Yellow fever

Yellow fever is a viral disease of typically short duration.[3] In most cases, symptoms include fever, chills, loss of appetite, nausea, muscle pains particularly in the back, and headaches.[3] Symptoms typically improve within five days.[3] In about 15 percent of people, within a day of improving the fever comes back, abdominal pain occurs, and liver damage begins causing yellow skin.[3][6] If this occurs, the risk of bleeding and kidney problems is increased.[3]

The disease is caused by yellow fever virus and is spread by the bite of an infected female mosquito.[3] It infects only humans, other primates, and several species of mosquitoes.[3] In cities, it is spread primarily by Aedes aegypti, a type of mosquito found throughout the tropics and subtropics.[3] The virus is an RNA virus of the genus Flavivirus.[7] The disease may be difficult to tell apart from other illnesses, especially in the early stages.[3] To confirm a suspected case, blood sample testing with polymerase chain reaction is required.[4]

A safe and effective vaccine against yellow fever exists, and some countries require vaccinations for travelers.[3] Other efforts to prevent infection include reducing the population of the transmitting mosquito.[3] In areas where yellow fever is common, early diagnosis of cases and immunization of large parts of the population are important to prevent outbreaks.[3] Once infected, management is symptomatic with no specific measures effective against the virus.[3] Death occurs in up to half of those who get severe disease.[3][8]

In 2013, yellow fever resulted in about 127,000 severe infections and 45,000 deaths,[3] with nearly 90 percent of these occurring in African nations.[4] Nearly a billion people live in an area of the world where the disease is common.[3] It is common in tropical areas of the continents of South America and Africa, but not in Asia.[3][9] Since the 1980s, the number of cases of yellow fever has been increasing.[3][10] This is believed to be due to fewer people being immune, more people living in cities, people moving frequently, and changing climate increasing the habitat for mosquitoes.[3] The disease originated in Africa and spread to South America with the slave trade in the 17th century.[1] Since the 17th century, several major outbreaks of the disease have occurred in the Americas, Africa, and Europe.[1] In the 18th and 19th centuries, yellow fever was seen as one of the most dangerous infectious diseases.[1] In 1927 yellow fever virus became the first human virus to be isolated.[7][11]

Yellow fever
Other namesYellow jack, yellow plague,[1] bronze john[2]
YellowFeverVirus
A TEM micrograph of yellow fever virus (234,000× magnification)
SpecialtyInfectious disease
SymptomsFever, chills, muscle pain, yellow skin[3]
ComplicationsLiver failure, bleeding[3]
Usual onset3–6 days post exposure[3]
Duration3–4 days[3]
CausesYellow fever virus spread by mosquitoes[3]
Diagnostic methodBlood test[4]
PreventionYellow fever vaccine[3]
TreatmentSupportive care[3]
Frequency~127,000 severe cases (2013)[3]
Deaths5,100 (2015)[5]

Signs and symptoms

Yellow fever begins after an incubation period of three to six days.[12] Most cases only cause a mild infection with fever, headache, chills, back pain, fatigue, loss of appetite, muscle pain, nausea, and vomiting.[13] In these cases, the infection lasts only three to four days.

In 15% of cases, however, people enter a second, toxic phase of the disease with recurring fever, this time accompanied by jaundice due to liver damage, as well as abdominal pain.[14] Bleeding in the mouth, the eyes, and the gastrointestinal tract cause vomit containing blood, hence the Spanish name for yellow fever, vómito negro ("black vomit").[15] There may also be kidney failure, hiccups, and delirium.[16][17]

Among those who develop jaundice the fatality rate is 20% to 50%, while the overall fatality rate is about 5%.[18] Severe cases may have a mortality greater than 50%.[19]

Surviving the infection provides lifelong immunity,[20] and normally no permanent organ damage results.[21]

Cause

Yellow fever virus
Virus classification
(unranked): Virus
Realm: Riboviria
(unranked): incertae sedis
Family: Flaviviridae
Genus: Flavivirus
Species:
Yellow fever virus

Yellow fever is caused by yellow fever virus, a 40– to 50-nm-wide enveloped RNA virus, the type species and namesake of the family Flaviviridae.[7] It was the first illness shown to be transmissible by filtered human serum and transmitted by mosquitoes, by Walter Reed around 1900.[22] The positive-sense, single-stranded RNA is around 11,000 nucleotides long and has a single open reading frame encoding a polyprotein. Host proteases cut this polyprotein into three structural (C, prM, E) and seven nonstructural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5); the enumeration corresponds to the arrangement of the protein coding genes in the genome.[23] Minimal yellow fever virus (YFV) 3'UTR region is required for stalling of the host 5'-3' exonuclease XRN1. The UTR contains PKS3 pseudoknot structure which serves as a molecular signal to stall the exonuclease and is the only viral requirement for subgenomic flavivirus RNA (sfRNA) production. The sfRNAs are a result of incomplete degradation of the viral genome by the exonuclease and are important for viral pathogenicity.[24] Yellow fever belongs to the group of hemorrhagic fevers.

The viruses infect, amongst others, monocytes, macrophages, and dendritic cells. They attach to the cell surface via specific receptors and are taken up by an endosomal vesicle. Inside the endosome, the decreased pH induces the fusion of the endosomal membrane with the virus envelope. The capsid enters the cytosol, decays, and releases the genome. Receptor binding, as well as membrane fusion, are catalyzed by the protein E, which changes its conformation at low pH, causing a rearrangement of the 90 homodimers to 60 homotrimers.[23]

After entering the host cell, the viral genome is replicated in the rough endoplasmic reticulum (ER) and in the so-called vesicle packets. At first, an immature form of the virus particle is produced inside the ER, whose M-protein is not yet cleaved to its mature form, so is denoted as precursor M (prM) and forms a complex with protein E. The immature particles are processed in the Golgi apparatus by the host protein furin, which cleaves prM to M. This releases E from the complex which can now take its place in the mature, infectious virion.[23]

Transmission

Aedes aegypti bloodfeeding CDC Gathany
Aedes aegypti feeding
Aedes aegypti E-A-Goeldi 1905
Adults of the yellow fever mosquito A. aegypti: The male is on the left, females are on the right. Only the female mosquito bites humans to transmit the disease.

