from South America are closely related to those from West Africa. This observation supports the supposition that yellow fever virus originated in West Africa.
In the 1930s, French and American investigators independently developed effective and safe vaccines. In 1932, a jungle transmission cycle was demonstrated. Vigorous measures of mosquito control (primary) and vaccination (secondary) led to the elimination of yellow fever during the early-to-mid 20th century from all areas of the world except parts of Africa, South America, and the Caribbean (Trinidad had intermittent transmission in 1954, 1959, and 1978). In 1942, the last major urban epidemic in the Western Hemisphere (Brazil) occurred. Jungle transmission persists in South America. Urban, intermediate, and jungle transmission persist in sub-Saharan African, where outbreaks have increased due to cessation of vaccination campaigns after 1960.
Overall, yellow fever reemergence has occurred since 1985, as reflected in the number of cases per year officially reported to the World Health Organization (WHO). See Frequency. Approximately 80-90% of the cases reported are from sub-Saharan Africa, and mostly from West Africa.
Yellow fever is reemerging in South America. Three factors contributing to this reemergence include (1) the reinvasion of Aedes aegypti since 1980 secondary to reduction in mosquito-control measures; (2) the juxtaposition of areas of jungle transmission and areas of A aegypti infestation, allowing the latter to become reinfected; and (3) the lack of yellow fever vaccination in densely populated areas outside of the traditional jungle transmission zone, creating huge populations at risk.
This female Aedes aegypti mosquito is shown here after landing on a human host. The A aegypti mosquito is a known transmitter of both dengue fever and yellow fever. A aegypti is sometimes referred to as the yellow fever mosquito. The viruses are transferred to the host when bitten by a female mosquito. Image courtesy of the Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO).
From 2007–2009, yellow fever cases in South America were reported outside the usual areas of risk in Argentina, Brazil, and Paraguay.
In Argentina, 5 cases of jungle yellow fever (with 1 death) were reported in the Misiones Province. To contain this outbreak, more than 1.4 million people in Argentina have received yellow fever vaccine (0.4 million in Misiones Province).
In Brazil, 45 cases of jungle yellow fever were reported, with 25 deaths among 4 states. Parts of the states of Sao Paulo and Minas Gerais reported cases outside their usual risk areas, and the state of Espirito Santo, which is on the coast and is not a usual risk area at all, reported cases; however, it is no longer considered a risk area as of late 2008. In December 2008, Rio Grande do Sul, which is also outside the usual reporting area, reported 18 cases, including 7 deaths. Because February 2009, the state of Sao Paulo has reported 25 yellow fever cases, including 9 deaths. To contain this outbreak, yellow fever vaccinations have been increased in these states and increased among travelers to these states, although yellow fever vaccination coverage is already extensive.
In Paraguay, the first cases of yellow fever in over 30 years were reported in 2008 (25 cases, 8 deaths), mostly jungle yellow fever but possibly urban yellow fever; San Lorenzo reported 9 cases with 3 deaths. These occurred in 3 departments (San Pedro, Central, Cuaagcu). To contain this outbreak, more than 1.2 million people in 15 departments of Paraguay have received yellow fever vaccine.
In Argentina and Brazil, the human outbreaks were preceded by weeks with an epizootic in monkeys.
Since 1980, A aegypti has repopulated large swaths of Central America, as well as the Caribbean coastal areas of the United States and most of Florida, allowing for the potential reemergence of yellow fever in these areas.
Urban, intermediate, and jungle transmissions of yellow fever persist in sub-Saharan Africa (West, Central, and East), with periodic large outbreaks, largely because of cessation of yellow fever vaccination campaigns after 1960. As a result, several significant outbreaks of yellow fever have occurred across sub-Saharan Africa threatening millions of people. This has led to a changed yellow fever strategy by WHO. The long term strategy is to include yellow fever vaccination in the national childhood routine vaccination schedule; however, at least 30 years are required for this strategy to have a major impact. The short term strategy is as follows:
- Stockpiling of the yellow fever vaccine (approximately 11 million doses per year) for use during outbreaks, such as those across South America and Africa (In Burkina Faso, 466,000 were immunized in Nov 2008; in the Central African Republic, 184,000 were immunized in October 2008; in Guinea, 140,000 were immunized in September 2008)
- Developing of adequate supplies for ongoing use for outbreaks and mass vaccination campaigns
- Establishment of vaccination for populations at highest risk for an epidemic
These strategies are being implemented by the World Health Organization (WHO) in conjunction with the Global Alliance for Vaccine and Immunization, the International Coordinating Group for Vaccine Provision for Epidemic Meningitis Control (yellow fever subgroup), United Nation's Children's Fund (UNICEF), the International Federation of the Red Cross and Red Crescent Societies, and Medicins sans Frontieres, among others.
