Datasets:

---

Recag

/

Rp_CommonC_69

like 0

ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMjMyMjQ0LW92ZXJ2aWV3\nDrugs & Diseases > Infectious Diseases\nAuthor: Dana M Blyth, MD; Chief Editor: John L Brusch, MD, FACP more...\nSections Yellow Fever\nSpecific Tests for Yellow Fever Virus\nEmergency Department Care\nDeterrence and Prevention\nHistamine H2 antagonists\nAntipyretics\nYellow fever is a mosquito-borne disease that is endemic to tropical South America and Sub-Saharan Africa (see the image below). Its presentation can range from asymptomatic illness to acute-onset viral hepatitis and hemorrhagic fever. [1, 2]\nThis 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).\nSee 11 Travel Diseases to Consider Before and After the Trip, a Critical Images slideshow, to help identify and manage infectious travel diseases.\nYellow fever is usually a mild, self-limited illness consisting of fever, headache, myalgia, and malaise. It is typically divided into three stages: the period of infection, period of remission, and period of intoxication.\nMore serious illness presents with the abrupt onset of the following during the period of infection:\nThis is followed by a period of remission, when the virus is cleared and when many infected individuals fully recover.\nIn 15%-25% of individuals with yellow fever, symptoms recur during the period of intoxication and can progress to fatal illness. This period is marked by the following:\nRenal failure\nPhysical findings in yellow fever include the following:\nRelative bradycardia for the degree of fever (Faget sign)\nConjunctival injection\nSkin flushing\nAs the disease progresses, additional physical findings include the following:\nScleral icterus\nEpigastric tenderness\nHepatomegaly\nThe following is also often apparent in severe disease:\nMucosal bleeding\nGastrointestinal bleeding (gross or occult)\nOrgan 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:\nHypothermia or hyperthermia\nIndividuals 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).\nChemistries\nLiver function tests (LFTs): Elevated levels of transaminases precede the appearance of jaundice, and the degree of liver dysfunction in the acute phase may be predictive of the clinical course.\nCoagulation studies\nChest 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.\nSpecific tests for yellow fever\nRapid detection methods (eg, polymerase chain reaction assay)\nSerologic tests (eg, enzyme-linked immunosorbent assay)\nImmunohistochemical tissue staining - To identify the yellow fever antigen\nNo 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:\nVasoactive medications\nFluid resuscitation\nVentilator management\nTreatment of disseminated intravascular coagulation (DIC), hemorrhage, secondary infections, and renal and hepatic dysfunction\nAdditional supportive care recommendations for patients with yellow fever include the following:\nA nasogastric or orogastric tube may be required to provide nutritional support\nPatients with renal failure or refractory acidosis may require dialysis\nSalicylates should be avoided because of the increased risk of bleeding secondary to platelet dysfunction\nThe currently available yellow fever vaccine confers near lifelong immunity in 95% of patients. [3]\nYellow 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 viruses, most of which are arthropod-borne, with 30 that are known to cause human disease. Other flaviviral infections include dengue, Japanese encephalitis, West Nile, Zika, 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.)\nYellow fever virus. Image courtesy of the Centers for Disease Control and Prevention.\nA mosquito-borne disease, yellow fever can manifest on a wide spectrum, ranging from asymptomatic illness to acute-onset viral hepatitis and hemorrhagic fever. (See Clinical and Workup.)\nFrom 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]\nThe 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.\nFascinating 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]\nIn 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]\nYellow 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 from West Africa by Dutch slave traders during the 17th century.\nThe 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.\nLarge 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]\nFlaviviruses, including those that cause yellow fever, also have a potential use as biologic weapons. [9]\nAs 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 (peridomestically versus within the forest canopy). 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: sylvatic (jungle), intermediate (savannah), and urban. (See the diagram below.)\nTransmission cycles of yellow fever in Africa and South America. Adapted from Annu Rev Entomol. 2007. 52:209-29.\nSylvatic (jungle) cycle\nIn tropical rainforests, yellow fever virus is endemic among lower primates. Infected monkeys pass the virus to canopy-dwelling mosquitoes that feed on them. Persons who subsequently enter the forest (often workers, eg, loggers, and travelers) are infected following the bite of an infected mosquito. In Africa, the principal vector of the jungle cycle is A africanus; in South America, Haemagogus species are the primary vector for jungle transmission. Nonhuman primates remain the preferred host and reservoir in this setting.\nIntermediate (savannah) cycle\nIn moist and semihumid areas of Africa, 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 and is also known as the zone of emergence. 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.