Yellow fever virus is mainly transmitted through the bite of the yellow fever mosquito Aedes aegypti, but other mostly Aedes mosquitoes such as the tiger mosquito (Aedes albopictus) can also serve as a vector for this virus. Like other arboviruses which are transmitted by mosquitoes, yellow fever virus is taken up by a female mosquito when it ingests the blood of an infected human or another primate. Viruses reach the stomach of the mosquito, and if the virus concentration is high enough, the virions can infect epithelial cells and replicate there. From there, they reach the haemocoel (the blood system of mosquitoes) and from there the salivary glands. When the mosquito next sucks blood, it injects its saliva into the wound, and the virus reaches the bloodstream of the bitten person. Transovarial and transstadial transmission of yellow fever virus within A. aegypti, that is, the transmission from a female mosquito to her eggs and then larvae, are indicated. This infection of vectors without a previous blood meal seems to play a role in single, sudden breakouts of the disease.[25]

Three epidemiologically different infectious cycles occur,[10] in which the virus is transmitted from mosquitoes to humans or other primates.[26] In the "urban cycle", only the yellow fever mosquito A. aegypti is involved. It is well adapted to urban areas, and can also transmit other diseases, including Zika fever, dengue fever, and chikungunya. The urban cycle is responsible for the major outbreaks of yellow fever that occur in Africa. Except for an outbreak in Bolivia in 1999, this urban cycle no longer exists in South America.

Besides the urban cycle, both in Africa and South America, a sylvatic cycle (forest or jungle cycle) is present, where Aedes africanus (in Africa) or mosquitoes of the genus Haemagogus and Sabethes (in South America) serve as vectors. In the jungle, the mosquitoes infect mainly nonhuman primates; the disease is mostly asymptomatic in African primates. In South America, the sylvatic cycle is currently the only way humans can become infected, which explains the low incidence of yellow fever cases on the continent. People who become infected in the jungle can carry the virus to urban areas, where A. aegypti acts as a vector. Because of this sylvatic cycle, yellow fever cannot be eradicated except by eradicating the mosquitoes that serve as vectors.[10]

In Africa, a third infectious cycle known as "savannah cycle" or intermediate cycle, occurs between the jungle and urban cycles. Different mosquitoes of the genus Aedes are involved. In recent years, this has been the most common form of transmission of yellow fever in Africa.[27]

Concern exists about yellow fever spreading to southeast Asia, where its vector A. aegypti already occurs.[28]

Pathogenesis

After transmission from a mosquito, the viruses replicate in the lymph nodes and infect dendritic cells in particular. From there, they reach the liver and infect hepatocytes (probably indirectly via Kupffer cells), which leads to eosinophilic degradation of these cells and to the release of cytokines. Apoptotic masses known as Councilman bodies appear in the cytoplasm of hepatocytes.[29][30]

Fatality may occur when cytokine storm, shock, and multiple organ failure follow.[18]

Diagnosis

Yellow fever is most frequently a clinical diagnosis, made from symptoms and where the infected person was before becoming ill. Mild courses of the disease can only be confirmed virologically. Since mild courses of yellow fever can also contribute significantly to regional outbreaks, every suspected case of yellow fever (involving symptoms of fever, pain, nausea, and vomiting 6–10 days after leaving the affected area) is treated seriously.

If yellow fever is suspected, the virus cannot be confirmed until 6–10 days after the illness. A direct confirmation can be obtained by reverse transcription polymerase chain reaction, where the genome of the virus is amplified.[4] Another direct approach is the isolation of the virus and its growth in cell culture using blood plasma; this can take 1–4 weeks.

Serologically, an enzyme-linked immunosorbent assay during the acute phase of the disease using specific IgM against yellow fever or an increase in specific IgG titer (compared to an earlier sample) can confirm yellow fever. Together with clinical symptoms, the detection of IgM or a four-fold increase in IgG titer is considered sufficient indication for yellow fever. Since these tests can cross-react with other flaviviruses, such as dengue virus, these indirect methods cannot conclusively prove yellow fever infection.

Liver biopsy can verify inflammation and necrosis of hepatocytes and detect viral antigens. Because of the bleeding tendency of yellow fever patients, a biopsy is only advisable post mortem to confirm the cause of death.

In a differential diagnosis, infections with yellow fever must be distinguished from other feverish illnesses such as malaria. Other viral hemorrhagic fevers, such as Ebola virus, Lassa virus, Marburg virus, and Junin virus, must be excluded as the cause.

Prevention

Personal prevention of yellow fever includes vaccination and avoidance of mosquito bites in areas where yellow fever is endemic. Institutional measures for prevention of yellow fever include vaccination programmes and measures of controlling mosquitoes. Programmes for distribution of mosquito nets for use in homes are providing reductions in cases of both malaria and yellow fever. Use of EPA-registered insect repellent is recommended when outdoors. Exposure for even a short time is enough for a potential mosquito bite. Long-sleeved clothing, long pants, and socks are useful for prevention. The awareness of peak mosquito exposure is from dusk to dawn. The application of larvicides to water-storage containers can help eliminate potential mosquito breeding sites. Adult mosquitos can be killed through insecticide spray usage, which decreases the transmission of yellow fever.[31]

  • Use insect repellent when outdoors such as those containing DEET, picaridin, ethyl butylacetylaminopropionate (IR3535), or oil of lemon eucalyptus on exposed skin.
  • Wear proper clothing to reduce mosquito bites. When weather permits, wear long sleeves, long pants, and socks when outdoors. Mosquitoes may bite through thin clothing, so spraying clothes with repellent containing permethrin or another EPA-registered repellent will give extra protection. Clothing treated with permethrin is commercially available. Mosquito repellents containing permethrin are not approved for application directly to the skin.
  • The peak biting times for many mosquito species are dusk to dawn. However, A. aegypti, one of the mosquitoes that transmits yellow fever virus, feeds during the daytime. Staying in accommodations with screened or air-conditioned rooms, particularly during peak biting times, also reduces the risk of mosquito bites.