Areas of Endemic Yellow Fever
In Africa, yellow fever occurs in areas between 15° north and 10° south of the Equator, a region encompassing 34 countries with a total population of nearly 500 million people.1
Yellow fever is also transmitted in Panama south of the canal zone and in Trinidad.
In South America and the Caribbean, enzootic countries include Bolivia, Brazil, British Guyana, Colombia, Ecuador, French Guyana, Panama (south of the Canal Zone), Peru, Surinam, Trinidad, and Venezuela. Human cases were reported in the 1990s in Bolivia, Brazil, Colombia, Ecuador, and Peru.
In Asia, although conditions currently exist for the transmission of yellow fever in Asia, no documented transmission has ever occurred there. Evidence suggests that previous infection with another flavivirus (eg, those causing dengue) may confer protection from yellow fever. This has been cited as the reason why yellow fever has not been observed in Asia.
Although conditions for the transmission of yellow fever are noted on the Indian subcontinent, no such transmission has ever been reported.
Transmission
In some publications, the term sylvatic (from the Latin, silva meaning wood) is used synonymously with intermediate cycle, in others, it is used synonymously with jungle cycle.
Jungle cycle
The mosquito transmits the virus to wild nonhuman primates (or possibly an incidental human host), and then it is transmitted to another mosquito. This cycle is confined to rain forests, and human hosts are usually males working in the forests clearing trees. In Africa, Aedes species not including A aegypti are implicated, while Haemagogus species are involved in South America.
Urban cycle
The mosquito transmits the virus to a human host, and then it is transmitted to another mosquito. Confined to urban areas, A aegypti, a domestic mosquito that breeds in human-made containers, is the primary vector.
Intermediate (savannah) cycle
The mosquito transmits the virus to wild nonhuman primates and human hosts, and then it is transmitted to another mosquito. Confined to moist savannas and forest savanna ecotones of Africa, this is the most common cycle for outbreaks in Africa. Many villages in a given area are affected simultaneously. Mortality appears to be lower with these outbreaks. Semidomestic mosquitoes that live in and outside of villages are the primary vectors. This cycle may act as a bridge between the jungle and urban areas, leading to spread to urban centers where, if contact is made between domestic mosquitoes and an unvaccinated human population, an urban epidemic can result.
Biology of the Mosquito Spreading Yellow Fever
Feeding habits
These mosquitos are diurnal feeders, and only females feed on blood. In humans, yellow fever virus is transmitted to the mosquito from an ill human only during the initial 3-4 days of illness. If the female is interrupted while feeding, it may seek another host on which to feed, leading to multiple transmissions during a feeding cycle. The extrinsic incubation period (interval from infection of the mosquito with yellow fever virus until the mosquito can transmit yellow fever to another host) is 12-21 days.
Vertical transmission
Yellow fever virus enters the ovum in the female mosquito and survives there during the dry season. Less than 1% of female mosquito progeny are infected. This is important for survival of the virus during the dry season.
Horizontal transmission
Uninfected female mosquitoes bite infected hosts, providing for viral amplification. This is essential for survival of the virus. Approximately 3-10 virions are necessary to infect a mosquito.
Breeding habits
Mosquitoes breed in stagnant water, including rainwater in tree holes, human-made water storage vessels, used vehicle tires, and in other collections of water in and about dwellings, such as broken coconut shells, flower vases, gutters, tin cans, and water drums. Seasonal transmission occurs, with peak transmission usually being the time of peak humidity and rainfall. In Africa, this is the mid rainy season to the early dry season. In South America, this occurs from January to March. However, transmission is not limited to the peak season.
Pathophysiology
Yellow fever virus is transferred from the infected female mosquito's salivary gland by means of saliva introduced into a bite wound during a blood meal. The virus replicates in local tissues and regional lymph nodes. The virus can then infect a feeding mosquito during the initial 3-4 days of the illness. No human-to-human transmission is known. Hematogenous spread to the bone marrow, kidney (probable), liver (main target), myocardium, and spleen ensues, where further replication occurs. Cerebral edema and cerebral petechial hemorrhages result from secondary factors. In the hemorrhagic diathesis that may follow, disseminated intravascular coagulation (DIC) involves decreased synthesis of coagulation factors, altered platelet function, and bleeding from the GI mucosa and abdominal/pleural serosa.
Myocardial fiber injury occurs secondary to direct virus activity, with cloudy swelling and fatty change. Shock and death can result from Yellow fever. Multiple organ insult involves the liver, kidney, brain, and heart. Other effects are hemorrhage and secondary effects of vasoactive cytokines. In an immune response, viral neutralizing antibodies are present by the end of the first week, and the virus is rapidly cleared. Immune response confers lifelong immunity. The role of immune response in pathogenesis has not yet been established.
