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Yellow Fever

  • Author: Mary T Busowski, MD; Chief Editor: Mark R Wallace, MD, FACP, FIDSA  more...
 
Updated: Jun 26, 2015
 

Practice Essentials

A mosquito-borne disease (see the image below), yellow fever can manifest as a spectrum of presentations ranging from asymptomatic illness to acute-onset viral hepatitis and hemorrhagic fever.[1, 2]

This female Aedes aegypti mosquito is shown after This female Aedes aegypti mosquito is shown after landing on a human host. The A aegypti mosquito is a known transmitter of dengue fever and yellow fever. A aegypti is sometimes referred to as the yellow fever mosquito. The viruses are transferred to the host when he or she has been bitten by a female mosquito. Image courtesy of the CDC/World Health Organization (WHO).

See 11 Travel Diseases to Consider Before and After the Trip, a Critical Images slideshow, to help identify and manage infectious travel diseases.

Signs and symptoms

History

Yellow fever is usually a mild, self-limiting illness consisting of fever, headache, myalgia, and malaise. More serious illness presents with the abrupt onset of the following:

  • General malaise
  • Fever
  • Chills
  • Headache
  • Lower back pain
  • Nausea
  • Dizziness

This is followed by a period of remission; the patient may then either recover or progress to fatal illness. The return of symptoms is marked by the following:

  • Fever
  • Vomiting
  • Abdominal pain
  • Renal failure
  • Hemorrhage

Physical examination

Physical findings in yellow fever include the following:

  • Fever
  • Relative bradycardia for the degree of fever (Faget sign)
  • Conjunctival injection
  • Skin flushing

As the disease progresses, additional physical findings include the following:

  • Scleral icterus
  • Jaundice
  • Epigastric tenderness
  • Hepatomegaly

The following will also often be apparent:

  • Petechiae
  • Purpura
  • Mucosal bleeding
  • Gastrointestinal bleeding (gross or occult)

Organ ischemia, which primarily affects the kidneys and central nervous system, leads to altered mental status and/or signs of volume overload. In the late stages of yellow fever, patients present with the following:

  • Tachycardia
  • Hypothermia or hyperthermia
  • Hypotension

Individuals who are severely hypoperfused appear mottled and cyanotic; they are also often obtunded. Tachypnea and hypoxia with impending respiratory failure may develop as a consequence of sepsis and acute respiratory distress syndrome (ARDS).

See Clinical Presentation for more detail.

Diagnosis

Laboratory studies

  • Complete blood count (CBC)
  • Coagulation studies
  • Chemistries
  • Urinalysis

Imaging studies

Chest radiography is used to evaluate the extent of pulmonary edema, to reveal secondary bacterial pulmonary infections, and to aid in ventilator management if intubation is required.

Liver function tests

Transaminitis precedes the appearance of jaundice, and the degree of liver dysfunction in the acute phase may be predictive of the clinical course.

Specific tests for yellow fever

  • Rapid detection methods (eg, polymerase chain reaction assay)
  • Serologic tests (eg, enzyme-linked immunosorbent assay)
  • Immunohistochemical tissue staining - To find the yellow fever antigen

See Workup for more detail.

Management

No specific treatment exists for yellow fever; however, supportive care is critical. Severely ill patients should be treated in an intensive care setting. The required management consists of the following:

  • Vasoactive medications
  • Fluid resuscitation
  • Ventilator management
  • Treatment of disseminated intravascular coagulation (DIC), hemorrhage, secondary infections, and renal and hepatic dysfunction

To manage coagulopathy in yellow fever, the following recommendations have been made:

  • In actively bleeding patients, administer fresh frozen plasma to maintain prothrombin time at 25-30 seconds
  • In patients with DIC, heparin has been recommended for treatment

Additional supportive care recommendations for patients with yellow fever include the following:

  • A nasogastric or orogastric tube may be required to provide nutritional support
  • Patients with renal failure or refractory acidosis may require dialysis
  • Salicylates should be avoided because of the increased risk of bleeding secondary to platelet dysfunction

Prevention

The currently available yellow fever vaccine confers near lifelong immunity in 95% of patients.[3] For travel certification, however, revaccination is recommended every 10 years.

See Treatment and Medication for more detail.