Vaccination

Yellow fever certificate
The cover of a certificate that confirms the holder has been vaccinated against yellow fever

Vaccination is recommended for those traveling to affected areas, because non-native people tend to develop more severe illness when infected. Protection begins by the 10th day after vaccine administration in 95% of people,[32] and had been reported to last for at least 10 years. The World Health Organization (WHO) now states that a single dose of vaccination is sufficient to confer lifelong immunity against yellow fever disease."[33] The attenuated live vaccine stem 17D was developed in 1937 by Max Theiler.[32] The WHO recommends routine vaccinations for people living in affected areas between the 9th and 12th month after birth.[4]

Up to one in four people experience fever, aches, and local soreness and redness at the site of injection.[34] In rare cases (less than one in 200,000 to 300,000),[32] the vaccination can cause yellow fever vaccine-associated viscerotropic disease, which is fatal in 60% of cases. It is probably due to the genetic morphology of the immune system. Another possible side effect is an infection of the nervous system, which occurs in one in 200,000 to 300,000 cases, causing yellow fever vaccine-associated neurotropic disease, which can lead to meningoencephalitis and is fatal in less than 5%[32] of cases.[4][18]

The Yellow Fever Initiative, launched by the WHO in 2006, vaccinated more than 105 million people in 14 countries in West Africa.[35] No outbreaks were reported during 2015. The campaign was supported by the GAVI Alliance, and governmental organizations in Europe and Africa. According to the WHO, mass vaccination cannot eliminate yellow fever because of the vast number of infected mosquitoes in urban areas of the target countries, but it will significantly reduce the number of people infected.[36]

Demand for the yellow fever vaccine has continued to increase due to the growing number of countries implementing yellow fever vaccination as part of their routine immunization programmes.[37] Recent upsurges in yellow fever outbreaks in Angola (2015), Democratic Republic of Congo (2016), Uganda (2016), and more recently in Nigeria and Brazil in 2017 have further increased demand, while straining global vaccine supply.[37][38] Therefore, to vaccinate susceptible populations in preventive mass immunization campaigns during outbreaks, fractional dosing of the vaccine is being considered as a dose-sparing strategy to maximize limited vaccine supplies.[37] Fractional dose yellow fever vaccination refers to administration of a reduced volume of vaccine dose, which has been reconstituted as per manufacturer recommendations.[37][39] The first practical use of fractional dose yellow fever vaccination was in response to a large yellow fever outbreak in the Democratic Republic of the Congo in mid-2016.[37]

In March 2017, the WHO launched a vaccination campaign in Brazil with 3.5 million doses from an emergency stockpile.[40] In March 2017 the WHO recommended vaccination for travellers to certain parts of Brazil.[41] In March 2018, Brazil shifted its policy and announced it planned to vaccinate all 77.5 million currently-unvaccinated citizens by April 2019.[42]

Compulsory vaccination

Some countries in Asia are theoretically in danger of yellow fever epidemics (mosquitoes with the capability to transmit yellow fever and susceptible monkeys are present), although the disease does not yet occur there. To prevent introduction of the virus, some countries demand previous vaccination of foreign visitors if they have passed through yellow fever areas. Vaccination has to be proved by the production of a vaccination certificate which is valid 10 days after the vaccination and lasts for 10 years. Although the WHO on 17 May 2013 advised that subsequent booster vaccinations are unnecessary, an older (than 10 years) certificate may not be acceptable at all border posts in all affected countries. A list of the countries that require yellow fever vaccination is published by the WHO.[43] If the vaccination cannot be conducted for some reasons, dispensation may be possible. In this case, an exemption certificate issued by a WHO-approved vaccination center is required. Although 32 of 44 countries where yellow fever occurs endemically do have vaccination programmes, in many of these countries, less than 50% of their population is vaccinated.[4]

Vector control

Luchemos todos contra el dengue
Information campaign for prevention of dengue and yellow fever in Paraguay

Control of the yellow fever mosquito A. aegypti is of major importance, especially because the same mosquito can also transmit dengue fever and chikungunya disease. A. aegypti breeds preferentially in water, for example in installations by inhabitants of areas with precarious drinking water supply, or in domestic waste, especially tires, cans, and plastic bottles. These conditions are common in urban areas in developing countries.

Two main strategies are employed to reduce mosquito populations. One approach is to kill the developing larvae. Measures are taken to reduce the water accumulations in which the larvae develop. Larvicides are used, as well as larvae-eating fish and copepods, which reduce the number of larvae. For many years, copepods of the genus Mesocyclops have been used in Vietnam for preventing dengue fever. It eradicated the mosquito vector in several areas. Similar efforts may be effective against yellow fever. Pyriproxyfen is recommended as a chemical larvicide, mainly because it is safe for humans and effective even in small doses.[4]

The second strategy is to reduce populations of the adult yellow fever mosquito. Lethal ovitraps can reduce Aedes populations, but with a decreased amount of pesticide because it targets the mosquitoes directly. Curtains and lids of water tanks can be sprayed with insecticides, but application inside houses is not recommended by the WHO. Insecticide-treated mosquito nets are effective, just as they are against the Anopheles mosquito that carries malaria.[4]

Treatment

As for other flavivirus infections, no cure is known for yellow fever. Hospitalization is advisable and intensive care may be necessary because of rapid deterioration in some cases. Different methods for acute treatment of the disease have been shown not to be very successful; passive immunization after the emergence of symptoms is probably without effect. Ribavirin and other antiviral drugs, as well as treatment with interferons, do not have a positive effect in patients.[18] Asymptomatic treatment includes rehydration and pain relief with drugs such as paracetamol. Acetylsalicylic acid should not be given because of its anticoagulant effect, which can be devastating in the case of internal bleeding that can occur with yellow fever.