\nUrban cycle\nA aegypti is responsible for the transmission of urban yellow fever in Africa and South America (see image below). A aegypti is well adapted as an urban vector: breeding in man-made water containers, feeding primarily on humans, biting multiple individuals during a single blood meal, and transmitting yellow fever efficiently in its saliva. Thus, A aegypti can infect large populations of unvaccinated individuals. Urban outbreaks were rare in South America, yet have been increasingly reported in both South America and Africa, with concern for potential of further spread. [12]\nRecommend 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.\nYellow 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.\nThe 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:\nCapsid protein C - Facilitates viral binding\nMembrane protein M - A minor glycoprotein\nE proteins - Initiate infection, mediate viral entry, and serve as principal targets for host immune response\nNonstructural protein 1 (NS1) - May play a role in RNA replication and immune evasion\nNS2A protein - Involved in RNA replication and packaging\nNS2B and NS3 - Form a complex and are involved in polyprotein processing and replication of RNA\nNS5 - Has a major role in RNA replication\nThe 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. [13] Yellow fever is primarily viscerotropic, with the liver being the most affected organ. [14]\nThe 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.\nThe 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 and necrosis, with recent data indicating apoptosis as the primary mechanism of cell death in the liver, corresponding with subsequent formation of Councilman bodies (degenerative eosinophilic hepatocytes). [13, 14]\nThe 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.\nCentral 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.\nThe terminal event of shock can be attributed to a combination of direct parenchymal damage and a systemic inflammatory response. This cytokine storm has been characterized by 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.\nOccurrence in the United States\nReports of yellow fever in the United States are exceedingly rare, with the last outbreak reported in New Orleans in 1905. It was a rare cause of illness in returning travelers; between 1970 and 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]\nWorld 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. [15] Without proper precautions, including vaccination, these travelers are at risk of contracting yellow fever.\nLess 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, 16]\nAfter 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. [17] 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. [18] Failure to sustain vector control campaigns has led to the reinvasion of A aegypti across the Americas, as evidenced by the recent chikungunya and Zika outbreaks. [12]\nInternational occurrence\nAfter adjustment for underreporting, broadly quoted estimates are that 200,000 cases of yellow fever occur annually in 47 countries, with 30,000 deaths per year. [10, 19] Accurate incidence reporting is limited by the occurrence of asymptomatic disease, underreporting of the disease, and lack of diagnostic capabilities in endemic areas. [3] A recent modeling study estimated that yellow fever may infect up to 1.8 million individuals in Africa annually, resulting in 180,000 cases and 78,000 deaths. [12]\nNinety percent of reported cases occur in Africa, [20] 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 15° south of the equator. [21] This region includes 34 countries in sub-Saharan Africa. (See the image below). [10]\nGlobal distribution of yellow fever. Image courtesy of the Centers for Disease Control and Prevention.\nThirty-four countries in Africa are at risk. Transmission in Africa is facilitated by the close proximity of vector mosquito populations to unvaccinated human populations. [20] The case-fatality rate of yellow fever in Africa approximates 20%. Infants and children are at highest risk. [22]\nIn 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. [21] Most of these cases occurred in young men via occupational exposures in forested areas.\nThe 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. [22]\nRecent outbreaks in urban areas of South America have been due to deforestation (leading to ground-level biting activity of canopy-dwelling vectors), unvaccinated population migration into endemic areas, 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, 14]\nThe 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). 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. [20] During the recent yellow fever outbreak in Angola, 11 imported cases were documented in China. These were the first yellow fever cases reported in Asia and have led to high levels of concern for potential introduction and urbanization of yellow fever in Asia. The scenario in Angola, which has a large community of nonimmune foreign Asian nationals (home to approximately 100,000 Chinese workers often working in the bush and building roads), coupled with high volumes of air travel to an area conducive to transmission in Asia with a susceptible population of 2 billion people and limited responsive infrastructure, is unprecedented.