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Background

Yellow fever is one of many causes of viral hemorrhagic fever. It is a member of the flavivirus family (group B arbovirus). The Flavivirus genus is composed of more than 70 arthropod-transmitted viruses, of which 30 are known to cause human disease. Other flaviviral infections include dengue, Japanese encephalitis, and tick-borne encephalitis. It is important to consider this group of viruses in the clinical differential of CNS infection, hemorrhagic fever, and acute febrile illnesses with arthropathy. Yellow fever virus is shown in the image below. (See Etiology.)

Yellow fever virus. Image courtesy of the Centers Yellow fever virus. Image courtesy of the Centers for Disease Control and Prevention.

A mosquito-borne disease, yellow fever can manifest as a spectrum of presentations, ranging from asymptomatic illness to acute-onset viral hepatitis and hemorrhagic fever. (See Clinical and Workup.)

From 1793-1822, yellow fever was one of the most dreaded diseases in US port cities. Yellow fever outbreaks in the United States shaped American history and influenced important national decisions. In the 1780s, yellow fever outbreaks in Philadelphia were responsible for killing one tenth of the city's population.[4]

The disease may have played a part in shaping the decision to move the nation's capital out of Philadelphia.[4] The disease had such an impact on the local economies that, in 1803, Napoleon, with his troops decimated by yellow fever, had few reservations about selling the affected Louisiana and western territories to the US government.

Fascinating accounts document how humankind's struggle with yellow fever has shaped world history. The French effort to develop the Panama Canal was not lost through engineering failures, but by disease. Frenchmen died of yellow fever in alarming numbers, leading to Panama being coined "the white man's graveyard."[5]

In the early 20th century, Carlos Findlay and Walter Reed's discovery of Aedes aegypti as a source of yellow fever transmission led to the eradication of yellow fever in parts of Latin America. Isolation of the virus and later development of the 17D vaccine by Max Theiler helped to eliminate A aegypti and yellow fever from countries in Africa and the Americas during the mid 20th century.[6]

Yellow fever is transmitted by tree-hole breeding mosquitoes (Haemagogus and Aedes species) during the tropical wet season and early dry season.[1] Genomic sequence analyses suggest that yellow fever evolved from other mosquito-borne viruses about 3000 years ago in Africa. It is surmised that the yellow fever virus was introduced to the Americas by Dutch slave traders during the 17th century.

The first documented epidemic occurred in the Yucatan Peninsula and spread through the Caribbean basin. This was the result of ship travel and the continued importation of slaves from West Africa. Vessels infested with A aegypti mosquitoes brought yellow fever into New England and several port cities throughout North America.

Large vaccination campaigns and A aegypti control programs have decreased the incidence of yellow fever worldwide. Nonetheless, yellow fever has reemerged across Africa and South America, despite the availability of an effective live-attenuated 17D vaccine. The populations at highest risk for the illness are those in countries that lack the funding and infrastructure to support a widespread vaccination program. (See Epidemiology and Treatment.)[7, 8]

Flaviviruses, including those that cause yellow fever, also have a potential use as biologic weapons.[9]

Transmission

As an arthropod-borne virus (ie, arbovirus), yellow fever is transferred from host to host by contaminated mouthparts of mosquitoes. Different species of the Aedes and Haemagogus genus breed in unique habitats. For example, Aedes aegypti, the first identified vector of yellow fever, is able to breed in small amounts of temporary standing water and, thus, in close association with humans.

In contrast, other mosquitoes are forest canopy dwellers and thrive only in rainforests. Consequently, these vectors transmit the virus in 3 ways: (1) between monkeys, (2) from monkeys to humans, and (3) from person to person.[10, 11] This variability has led to 3 types of transmission cycles (depicted in the diagram below): sylvatic (jungle), intermediate (savannah), and urban. (See the diagram below.)

Transmission cycles of yellow fever in Africa and Transmission cycles of yellow fever in Africa and South America. Adapted from Annu Rev Entomol. 2007. 52:209-29.

Sylvatic (jungle) cycle

In tropical rainforests, yellow fever virus is endemic among lower primates. Infected monkeys pass the virus to mosquitoes that feed on them. Persons who subsequently enter the forest (often workers, eg, loggers, and travelers) are infected with this form of disease. In Africa, the principal vector of the jungle cycle is A africanus; in South America, H janthinomys is the primary vector for jungle transmission. Nonhuman primates remain the preferred host in this setting.