Epidemiology

Yellow fever is common in tropical and subtropical areas of South America and Africa. Worldwide, about 600 million people live in endemic areas. The WHO estimates 200,000 cases of disease and 30,000 deaths a year occur; the number of officially reported cases is far lower.

Africa

Yellow fever Africa 2009.jpeg
Areas with risk of yellow fever in Africa (2017)

An estimated 90% of the infections occur on the African continent.[4] In 2008, the largest number of recorded cases was in Togo. In 2016, a large outbreak originated in Angola and spread to neighboring countries before being contained by a massive vaccination campaign. In March and April, 11 cases were reported in China, the first appearance of the disease in Asia in recorded history.[44][45]

Phylogenetic analysis has identified seven genotypes of yellow fever viruses, and they are assumed to be differently adapted to humans and to the vector A. aegypti. Five genotypes (Angola, Central/East Africa, East Africa, West Africa I, and West Africa II) occur only in Africa. West Africa genotype I is found in Nigeria and the surrounding areas.[46] This appears to be especially virulent or infectious, as this type is often associated with major outbreaks. The three genotypes in East and Central Africa occur in areas where outbreaks are rare. Two recent outbreaks in Kenya (1992–1993) and Sudan (2003 and 2005) involved the East African genotype, which had remained unknown until these outbreaks occurred.[47]

South America

Yellow fever South America 2009.jpeg
Areas with risk of yellow fever in South America (2018)

In South America, two genotypes have been identified (South American genotypes I and II).[10] Based on phylogenetic analysis these two genotypes appear to have originated in West Africa[48] and were first introduced into Brazil.[49] The date of introduction into South America appears to be 1822 (95% confidence interval 1701 to 1911).[49] The historical record shows an outbreak of yellow fever occurred in Recife, Brazil, between 1685 and 1690. The disease seems to have disappeared, with the next outbreak occurring in 1849. It was likely introduced with the importation of slaves through the slave trade from Africa. Genotype I has been divided into five subclades, A through E.[50]

In late 2016, a large outbreak began in Minas Gerais state of Brazil that was characterized as a sylvan or jungle epizootic.[51] It began as an outbreak in brown howler monkeys,[52] which serve as a sentinel species for yellow fever, that then spread to men working in the jungle. No cases had been transmitted between humans by the A. aegypti mosquito, which can sustain urban outbreaks that can spread rapidly. In April 2017, the sylvan outbreak continued moving toward the Brazilian coast, where most people were unvaccinated.[53] By the end of May the outbreak appeared to be declining after more than 3,000 suspected cases, 758 confirmed and 264 deaths confirmed to be yellow fever.[54] The Health Ministry launched a vaccination campaign and was concerned about spread during the Carnival season in February and March.[55] The CDC issued a Level 2 alert (practice enhanced precautions.)[56]

A Bayesian analysis of genotypes I and II has shown that genotype I accounts for virtually all the current infections in Brazil, Colombia, Venezuela, and Trinidad and Tobago, while genotype II accounted for all cases in Peru.[57] Genotype I originated in the northern Brazilian region around 1908 (95% HPD: 1870–1936). Genotype II originated in Peru in 1920 (95% HPD: 1867–1958). The estimated rate of mutation for both genotypes was about 5 × 10−4 substitutions/site/year, similar to that of other RNA viruses.

Asia

The main vector (A. aegypti) also occurs in tropical and subtropical regions of Asia, the Pacific, and Australia, but yellow fever has never occurred there, until jet travel introduced 11 cases from the 2016 Angola and DR Congo yellow fever outbreak in Africa. Proposed explanations include:

  • That the strains of the mosquito in the east are less able to transmit yellow fever virus.
  • That immunity is present in the populations because of other diseases caused by related viruses (for example, dengue).
  • That the disease was never introduced because the shipping trade was insufficient.

But none is considered satisfactory.[58][59] Another proposal is the absence of a slave trade to Asia on the scale of that to the Americas.[60] The trans-Atlantic slave trade probably introduced yellow fever into the Western Hemisphere from Africa.[61]

History

The evolutionary origins of yellow fever most likely lie in Africa, with transmission of the disease from nonhuman primates to humans.[62][63] The virus is thought to have originated in East or Central Africa and spread from there to West Africa. As it was endemic in Africa, the natives had developed some immunity to it. When an outbreak of yellow fever would occur in an African village where colonists resided, most Europeans died, while the native population usually suffered nonlethal symptoms resembling influenza.[64] This phenomenon, in which certain populations develop immunity to yellow fever due to prolonged exposure in their childhood, is known as acquired immunity.[65] The virus, as well as the vector A. aegypti, were probably transferred to North and South America with the importation of slaves from Africa, part of the Columbian Exchange following European exploration and colonization.

The first definitive outbreak of yellow fever in the New World was in 1647 on the island of Barbados.[66] An outbreak was recorded by Spanish colonists in 1648 in the Yucatán Peninsula, where the indigenous Mayan people called the illness xekik ("blood vomit"). In 1685, Brazil suffered its first epidemic, in Recife. The first mention of the disease by the name "yellow fever" occurred in 1744.[67] McNeill argues that the environmental and ecological disruption caused by the introduction of sugar plantations created the conditions for mosquito and viral reproduction, and subsequent outbreaks of yellow fever.[68] Deforestation reduced populations of insectivorous birds and other creatures that fed on mosquitoes and their eggs.

Affinerie des sucres (1)
Sugar curing house, 1762: Sugar pots and jars on sugar plantations served as breeding place for larvae of A. aegypti, the vector of yellow fever.