Frequency
United States
Since 1996, 3 fatal cases of yellow fever have been reported in American travelers to the Amazon. None of the patients were immunized against yellow fever. The CDC estimates that yellow fever immunization of travelers to yellow fever endemic areas has declined 50% from 1992-1998. The first 2 did receive other pretravel vaccinations, including the hepatitis A vaccine. The third person did not receive a medical consultation, yellow fever vaccine, or malaria prophylaxis before traveling. Because patients with yellow fever can present with a mild influenzalike illness, yellow fever may not be recognized and go unreported.
In addition, the outfitter of one of the patients stated, "The International medical community suggests yellow fever and malaria prophylaxis for the Amazon region. This is not a requirement to enter Brazil, but merely a suggestion." The brochure of a travel agent stated, "We do not suggest any inoculations of any kind for this trip...But to make sure you are worry free, consult with your personal physician."
These cases illustrate that some outfitters, travel agents, and physicians may underestimate health risks of travelers.
In 1996, a 45-year-old man spent 9 days in the jungles of Brazil. He returned to the United States with headache, myalgias, arthralgias, and chills. During an initial visit to an emergency department, he had fever, leukopenia, thrombocytopenia, and mild elevations in hepatic transaminase values. He subsequently developed jaundice and hemorrhagic manifestations and died 10 days after developing symptoms. Yellow fever virus was isolated from tissue specimens.
In 1999, a 48-year-old man returned to the United States after a 10-day trip to a forested area of Venezuela. During his trip, he received multiple mosquito bites. On the day of his return, he developed fever, chills, headache, photophobia, myalgias, arthralgias, nausea, vomiting, constipation, upper abdominal discomfort, and weakness. He developed hemorrhagic manifestations and died 9 days after developing symptoms. Yellow fever viral antigens were isolated from postmortem liver specimens by using immunohistochemical methods.
In 2002, a 47-year-old man traveled to the Brazilian Amazon to fish. He slept in an air-conditioned boat and wore clothing impregnated with N, N -diethyl-m-toluamide (DEET). He returned to Texas and presented to an emergency department the same day, complaining of 4 days of crampy abdominal pain, 1 day of fever (102.8°F [39.3°C]), and severe headache. He was treated for presumed rickettsial infection and sent home.
Two days later, he was admitted for intractable vomiting. On initial evaluation, he had leukopenia (WBC count 2.3 X 109 [2300/µL]), coagulopathy, hepatic failure, and renal failure. He was treated for malaria. Bacterial cultures of blood, urine, and cerebrospinal fluid (CSF) were negative, as were malaria smears. On the fourth day, he developed shock and seizures. On the fifth day, he died. Serum tests for immunoglobulin G (IgG) and immunoglobulin M (IgM) were negative for yellow fever on days 2-7. Reverse-transcriptase polymerase chain reaction (PCR) assay of serum samples obtained on days 4,5, and 7 and a postmortem liver specimen demonstrated yellow fever virus RNA.
International
Each year, an estimated 200,000 cases of yellow fever occur in Africa and South America combined, causing an estimated 30,000 deaths. The number of total cases reported to the WHO each year from Africa and South America ranges from hundreds to a few thousand. The true incidence is estimated to be at least 40 times more than this in Africa and 10 times more than this in South America.
Underreporting occurs because many cases are mild or asymptomatic, because cases occur in remote regions, because populations are moving or displaced, and/or because the public health infrastructure is nonexistent, particularly in Africa where regional conflicts are ongoing.
Since 1980, yellow fever has been reemerging, with more cases being reported now than in the late 1940s. This trend is evident in Africa, where the number of countries reporting cases and the number of small-scale outbreaks have increased, where large populations are losing immunity (due to the end of mass-prevention campaigns in the early1960s), and where vectors are present in urban areas. In addition, urban populations are markedly increasing by 4.8% per year), populations are migrating (forced and unforced), and vaccine cannot be procured because of the expense.
In South America, A aegypti is now present in urban areas. A aegypti is the vector of urban yellow fever. It breeds in domestic and peridomestic containers. In the past 30 years, A aegypti has reinfested most countries, where its eradication was previously accomplished.
In 2008, A aegypti was present in the southern United States, Central America, the Caribbean, most major urban centers in tropical South America, the Indian subcontinent, Southeast Asia, Oceania, and northeast Australia. A legitimate concern is that yellow fever could be reintroduced into these areas at any time because of global travel and trade and because of migrating populations. That said, yellow fever has never been reported endemic to Asia.
Travel to countries where yellow fever is endemic poses a threat to the unimmunized traveler. Each year, an estimated 9 million travelers from North America, Europe, and Asia travel to endemic countries. At least one third of these travelers are exposed to areas where active transmission is known or unknown to be occurring. Since 1979, at least 9 cases of traveler-related yellow fever have been reported. Seven individuals, all unimmunized, died. Of the 2 survivors, 1 had been immunized. All traveled to rural areas, where no epidemics were known to be occurring.