Intermediate (savannah) cycle

In moist and semihumid areas of Africa, semi-domestic mosquitoes (which breed in the wild and around households) feed primarily on monkeys but will also feed on humans when the opportunity arises. This cycle likely reflects the evolution of yellow fever into an epidemic human disease. It is the most common cycle present in Africa and frequently leads to small-scale outbreaks in villages. However, transmission can potentially lead to large-scale epidemics if an infected individual carries the disease into an urban region. This cycle has not been identified in South America.

Urban cycle

A aegypti is responsible for the transmission of urban yellow fever in Africa and South America. This mosquito can breed in urban water containers, allowing mosquito transmission of the yellow fever virus from human to human. Thus, A aegypti can infect large populations of unvaccinated individuals. Urban outbreaks are rare in South America, yet they are still occasionally reported in densely populated regions in Africa. (See the image below.)

This female Aedes aegypti mosquito is shown after This female Aedes aegypti mosquito is shown after landing on a human host. The A aegypti mosquito is a known transmitter of dengue fever and yellow fever. A aegypti is sometimes referred to as the yellow fever mosquito. The viruses are transferred to the host when he or she has been bitten by a female mosquito. Image courtesy of the CDC/World Health Organization (WHO).

Patient education

Recommend yellow fever vaccination for international travelers going to endemic regions. Current information, including new outbreaks and information for travelers, can be obtained online from the World Health Organization and the Centers for Disease Control and Prevention.

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Etiology

Yellow fever virus is a positive-sense, single-stranded, ribonucleic acid (RNA) ̶ enveloped flavivirus with a diameter of about 50-60 nm. The virus is transmitted via the saliva of an infected mosquito. Local replication of the virus takes place in the skin and regional lymph nodes. Viremia and dissemination follow.

The virus gains entrance through receptor-mediated endocytosis. RNA synthesis occurs in the cytoplasm and protein synthesis takes place in the endoplasmic reticulum. Virions are released through the cell membrane. The viral envelope contains a lipid bilayer taken from the infected cell. Virulence factors include the following:

  • Capsid protein C - Facilitates viral binding
  • Membrane protein M - A minor glycoprotein
  • E proteins - Initiate infection and mediate viral entry
  • Nonstructural protein 1 (NS1) - May play a role in RNA replication
  • NS2A protein - Involved in RNA replication and packaging
  • NS2B and NS3 - Form a complex and are involved in polyprotein processing and replication of RNA
  • NS5 - Has a major role in RNA replication

The E protein interacts with the cellular receptor, and virions are endocytosed into the dendritic cells. Subsequently, epidermal dendritic cells and lymph channels disseminate virions. After invasion in the host, Kupffer cells (fixed liver macrophages) are infected within 24 hours.

The infection quickly disseminates to the kidneys, lymph nodes, spleen, and bone marrow. Renal failure occurs as renal tubules undergo fatty change and eosinophilic degeneration, likely due to direct viral effect, hypotension, and hepatic involvement.

The liver is the most important organ affected in yellow fever. The disease was labeled "yellow" based on the profound jaundice observed in affected individuals. Hepatocellular damage is characterized by lobular steatosis, necrosis, and apoptosis with subsequent formation of Councilman bodies (degenerative eosinophilic hepatocytes).[12]

The kidneys also undergo significant pathologic changes. Albuminuria and renal insufficiency evolve secondary to the prerenal component of yellow fever; consequently, acute tubular necrosis develops in advanced disease. Hemorrhage and erosion of the gastric mucosa lead to hematemesis, popularly known as black vomit. Fatty infiltration of the myocardium, including the conduction system, can lead to myocarditis and arrhythmias.

Central nervous system (CNS) findings can be attributed to cerebral edema and hemorrhages compounded on metabolic disturbances. The bleeding diathesis of this disease is secondary to reduced hepatic synthesis of clotting factors, thrombocytopenia, and platelet dysfunction. The terminal event of shock can be attributed to a combination of direct parenchymal damage and a systemic inflammatory response.