Although yellow fever is most prevalent in tropical-like climates, the northern United States were not exempted from the fever. The first outbreak in English-speaking North America occurred in New York City in 1668. English colonists in Philadelphia and the French in the Mississippi River Valley recorded major outbreaks in 1669, as well as additional yellow fever epidemics in Philadelphia, Baltimore, and New York City in the 18th and 19th centuries. the disease traveled along steamboat routes from New Orleans, causing caused some 100,000–150,000 deaths in total.[69] The yellow fever epidemic of 1793 in Philadelphia, which was then the capital of the United States, resulted in the deaths of several thousand people, more than 9% of the population.[70] The national government fled the city, including President George Washington.[71]

The southern city of New Orleans was plagued with major epidemics during the 19th century, most notably in 1833 and 1853. Its residents called the disease "yellow jack". Urban epidemics continued in the United States until 1905, with the last outbreak affecting New Orleans.[72]

At least 25 major outbreaks took place in the Americas during the 18th and 19th centuries, including particularly serious ones in Cartagena, Chile, in 1741; Cuba in 1762 and 1900; Santo Domingo in 1803; and Memphis, Tennessee, in 1878.[73]

Yellow Fever Deaths Lafayette Cemetery 1 New Orleans
Headstones of people who died in the yellow fever epidemic of 1878 can be found in New Orleans' cemeteries.

In 1853, Cloutierville, Louisiana, had a late-summer outbreak of yellow fever that quickly killed 68 of the 91 inhabitants. A local doctor concluded that some unspecified infectious agent had arrived in a package from New Orleans.[74][75] 650 residents of Savannah, Georgia died from yellow fever in 1854.[76] In 1858, St. Matthew's German Evangelical Lutheran Church in Charleston, South Carolina, suffered 308 yellow fever deaths, reducing the congregation by half.[77] A ship carrying persons infected with the virus arrived in Hampton Roads in southeastern Virginia in June 1855.[78] The disease spread quickly through the community, eventually killing over 3,000 people, mostly residents of Norfolk and Portsmouth. In 1873, Shreveport, Louisiana lost 759 citizens in an 80-day period to a Yellow fever epidemic, with over 400 additional victims eventually succumbing. The total death toll from August through November was approximately 1,200,[79][80]

In 1878, about 20,000 people died in a widespread epidemic in the Mississippi River Valley.[81] That year, Memphis had an unusually large amount of rain, which led to an increase in the mosquito population. The result was a huge epidemic of yellow fever.[82] The steamship John D. Porter took people fleeing Memphis northward in hopes of escaping the disease, but passengers were not allowed to disembark due to concerns of spreading yellow fever. The ship roamed the Mississippi River for the next two months before unloading her passengers.[83] The last major U.S. outbreak was in 1905 in New Orleans.[10][84]

Major outbreaks have also occurred in southern Europe. Gibraltar lost many to outbreaks in 1804, 1814, and 1828.[85] Barcelona suffered the loss of several thousand citizens during an outbreak in 1821. The Duke de Richelieu deployed 30,000 French troops to the border between France and Spain in the Pyrenees Mountains, to establish a cordon sanitaire in order to prevent the epidemic from spreading from Spain into France.[86]

In Colonial times and during the Napoleonic Wars, the West Indies were known as a particularly dangerous posting for soldiers due to yellow fever being endemic in the area. The mortality rate in British garrisons in Jamaica was seven times that of garrisons in Canada, mostly because of yellow fever and other tropical diseases.[87] Both English and French forces posted there were seriously affected by the "yellow jack". Wanting to regain control of the lucrative sugar trade in Saint-Domingue (Hispaniola), and with an eye on regaining France's New World empire, Napoleon sent an army under the command of his brother-in-law General Charles Leclerc to Saint-Domingue to seize control after a slave revolt. The historian J. R. McNeill asserts that yellow fever accounted for about 35,000 to 45,000 casualties of these forces during the fighting.[88] Only one-third of the French troops survived for withdrawal and return to France. Napoleon gave up on the island and his plans for North America, selling the Louisiana Purchase to the US in 1803. In 1804, Haiti proclaimed its independence as the second republic in the Western Hemisphere. Considerable debate exists over whether the number of deaths caused by disease in the Haitian Revolution was exaggerated.[89]

Discovery of causes and transmission

Ezekiel Stone Wiggins, known as the Ottawa Prophet, proposed that the cause of a yellow fever epidemic in Jacksonville, Florida, in 1888, was astrological.

The planets were in the same line as the sun and earth and this produced, besides Cyclones, Earthquakes, etc., a denser atmosphere holding more carbon and creating microbes. Mars had an uncommonly dense atmosphere, but its inhabitants were probably protected from the fever by their newly discovered canals, which were perhaps made to absorb carbon and prevent the disease.[90]

In 1848, Josiah C. Nott suggested that yellow fever was spread by insects such as moths or mosquitoes, basing his ideas on the pattern of transmission of the disease.[91] Carlos Finlay, a Cuban doctor and scientist, proposed in 1881 that yellow fever might be transmitted by mosquitoes rather than direct human contact.[92][93] Since the losses from yellow fever in the Spanish–American War in the 1890s were extremely high, Army doctors began research experiments with a team led by Walter Reed, and composed of doctors James Carroll, Aristides Agramonte, and Jesse William Lazear. They successfully proved Finlay's ″mosquito hypothesis″. Yellow fever was the first virus shown to be transmitted by mosquitoes. The physician William Gorgas applied these insights and eradicated yellow fever from Havana. He also campaigned against yellow fever during the construction of the Panama Canal. A previous effort of canal building by the French had failed (in part due to mortality from the high incidence of yellow fever and malaria, which killed many workers).[10]