The overall risk to an unimmunized traveler in Africa who is entering an area with epidemic activity is 1:267 for yellow fever illness and 1:1333 for yellow fever death during a 2-week trip. If the area is undergoing a silent period (ie, existing surveillance methods fail to detect active transmission), the risk is 1:2000 for yellow fever illness and 1:10,000 for yellow fever death for a 2-week trip. In the South America the risk is estimated to be one tenth as much.
In West Africa, the most dangerous time of year is July-October. In Brazil, it is January-March. In South America, Iguarzú Falls on the Argentine-Brazil border is not considered a high risk destination, but the risk is not zero. For example, in 1996 and 2001, risk increased because of epizootic expansion. This example illustrates how the status of yellow fever transmission in endemic countries is constantly shifting and unpredictable.
Mortality/Morbidity
Mortality rates due to the toxic form of disease vary from 25-50%, but the mortality rate has been reported to be as low as 1%. The number of reported deaths from yellow fever among travelers over the past 10 years has increased, and more can be expected unless yellow fever vaccine is most appropriately used.
Morbidity is minimal unless complications develop from the toxic form of the disease. Recovery from the disease confers long-lasting immunity.
Race
No racial predilection is known.
Sex
No sex predilection is known. More men than women are infected in jungles and forests because of occupational exposure.
Age
No age predilection is known. However, most infections in endemic countries occur in persons younger than 15 years because that is the largest population of nonimmune individuals. Occupational or recreational exposure may be increased among children as well.
Clinical
History
The clinical spectrum of yellow fever (YF) ranges from a minimally symptomatic flulike illness to a catastrophic illness complicated by hemorrhage and organ failure (primarily the liver and kidney). Several distinct phases of yellow fever are outlined below.
- Incubation period (3-6 d): No prodromal symptoms occur.
- Period of infection (3-4 d)
- Viremia is present. Susceptible biting mosquitoes can be infected with yellow fever.
- Symptoms typically begin abruptly with fever, chills, malaise, prostration, headache, dizziness, myalgia (particularly lumbosacral area), anorexia, nausea, and vomiting.
- Period of remission (2-24 h): Symptoms and fever abate.
- Abortive phase (>1 d): Recovery occurs without further symptoms.
- Period of intoxication (3-5 d): Liver failure, hemorrhagic diathesis, and kidney failure occur.
- This period develops in approximately 15% of all cases.
- This stage is fatal in 1-50% of cases that develop toxicity.
- Previous symptoms and new symptoms include fever with high temperatures, chills, anxiety, confusion, lethargy, prostration, jaundice, epistaxis, anorexia, epigastric pain, nausea, vomiting, hematemesis, melena, lumbosacral pain, and decreased urine output.
- Complications include bacterial pneumonia and sepsis.
- Period of convalescence (days to weeks)
- The patient completely recovers without sequelae.
- Complications may include protracted weakness and fatigability.
Physical
The Pan American Health Organization has published a case definition for yellow fever to aid in surveillance.
- The clinical case definition is as follows: An illness characterized by acute onset of fever followed by jaundice within 2 weeks of onset of first symptoms plus 1 of the following:
- Bleeding from the nose, gums, GI tract, or skin
- Death within 3 weeks of illness onset
- A case of yellow fever is classified as suspected if it meets the clinical definition or if other causes of fever or jaundice are excluded.
- A suspected yellow fever case can be confirmed by laboratory criteria or when it is epidemiologically linked to a laboratory-confirmed case or outbreak.
- Data to be reported to public health authorities include patient-specific identifier, age or date of birth, location, laboratory results, vaccination history, outcome of infection (alive, dead, unknown), case classification, and date of death (if dead).
- Physical examination findings are nonspecific and may include the following:
- Fever
- Pulse - Slow, inversely proportional to temperature (Faget sign)
- Anxiety, lethargy, prostration, confusion, coma
- Facies - Flushed
- Conjunctival injection
- Abdominal tenderness
- Hemorrhagic manifestations - Epistaxis, gingival bleeding, hematosis, melena, hematuria
- Urine output - Decreased
- Shock
Causes
- See Pathophysiology
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Further Reading
Keywords
yellow fever, YF, Flaviviridae, tropical infections, viral infections, yellow fever virus, yellow jack, proteinuria, mosquito, Aedes aegypti, disseminated intravascular coagulation, DIC, high temperatures, chills, anxiety, confusion, lethargy, prostration, jaundice, epistaxis, anorexia, epigastric pain, nausea, vomiting, hematemesis, melena, lumbosacral pain, pneumonia, sepsis, infection, treatment, diagnosis