Finally, circulatory shock develops secondary to cytokine storm, with evidence of increased levels of interleukin (IL)-6, IL-1 receptor antagonist, interferon-inducible protein-10, and tumor necrosis factor (TNF)–alpha. Viral antigens are found diffusely in kidneys, myocardium, and hepatocytes. In individuals who survive yellow fever, the recovery is complete, with no residual fibrosis.

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Epidemiology

Occurrence in the United States

Reports of yellow fever in the United States are exceedingly rare, with the last outbreak reported in New Orleans in 1905. It is a rare cause of illness in returning travelers; between 1970-2002, 9 cases of yellow fever were reported in unimmunized travelers from the United States and Europe. In these individuals, the disease was acquired in Brazil, Senegal, Venezuela, Ivory Coast, Gambia, and West Africa. Seven of these cases were fatal.[11, 3]

World Health Organization (WHO) data suggest that the rate of yellow fever transmission is increasing, especially in sub-Saharan Africa. In addition, the number of US residents traveling to South America and Africa is also increasing. The WHO estimates that travelers from the United States to endemic areas has doubled since 1988.[13] Without proper precautions, including vaccination, these travelers are at risk of contracting yellow fever.

Less fervent mosquito control efforts in the United States have led to the reemergence of Aedes aegypti in the last 30 years. A aegypti has been found in 23 states in the southeastern US. It is still a common mosquito in subtropical regions of southeastern Florida and along the Gulf of Mexico.[10, 14]

After 21st century outbreaks of dengue fever in Hawaii and along the Texas-Mexico border, it has been hypothesized that yellow fever could reemerge in the United States.[15] Virology research has isolated Flaviviridae strains from mosquitoes in eastern Texas, making transmission of urban yellow fever a potential threat for the United States in the future.[16]

International occurrence

After adjustment for underreporting, an estimated 200,000 cases of yellow fever occur annually, with 30,000 deaths per year.[10] Accurate incidence reporting is limited by the occurrence of asymptomatic disease, underreporting of the disease, and lack of diagnostic capabilities in endemic areas.[3]

Ninety percent of reported cases occur in Africa,[17] where Aaegypti is rampant. Transmission occurs in largely unvaccinated populations of sub-Saharan Africa. The countries at greatest risk lie within a band from 15° north to 10° south of the equator.[18] This region includes 32 countries in sub-Saharan Africa. (See the image below).[10]

Global distribution of yellow fever. Image courtes Global distribution of yellow fever. Image courtesy of the Centers for Disease Control and Prevention.

Thirty-three countries in Africa are at risk. Transmission in Africa is facilitated by the close proximity of vector mosquito populations to unvaccinated human populations.[17] The case-fatality rate of yellow fever in Africa approximates 20%. Infants and children are at highest risk.[19]

In South America, the rate of transmission of yellow fever is lower than in Africa. Historically, yellow fever outbreaks in South America occurred in the Amazon region.[3] The Haemagogus species of mosquitoes transmitted the virus in this area; affected individuals developed the sylvatic form of yellow fever.[18] Most of these cases occurred in young men working in the forests.

Yellow fever is endemic in 9 South American countries and several Caribbean islands. Bolivia, Brazil, Ecuador, and Peru are considered at highest risk.[17] The incidence of yellow fever in South America is lower than in Africa because the infected monkeys in the rain forest canopy do not often come in contact with human populations. Indigenous human populations have immunity as a part of mass immunization campaigns.[19] Yellow fever occurs most frequently in young men through occupational exposure in forested areas.

Recent outbreaks in urban areas of South America have been due to deforestation, population migration, and the resultant emergence of A aegypti species. Currently, 13 endemic countries within South America have been identified, with Bolivia, Brazil, Columbia, Ecuador, and Peru at greatest risk.[10] The range of yellow fever continues to expand, now including areas in which it previously was believed to be eradicated (eg, eastern and southern African countries). Although yellow fever has never been reported in Asia, this region is at risk because the appropriate primates and mosquitoes are present.[18]

Outbreaks of yellow fever have not been reported in Asia, but this region remains at risk because of the presence of competent vector mosquitoes and nonhuman primates.[17]

A traveler's risk of acquiring yellow fever depends on the location of travel, immunization status, season, duration of travel, and types of occupational or recreational activities. For travelers, the risk of illness and death due to yellow fever is estimated to be 10 times greater in West Africa than in South America.[19]