Although Dr. Walter Reed has received much of the credit in United States history books for "beating" yellow fever, he had fully credited Dr. Finlay with the discovery of the yellow fever vector, and how it might be controlled. Reed often cited Finlay's papers in his own articles, and also credited him for the discovery in his personal correspondence.[94] The acceptance of Finlay's work was one of the most important and far-reaching effects of the Walter Reed Commission of 1900.[95] Applying methods first suggested by Finlay, the United States government and Army eradicated yellow fever in Cuba and later in Panama, allowing completion of the Panama Canal. While Reed built on the research of Finlay, historian François Delaporte notes that yellow fever research was a contentious issue. Scientists, including Finlay and Reed, became successful by building on the work of less prominent scientists, without always giving them the credit they were due.[96] Reed's research was essential in the fight against yellow fever. He is also credited for using the first type of medical consent form during his experiments in Cuba, an attempt to ensure that participants knew they were taking a risk by being part of testing.[97]

Like Cuba and Panama, Brazil also led a highly successful sanitation campaign against mosquitoes and yellow fever. Beginning in 1903, the campaign led by Oswaldo Cruz, then director general of public health, not only resulted in eradicating the disease, but also reshaped the physical landscape of Brazilian cities, such as Rio de Janeiro. During rainy seasons, Rio de Janeiro had regularly suffered floods, as water from the bay surrounding the city overflowed into Rio's narrow streets. Coupled with the poor drainage systems found throughout Rio, this created swampy conditions in the city's neighborhoods. Pools of stagnant water stood year long in city streets and proved to be a fertile ground for disease-carrying mosquitoes. Thus, under Cruz's direction, public health units known as "mosquito inspectors" fiercely worked to combat yellow fever throughout Rio by spraying, exterminating rats, improving drainage, and destroying unsanitary housing. Ultimately, the city's sanitation and renovation campaigns reshaped Rio de Janeiro's neighborhoods. Its poor residents were pushed from city centers to Rio's suburbs, or to towns found in the outskirts of the city. In later years, Rio's most impoverished inhabitants would come to reside in favelas.[98]

During 1920–23, the Rockefeller Foundation’s International Health Board undertook an expensive and successful yellow fever eradication campaign in Mexico.[99] The IHB gained the respect of Mexico’s federal government because of the success. The eradication of yellow fever strengthened the relationship between the US and Mexico, which had not been very good in the past. The eradication of yellow fever was also a major step toward better global health.[100]

In 1927, scientists isolated yellow fever virus in West Africa.[101] Following this, two vaccines were developed in the 1930s. The vaccine 17D was developed by the South African microbiologist Max Theiler at the Rockefeller Institute in New York City. This vaccine was widely used by the U.S. Army during World War II.[66] Following the work of Ernest Goodpasture, Theiler used chicken eggs to culture the virus and won a Nobel Prize in 1951 for this achievement. A French team developed the French neurotropic vaccine (FNV), which was extracted from mouse brain tissue. Since this vaccine was associated with a higher incidence of encephalitis, FNV was not recommended after 1961. Vaccine 17D is still in use, and more than 400 million doses have been distributed. Little research has been done to develop new vaccines. Some researchers worry that the 60-year-old technology for vaccine production may be too slow to stop a major new yellow-fever epidemic. Newer vaccines, based on vero cells, are in development and should replace 17D at some point.[4]

Using vector control and strict vaccination programs, the urban cycle of yellow fever was nearly eradicated from South America. Since 1943, only a single urban outbreak in Santa Cruz de la Sierra, Bolivia, has occurred. Since the 1980s, though, the number of yellow fever cases has been increasing again, and A. aegypti has returned to the urban centers of South America. This is partly due to limitations on available insecticides, as well as habitat dislocations caused by climate change. It is also because the vector control program was abandoned. Although no new urban cycle has yet been established, scientists believe this could happen again at any point. An outbreak in Paraguay in 2008 was thought to be urban in nature, but this ultimately proved not to be the case.[4]

In Africa, virus eradication programs have mostly relied upon vaccination. These programs have largely been unsuccessful because they were unable to break the sylvatic cycle involving wild primates. With few countries establishing regular vaccination programs, measures to fight yellow fever have been neglected, making the future spread of the virus more likely.[4]

Research

In the hamster model of yellow fever, early administration of the antiviral ribavirin is an effective early treatment of many pathological features of the disease.[102] Ribavirin treatment during the first five days after virus infection improved survival rates, reduced tissue damage in the liver and spleen, prevented hepatocellular steatosis, and normalised levels of alanine aminotransferase, a liver damage marker. The mechanism of action of ribavirin in reducing liver pathology in yellow fever virus infection may be similar to its activity in treatment of hepatitis C, a related virus.[102] Because ribavirin had failed to improve survival in a virulent rhesus model of yellow fever infection, it had been previously discounted as a possible therapy.[103] Infection was reduced in mosquitoes with the wMel strain of Wolbachia.[104]

Yellow fever has been researched by several countries as a potential biological weapon.[105]

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Further reading

  • Crosby, M. (2006). The American Plague: The Untold Story of Yellow Fever, the Epidemic that Shaped Our History. New York: The Berkley Publishing Group. ISBN 978-0-425-21202-8.
  • Espinosa, M. (2009). Epidemic Invasions: Yellow Fever and the Limits of Cuban Independence, 1878–1930. Chicago: University of Chicago Press. ISBN 978-0-226-21811-3.
  • Gessner, I. (2016). Yellow Fever Years: An Epidemiology of Nineteenth-Century American Literature and Culture. Frankfurt/Main: Peter Lang. ISBN 978-3-631-67412-3.
  • Murphy, J. (2003). An American Plague: The True and Terrifying Story of the Yellow Fever Epidemic of 1793. New York: Clarion Books. ISBN 978-0-395-77608-7.
  • Nuwer, D. S. (2009). Plague Among the Magnolias: The 1878 Yellow Fever Epidemic in Mississippi. University of Alabama Press. ISBN 978-0-8173-1653-2.