\nThe prior failure of yellow fever to become established in Asia-Pacific, in contrast to similar hyperendemic dengue, suggests local factors may have prevented yellow fever from gaining a foothold in the region. This may be related to local vector characteristics, preceding high levels of cross-immunity from dengue and other flaviviruses, prior low risk of importation of viremic travelers, and regional differences in yellow fever geographic strains. However the recent chikungunya and Zika experience has illustrated that a shared vector and prior population exposure do not necessarily constrain the entry of a new arbovirus into dengue-endemic regions. The experience in South America has illustrated 4 main conditions to support yellow fever introduction into a new population, as follows: [12]\nIntense and sustained migratory flow of viremic individuals\nHigh density of competent vectors in receptive ecological conditions\nSusceptible or partially susceptible human and monkey populations\nInadequate surveillance and delayed recognition and ineffective vaccination programs\nA 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. US travel data from 1996-2004 describes the overall risk for serious illness and death due to yellow fever to be 0.05-0.5 per 100,000 travelers to yellow fever–endemic areas. [22] Although 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. 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. [22, 23]\nSex-related demographics\nSouth 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. [21]\nIn African cases, in which undervaccination of endemic populations has led to higher infection rates in children, yellow fever is slightly more common in males.\nAge-related demographics\nAfrican cases of yellow fever occur seasonally in villages in contact with semidomestic mosquitoes. In these populations, nonimmunized children are at the highest risk.\nSylvatic 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. [21]\nYellow 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. [13] In those who become symptomatic but recover, weakness and fatigue can last for months. [22]\nThe 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%. [24]\nDeath usually follows within 7-10 days of the onset of the toxic phase of yellow fever. [13] Infancy and age older than 50 years are associated with increased severity of illness and lethality. [3]\nUnvaccinated 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 potential strain-specific virulence. [20]\nThe rare cases of postvaccination neurologic and viscerotropic disease have infrequently led to death. Most individuals diagnosed with yellow fever vaccine–associated neurologic disease (YEL-AND) recover without 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, 25]\nComplications include:\nPulmonary edema\nSecondary bacterial infections\nHemorrhage or disseminated intravascular coagulation\nEncephalitis (rare)\nShock or death\nSecondary bacterial infections are frequent complications in patients who survive the critical period of illness.\nCleri 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].\nQuaresma 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].\nBarnett ED, Wilder-Smith A, Wilson ME. Yellow fever vaccines and international travelers. Expert Rev Vaccines. 2008 Jul. 7(5):579-87. [Medline].\nBob Arnebeck. A Short History of Yellow Fever in the US. Available at http://www.geocities.com/bobarnebeck/history.html. Accessed: November 11, 2008.\nKean 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.\nBryan CS, Moss SW, Kahn RJ. Yellow fever in the Americas. Infect Dis Clin North Am. 2004. 18:275-279.\nRoukens AH, Visser LG. Yellow fever vaccine: past, present and future. Expert Opin Biol Ther. 2008 Nov. 8(11):1787-95. [Medline].\nBhatiasevi 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.\nTsai 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.\nWorld Health Organization. Yellow fever factsheet (revised in December 2009). Weekly Epidemiological Record. Jan 2010.\nBarrett AD, Higgs S. Yellow fever: A disease that has yet to be conquered. Annu Rev Entomol. 2007. 52:209-229.\nWasserman S, Tambyah PA, Lim PL. Yellow fever cases in Asia: primed for an epidemic. Int J Infect Dis. 2016 Jul. 48:98-103. [Medline].\nMonath TP. Treatment of yellow fever. Antiviral Res. 2008 Apr. 78(1):116-24. [Medline].\nMonath TP, Vasconcelos PF. Yellow fever. J Clin Virol. 2015 Mar. 64:160-73. [Medline].\nCenters 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].\nDarsie RF, Ward RA. Gainesville FL. Identification and Geographical Distribution of the Mosquitoes of North America. University of Florida Press; 2005.\nMorens 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].\nKim 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].\nChen LH, Kozarsky PE, Visser LG. What's old is new again: the re-emergence of yellow fever in Brazil and vaccine shortages. Clin Infect Dis. 2018 Sep 10. [Medline].\nBarnett ED. Yellow fever: epidemiology and prevention. Clin Infect Dis. 2007 Mar 15. 44(6):850-6. [Medline].\nWorld 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.\nCenters for Disease Control and Prevention. Traveler’s Health. CDC. Available at http://wwwnc.cdc.gov/travel. Accessed: Aug 16 2011.\nWorld Health Organization. WHO position paper: Yellow fever vaccine. Geneva, Switzerland: Oct 2003. Weekly Epidemiological Record; [Full Text].\nWorld Health Organization. Update on progress controlling yellow fever in Africa, 2004-2008. Geneva, Switzerland: Dec 2008. Weekly Epidemiological Record;\nReceveur 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.\nThwaites GE, Day NP. Approach to Fever in the Returning Traveler. N Engl J Med. 2017 Feb 9. 376 (6):548-560. [Medline].\nWorld Health Organization. Yellow fever laboratory diagnostic testing in Africa, Interim guidance. World Health Organization. Available at http://apps.who.int/iris/bitstream/10665/246226/1/WHO-OHE-YF-LAB-16.1-eng.pdf. July 2016; Accessed: 12 December 2016.