Though transmission rates vary by year and season, it is estimated that an unvaccinated traveler spending 2 weeks in sub-Saharan Africa carries a 1:267 risk of contracting yellow fever, with a 1:1333 risk of death from illness. The corresponding risks for persons traveling to South America are about 10% lower.[20]

US travel data from 1996-2004 describes the overall risk for serious illness and death due to yellow fever estimated to be 0.05-0.5 per 100,000 travelers to yellow fever–endemic areas.[19]

Sex-related demographics

South American cases of yellow fever are sporadic and usually occur in the population exposed to tropical rain forests. Men aged 14-45 years are most often infected through occupational exposure.[18]

In African cases, in which undervaccination of endemic populations has led to higher infection rates in children, yellow fever is slightly more common in males.

Age-related demographics

African cases of yellow fever occur seasonally in villages in contact with semidomestic mosquitoes. In these populations, nonimmunized children are at the highest risk.

Sylvatic disease primarily affects individuals aged 15-45 years who work outdoors in agriculture and forestry. Urban yellow fever and intermediate yellow fever, which occurs primarily in the humid savannas of Africa, affect individuals of all ages.[18]

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Prognosis

Yellow fever ranges in severity from a self-limited infection to life-threatening hemorrhagic fever. About 15-25% of affected individuals develop a more severe phase of disease that involves fever, jaundice, and liver and renal failure. Case-fatality rates in South America are reportedly higher than in West Africa.[3] Mortality is a function of patient susceptibility and of the virulence of the infecting strain.[12]

The case-fatality rate for yellow fever has been reported at 5%-70%. In recent outbreaks, the fatality rate was approximately 20% among patients with jaundice. The mortality risk in patients who present in the toxic stage of yellow fever is up to 50%.[21]

Death usually follows within 7-10 days of the onset of the toxic phase of yellow fever; however, mortality is a function of host susceptibility and the virulence of the infecting strain.[12] Infancy and age older than 50 years is associated with increased severity of illness and lethality.[3]

Unvaccinated travelers entering endemic regions have a greater risk of developing symptomatic disease than natives who have developed significant immunity.[1] An association has been made between recurrent outbreaks in West Africa and a unique strain in that region, suggesting that it may be more virulent in humans.[17]

The rare cases of postvaccination neurologic and system disease have infrequently led to death. Most individuals diagnosed with yellow fever vaccine-associated neurologic disease (YEL-AND) recover withoout sequelae; the case-fatality rate has been reported as less than 5%. Even fewer cases of fatal yellow fever vaccine-associated viscerotropic disease (YEL-AVD) have been documented.[3, 22]

Complications

Complications include:

  • Liver failure
  • Renal failure
  • Pulmonary edema
  • Myocarditis
  • Secondary bacterial infections
  • Hemorrhage or disseminated intravascular coagulation
  • Encephalitis (rare)
  • Shock or death

Secondary bacterial infections are frequent complications in patients who survive the critical period of illness.

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Contributor Information and Disclosures
Author

Mary T Busowski, MD Chief, Division of Infectious Diseases, Orlando VA Medical Center; Infectious Disease Faculty Practice/Internal Medicine Faculty Practice, Orlando Health; Assistant Professor of Medicine, Florida State University College of Medicine; Assistant Professor of Medicine, University of Central Florida College of Medicine

Mary T Busowski, MD is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American College of Physicians, American Medical Association, Florida Medical Association, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)

Mark R Wallace, MD, FACP, FIDSA Clinical Professor of Medicine, Florida State University College of Medicine; Clinical Professor of Medicine, University of Central Florida College of Medicine

Mark R Wallace, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, International AIDS Society, Florida Infectious Diseases Society

Disclosure: Nothing to disclose.

Janelle L Robertson, MD Staff Physician, Department of Infectious Diseases, Wilford Hall Medical Center

Janelle L Robertson, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Chief Editor

Mark R Wallace, MD, FACP, FIDSA Clinical Professor of Medicine, Florida State University College of Medicine; Clinical Professor of Medicine, University of Central Florida College of Medicine

Mark R Wallace, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, International AIDS Society, Florida Infectious Diseases Society

Disclosure: Nothing to disclose.