External links

External resources
1793 Philadelphia yellow fever epidemic

During the Yellow Fever Epidemic of 1793 in Philadelphia, 5,000 or more people were listed in the official register of deaths between August 1 and November 9. The vast majority of them died of yellow fever, making the epidemic in the city of 50,000 people one of the most severe in United States history. By the end of September, 20,000 people had fled the city. The mortality rate peaked in October, before frost finally killed the mosquitoes and brought an end to the epidemic in November. Doctors tried a variety of treatments, but knew neither the origin of the fever nor that it was transmitted by mosquitoes (which was not verified until the late nineteenth century).

The mayor and a committee of two dozen organized a fever hospital at Bush Hill and other crisis measures. The assistance of the Free African Society was requested by the city and readily agreed to by the members, based on the mistaken assumption that native Africans would have the same partial immunity to the new disease as many had to malaria, the most common source of fever epidemics during the summer months. Black nurses aided the sick and the group's leaders hired additional men to take away corpses, which most people would not touch. Blacks in the city died at the same rate as whites, about 240 altogether.

Some neighboring towns refused to let refugees in from Philadelphia, for fear they were carrying the fever. Major port cities such as Baltimore and New York had quarantines against refugees and goods from Philadelphia although New York sent financial aid to the city. The once thriving city soon became distraught under the raging epidemic, leaving many to fight for their own lives.

Acacia

Acacia, commonly known as the wattles or acacias, is a large genus of shrubs and trees in the subfamily Mimosoideae of the pea family Fabaceae. Initially it comprised a group of plant species native to Africa and Australia, with the first species A. nilotica described by Linnaeus. Controversy erupted in the early 2000s when it became evident that the genus as it stood was not monophyletic, and that several divergent lineages needed to be placed in separate genera. It turned out that one lineage comprising over 900 species mainly native to Australia was not closely related to the mainly African lineage that contained A. nilotica—the first and type species. This meant that the Australian lineage (by far the most prolific in number of species) would need to be renamed. Botanist Les Pedley named this group Racosperma, which was inconsistently adopted. Australian botanists proposed that this would be more disruptive than setting a different type species (A. penninervis) and allowing this large number of species to remain Acacia, resulting in the two African lineages being renamed Vachellia and Senegalia, and the two New World lineages renamed Acaciella and Mariosousa. This was officially adopted, but many botanists from Africa and elsewhere disagreed that this was necessary.

A number of species have been introduced to various parts of the world, and two million hectares of commercial plantations have been established. The heterogeneous group varies considerably in habit, from mat-like subshrubs to canopy trees in forest.

Aedes

Aedes is a genus of mosquitoes originally found in tropical and subtropical zones, but now found on all continents except Antarctica. Some species have been spread by human activity. Aedes albopictus, a most invasive species, was recently spread to the New World, including the United States, by the used-tire trade. First described and named by German entomologist Johann Wilhelm Meigen in 1818, the generic name comes from the Ancient Greek ἀηδής, aēdēs, meaning "unpleasant" or "odious". The type species for Aedes is Aedes cinereus. Some species of this genus transmit serious diseases, including dengue fever, yellow fever, the Zika virus, and chikungunya. In Polynesia, the species Aedes polynesiensis is responsible for the transmission of human lymphatic filariasis.

Aedes can be detected and monitored by ovitraps.

The yellow fever mosquito (Aedes aegypti) genome was sequenced by the Broad Institute and The Institute for Genomic Research. The initial assembly was released in August 2005; a draft sequence of the genome and preliminary analysis was published in June 2007. The annotated genome is available at VectorBase.

Aedes aegypti

Aedes aegypti, the yellow fever mosquito, is a mosquito that can spread dengue fever, chikungunya, Zika fever, Mayaro and yellow fever viruses, and other disease agents. The mosquito can be recognized by white markings on its legs and a marking in the form of a lyre on the upper surface of its thorax. This mosquito originated in Africa, but is now found in tropical, subtropical and temperate regions throughout the world.

Carlos Finlay

Carlos Juan Finlay (December 3, 1833 – August 20, 1915) was a Cuban epidemiologist recognized as a pioneer in the research of yellow fever, determining that it was transmitted through mosquitoes Aedes aegypti.

Carte Jaune

The Carte Jaune or Yellow Card is an international certificate of vaccination (ICV). It is issued by the World Health Organization. It is recognised internationally and may be required for entry to certain countries where there are increased health risks for travellers. The Yellow Card should be kept in the holder's passport, as it is a medical passport of sorts.

Note that the example shown here is the American version of the WHO-ICV, issued by U.S. Department of Health and Human Services. It is available through the Government Printing Office. The original ICV printed and distributed by WHO is found in two versions: 1) English - French (bilingual) or 2) English - French - Arabic (trilingual). These WHO versions do not have pages to show medical contraindication to vaccination, personal health history, state of health, medical treatments, known sensitivities, medications taken regularly, and ophthalmic information. The WHO versions are available from the WHO Bookstore, and they can be ordered in quantities of 5,000 or more, for overprint. The Yellow Fever section is the most important part of the certificate. Other variants of the Yellow Fever certificate are valid only if the card follows the standardized format, and has been officially approved by WHO.

There has been a revision in the format, title and the rules on the 2007 issue. It is now called, "International Certificate of Vaccination or Prophylaxis", and the overprint service is no longer available.

Charles Leclerc (general)

Charles Victoire Emmanuel Leclerc (17 March 1772 – 2 November 1802) was a French Army general who served under Napoleon Bonaparte during the French Revolution. He was husband to Pauline Bonaparte, sister to Napoleon. In 1801, he was sent to Saint-Domingue (Haiti), where an expeditionary force under his command captured and deported the Haitian leader Toussaint L'Ouverture, as part of an unsuccessful attempt to reassert imperial control over the Saint-Domingue government. Leclerc died of yellow fever during the failed expedition.