\nMonath TP. Yellow fever: an update. Lancet Infect Dis. 2001 Aug. 1 (1):11-20. [Medline].\nPatel D, Simons H. Yellow fever vaccination: Is one dose always enough?. Travel Med Infect Dis. 2013 Sep 5. [Medline].\nStaples 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].\nWorld 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.\nBeck AS, Barrett AD. Current status and future prospects of yellow fever vaccines. Expert Rev Vaccines. 2015. 14 (11):1479-92. [Medline].\nCampi-Azevedo AC, de Almeida Estevam P, Coelho-Dos-Reis JG, et al. Subdoses of 17DD yellow fever vaccine elicit equivalent virological/immunological kinetics timeline. BMC Infect Dis. 2014 Jul 15. 14:391. [Medline].\nJonker EF, Visser LG, Roukens AH. Advances and controversies in yellow fever vaccination. Ther Adv Vaccines. 2013 Nov. 1 (4):144-52. [Medline].\nMartins RM, Maia Mde L, Farias RH, Camacho LA, Freire MS, Galler R, et al. 17DD yellow fever vaccine: a double blind, randomized clinical trial of immunogenicity and safety on a dose-response study. Hum Vaccin Immunother. 2013 Apr. 9 (4):879-88. [Medline].\nChen LH, Hamer DH. Vaccination Challenges in Confronting the Resurgent Threat From Yellow Fever. JAMA. 2017 Nov 7. 318 (17):1651-1652. [Medline].\nWHO. Summary of WHO position on use of fractional doses of Yellow fever vaccine, June 2017. Available at https://www.who.int/immunization/documents/who_pp_yf_fractional_dose_june2017_summary.pdf. June 2017; Accessed: June 21, 2019.\nJulander 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].\nBruyand 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].\nBarber 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.\nHill DR. Mapping the risk of yellow Fever infection. Curr Infect Dis Rep. 2012 Jun. 14(3):246-55. [Medline].\nPaessler S, Walker DH. Pathogenesis of the viral hemorrhagic fevers. Annu Rev Pathol. 2013 Jan 24. 8:411-40. [Medline].\nMoreno-Madriñán MJ, Turell M. History of Mosquitoborne Diseases in the United States and Implications for New Pathogens. Emerg Infect Dis. 2018 May. 24 (5):821-826. [Medline].\nDana M Blyth, MD Assistant Professor, Department of Medicine, Uniformed Services University of the Health Sciences; Adjunct Assistant Professor, Department of Medicine, University of Texas Health Science Center at San Antonio School of Medicine; Staff Physician, Department of Medicine, Infectious Disease Service, Brooke Army Medical Center, San Antonio Military Medical Center, San Antonio Uniformed Services Health Education Consortium (SAUSHEC)\nDana M Blyth, MD is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America\nJohn L Brusch, MD, FACP Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance\nJohn L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America\nJanelle L Robertson, MD Staff Physician, Department of Infectious Diseases, Wilford Hall Medical Center\nJanelle L Robertson, MD is a member of the following medical societies: American College of Physicians\nMary 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\nMary 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\nJoseph U Becker, MD Fellow, Global Health and International Emergency Medicine, Stanford University School of Medicine\nJoseph 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\nRichard B Brown, MD, FACP Chief, Division of Infectious Diseases, Baystate Medical Center; Professor, Department of Internal Medicine, Tufts University School of Medicine\nRichard 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\nDan Danzl, MD Chair, Professor, Department of Emergency Medicine, University of Louisville Hospital\nDan 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\nAleksandr 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\nAleksandr Gleyzer, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and International Society of Travel Medicine\nThomas E Herchline, MD Professor of Medicine, Wright State University, Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio\nThomas 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\nEmily Nichols, MD Clinical Assistant Instructor, State University of New York Downstate Medical Center, Kings County Hospital Center\nEmily 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\nMark L Plaster, MD, JD Executive Editor, Emergency Physicians Monthly\nMark L Plaster, MD, JD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians\nDisclosure: M L Plaster Publishing Co LLC Ownership interest Management position\nMark 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\nMark 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\nencoded search term (Yellow Fever) and Yellow Fever\nTropical Myeloneuropathies\nTropical Sprue\nCutaneous Larva Migrans\nVaccinations, Travel\nMiliaria\nAinhum\nEbola Just 'A Plane Ride Away'\nTravel health: Keeping Up-to-Date With The Risks of Insect-Borne Disease\nCDC Clarifies Diagnostic Testing for Individuals Who Could Have Either Dengue or Zika\nInfant Outcomes of Zika in Pregnancy: New Data\nAccording to Infectious Disease Physicians\nNever Seen Measles? 5 Things to Know\nGuidelines Nix Annual TB Testing for Most Healthcare Workers\nCandida auris Spreads Through US Hospitals\nDangerous 'Kissing' Bug Marches North in US\nMultidrug-Resistant Bacteria Found on Patient Hands, Surfaces\nNews Tropical Skin Conditions on the Rise, Difficult to Detect\nNews New WHO Regional Chief Must Battle Lifestyle Conditions, Tropical Diseases\nNews FDA OKs Triclabendazole (Egaten) for Neglected Tropical Disease Fascioliasis\n2010 /viewarticle/906548 Practice Guideline\nPractice Guideline Neurocysticercosis Clinical Practice Guidelines (2018)"