Acknowledgements

Joseph U Becker, MD Fellow, Global Health and International Emergency Medicine, Stanford University School of Medicine

Joseph U Becker, MD is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Richard B Brown, MD, FACP Chief, Division of Infectious Diseases, Baystate Medical Center; Professor, Department of Internal Medicine, Tufts University School of Medicine

Richard B Brown, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Dan Danzl, MD Chair, Professor, Department of Emergency Medicine, University of Louisville Hospital

Dan Danzl, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Kentucky Medical Association, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Aleksandr Gleyzer, MD, FAAEM Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center; Attending Physician, Department of Emergency Medicine, Kings County Medical Center and Brooklyn Veterans Affairs Medical Center

Aleksandr Gleyzer, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and International Society of Travel Medicine

Disclosure: Nothing to disclose.

Thomas E Herchline, MD Professor of Medicine, Wright State University, Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio

Thomas E Herchline, MD is a member of the following medical societies: Alpha Omega Alpha, Infectious Diseases Society of America, and Infectious Diseases Society of Ohio

Disclosure: Nothing to disclose.

Emily Nichols, MD Clinical Assistant Instructor, State University of New York Downstate Medical Center, Kings County Hospital Center

Emily Nichols, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Emergency Medicine Residents Association, and National Medical Association

Disclosure: Nothing to disclose.

Mark L Plaster, MD, JD Executive Editor, Emergency Physicians Monthly

Mark L Plaster, MD, JD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: M L Plaster Publishing Co LLC Ownership interest Management position

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Mark R Wallace, MD, FACP, FIDSA Clinical Professor of Medicine, Florida State University College of Medicine; Head of Infectious Disease Fellowship Program, Orlando Regional Medical Center

Mark R Wallace, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

References
  1. Cleri DJ, Ricketti AJ, Porwancher RB, Ramos-Bonner LS, Vernaleo JR. Viral hemorrhagic fevers: current status of endemic disease and strategies for control. Infect Dis Clin North Am. 2006 Jun. 20(2):359-93, x. [Medline].

  2. Quaresma JA, Pagliari C, Medeiros DB, Duarte MI, Vasconcelos PF. Immunity and immune response, pathology and pathologic changes: progress and challenges in the immunopathology of yellow fever. Rev Med Virol. 2013 Sep. 23(5):305-18. [Medline].

  3. Barnett ED, Wilder-Smith A, Wilson ME. Yellow fever vaccines and international travelers. Expert Rev Vaccines. 2008 Jul. 7(5):579-87. [Medline].

  4. Bob Arnebeck. A Short History of Yellow Fever in the US. Available at http://www.geocities.com/bobarnebeck/history.html. Accessed: November 11, 2008.

  5. Kean BH, Dahlby T. Coming of age in Panama. One Doctor's Adventures Among the Famous and Infamous from the Jungles of Panama to a Park Avenue Practice. New York, NY: Ballantine Books; 1990. Ch 2.

  6. Bryan CS, Moss SW, Kahn RJ. Yellow fever in the Americas. Infect Dis Clin North Am. 2004. 18:275-279.

  7. Roukens AH, Visser LG. Yellow fever vaccine: past, present and future. Expert Opin Biol Ther. 2008 Nov. 8(11):1787-95. [Medline].

  8. Bhatiasevi A, Moen C. More funding urged for yellow fever vaccine stockpile. WHO News Releases 2009. Available at http://www.who.int/mediacentre/news/releases/2009/yellow_fever_vaccine_20090526/en/index.html. Accessed: May 31, 2009.

  9. Tsai TF, Vaughn DW, Solomon T. Flaviviruses. Mandell GL, Bennett JE, Dolin R, eds. Principles and Practice of Infectious Diseases. 6th ed. Philadelphia, Pennsylvania: Elsevier, Inc.; 2005. Vol 2: Ch 149; 1926-9.

  10. World Health Organization. Yellow fever factsheet (revised in December 2009). Weekly Epidemiological Record. Jan 2010.

  11. Barrett AD, Higgs S. Yellow fever: A disease that has yet to be conquered. Annu Rev Entomol. 2007. 52:209-229.

  12. Monath TP. Treatment of yellow fever. Antiviral Res. 2008 Apr. 78(1):116-24. [Medline].

  13. Centers for Disease Control and Prevention. Fatal Yellow Fever in a Traveler Returning from Venezula, 1999. CDC. Apr 14 2000. 49(14):303-5. [Full Text].

  14. Darsie RF, Ward RA. Gainesville FL. Identification and Geographical Distribution of the Mosquitoes of North America. University of Florida Press; 2005.

  15. Morens DM, Fauci AS. Dengue and hemorrhagic fever: a potential threat to public health in the United States. JAMA. 2008 Jan 9. 299(2):214-6. [Medline].

  16. Kim DY, Guzman H, Bueno R Jr, et al. Characterization of Culex Flavivirus (Flaviviridae) strains isolated from mosquitoes in the United States and Trinidad. Virology. 2009 Mar 30. 386(1):154-9. [Medline].

  17. Barnett ED. Yellow fever: epidemiology and prevention. Clin Infect Dis. 2007 Mar 15. 44(6):850-6. [Medline].

  18. World Health Organization. Media centre fact sheets: Yellow fever. Updated December 2001. World Health Organization. Available at http://www.who.int/mediacentre/factsheets/fs100/en/. Accessed: May 13, 2009.

  19. Centers for Disease Control and Prevention. Traveler’s Health. CDC. Available at http://wwwnc.cdc.gov/travel. Accessed: Aug 16 2011.

  20. World Health Organization. WHO position paper: Yellow fever vaccine. Geneva, Switzerland: Oct 2003. Weekly Epidemiological Record; [Full Text].

  21. World Health Organization. Update on progress controlling yellow fever in Africa, 2004-2008. Geneva, Switzerland: Dec 2008. Weekly Epidemiological Record;

  22. Receveur MC, Bruyand M, Pistone T, Malvy D. Yellow fever vaccination: Update on rare and severe adverse effects. Médecine et Maladies Infectieuses. 2009. 39:239-241.

  23. Patel D, Simons H. Yellow fever vaccination: Is one dose always enough?. Travel Med Infect Dis. 2013 Sep 5. [Medline].

  24. Staples JE, Bocchini JA Jr, Rubin L, Fischer M. Yellow Fever Vaccine Booster Doses: Recommendations of the Advisory Committee on Immunization Practices, 2015. MMWR Morb Mortal Wkly Rep. 2015 Jun 19. 64 (23):647-50. [Medline]. [Full Text].

  25. World Health Organization. Weekly Epidemiological Record. WHO. May 17 2013;88:208-10. Available at http://www.who.int/wer/2013/wer8820.pdf. Accessed: May 29 2013.

  26. Julander JG, Furuta Y, Shafer K, Sidwell RW. Activity of T-1106 in a hamster model of yellow Fever virus infection. Antimicrob Agents Chemother. 2007 Jun. 51(6):1962-6. [Medline]. [Full Text].

  27. Bruyand M, Receveur MC, Pistone T, Verdiere CH, Thiebaut R, Malvy D. [Yellow fever vaccination in non-immunocompetent patients]. Med Mal Infect. 2008 Oct. 38(10):524-32. [Medline].

  28. Barber J. Yellow Fever Vaccination: No Booster Needed for Immunity. Medscape Medical News. May 20 2013. Available at http://www.medscape.com/viewarticle/804480. Accessed: May 29 2013.

  29. Hill DR. Mapping the risk of yellow Fever infection. Curr Infect Dis Rep. 2012 Jun. 14(3):246-55. [Medline].

  30. Paessler S, Walker DH. Pathogenesis of the viral hemorrhagic fevers. Annu Rev Pathol. 2013 Jan 24. 8:411-40. [Medline].

 
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Yellow fever virus. Image courtesy of the Centers for Disease Control and Prevention.
This female Aedes aegypti mosquito is shown after landing on a human host. The A aegypti mosquito is a known transmitter of dengue fever and yellow fever. A aegypti is sometimes referred to as the yellow fever mosquito. The viruses are transferred to the host when he or she has been bitten by a female mosquito. Image courtesy of the CDC/World Health Organization (WHO).
Global distribution of yellow fever. Image courtesy of the Centers for Disease Control and Prevention.
Transmission cycles of yellow fever in Africa and South America. Adapted from Annu Rev Entomol. 2007. 52:209-29.
 
 
 
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