Flaviviridae

Flaviviridae is a family of viruses. Humans and other mammals serve as natural hosts. They are primarily spread through arthropod vectors (mainly ticks and mosquitoes). The family gets its name from the yellow fever virus, the type virus of Flaviviridae; flavus is Latin for "yellow", and Yellow fever in turn was named because of its propensity to cause jaundice in victims. There are currently over 100 species in this family, divided among four genera. Diseases associated with this family include: hepatitis (hepaciviruses), hemorrhagic syndromes, fatal mucosal disease (pestiviruses), hemorrhagic fever, encephalitis, and the birth defect microcephaly (flaviviruses).

Flavivirus

Flavivirus is a genus of viruses in the family Flaviviridae. This genus includes the West Nile virus, dengue virus, tick-borne encephalitis virus, yellow fever virus, Zika virus and several other viruses which may cause encephalitis, as well as insect-specific flaviviruses (ISFs) such as cell fusing agent virus (CFAV), Palm Creek virus (PCV), and Parramatta River virus (PaRV).Flaviviruses are named from the yellow fever virus, the type virus for the family; the word flavus means "yellow" in Latin and the yellow fever in turn is named from its propensity to cause yellow jaundice in victims.Flaviviruses share several common aspects: common size (40–65 nm), symmetry (enveloped, icosahedral nucleocapsid), nucleic acid (positive-sense, single-stranded RNA around 10,000–11,000 bases), and appearance in the electron microscope.

Most of these viruses are transmitted by the bite from an infected arthropod (mosquito or tick), and hence are classified as arboviruses. Human infections with most of these arboviruses are incidental, as humans are unable to replicate the virus to high enough titers to reinfect the arthropods needed to continue the virus lifecycle – humans are then a dead end host. The exceptions to this are the yellow fever, dengue, and zika viruses. These three viruses still require mosquito vectors, but are well-enough adapted to humans as to not necessarily depend upon animal hosts (although they continue to have important animal transmission routes, as well).

Other virus transmission routes for arboviruses include handling infected animal carcasses, blood transfusion, child birth and consumption of unpasteurised milk products. Transmission from nonhuman vertebrates to humans without an intermediate vector arthropod is thought to be unlikely. For example, early tests with yellow fever showed that the disease is not contagious.

The known non-arboviruses of the flavivirus family reproduce in either arthropods or vertebrates, but not both, with one odd member of the genus affecting a nematode.

List of epidemics

This article is a list of epidemics of infectious disease. Widespread and chronic complaints such as heart disease and allergy are not included if they are not thought to be infectious.

List of notifiable diseases

The following is a list of notifiable diseases arranged by country.

Luke P. Blackburn

Luke Pryor Blackburn (June 16, 1816 – September 14, 1887) was an American physician, philanthropist, and politician from Kentucky. He was elected the 28th governor of Kentucky, serving from 1879 to 1883. Until the election of Ernie Fletcher in 2003, Blackburn was the only physician to serve as governor of Kentucky.

After earning a medical degree at Transylvania University, Blackburn moved to Natchez, Mississippi, and gained national fame for implementing the first successful quarantine against yellow fever in the Mississippi River valley in 1848. He came to be regarded as an expert on yellow fever and often worked pro bono to combat outbreaks. Among his philanthropic ventures was the construction of a hospital for boatmen working on the Mississippi River using his personal funds. He later successfully lobbied Congress to construct a series of similar hospitals along the Mississippi.

Although too old to serve in the military, Blackburn supported the Confederate cause during the Civil War. In the early days of the war, he acted as a civilian agent for the governments of Kentucky and Mississippi. By 1863, he was aiding Confederate blockade runners in Canada. In 1864, he traveled to Bermuda to help combat a yellow fever outbreak that threatened Confederate blockade running operations there. Shortly after the war's end, a Confederate double agent accused him of having carried out a plot to start a yellow fever epidemic in the Northern United States that would have hampered the Union war effort. Blackburn was accused of collecting linens and garments used by yellow fever patients and smuggling them into the Northern states to be sold. The evidence against Blackburn was considerable, although much of it was either circumstantial or provided by witnesses of questionable reputation. Although he was acquitted by a Toronto court, public sentiment was decidedly against him throughout much of the United States. Today, historians still disagree as to the strength of the evidence supporting Blackburn's role in the alleged plot. Any plot of this nature was destined to fail, however; in 1900, Walter Reed discovered that yellow fever is spread by mosquitoes, not by contact.

Blackburn remained in Canada to avoid prosecution by U.S. authorities, but he returned to his home country in 1868 to help combat a yellow fever outbreak along the Gulf Coast of Texas and Louisiana. Although the charges against him had not been dropped, he was not arrested or prosecuted. He rehabilitated his public image by rendering aid in yellow fever outbreaks in Memphis, Tennessee, in 1873, Fernandina, Florida, in 1877, and Hickman, Kentucky, in 1878. Dubbed the "Hero of Hickman", Blackburn's ministrations propelled him to the Democratic gubernatorial nomination the following year. In the general election, he defeated Republican Walter Evans by a wide margin. As governor, Blackburn won passage of several reforms in the areas of state finance and internal improvements, but his signature accomplishments were in the area of penal reform. Troubled by the conditions at the penitentiary in Frankfort, Blackburn attempted to ease overcrowding through liberal use of his gubernatorial pardon, earning him the derisive nickname "Lenient Luke". He also secured approval of the construction of a new penitentiary at Eddyville, the adoption of a warden system to replace the corrupt private oversight of the old penitentiary, and the implementation of the state's first parole system. Although his record of reform led historians to laud him as "the father of prison reform in Kentucky", his liberal pardon record and expenditure of scarce taxpayer money to improve the living conditions of prisoners was unpopular at the time, and he was booed and shouted down at his own party's nominating convention in 1883. After his term as governor, he returned to his medical practice and died in 1887. The Blackburn Correctional Complex, a minimum-security penal facility near Lexington, Kentucky, was named in his honor in 1972.

Max Theiler

Max Theiler (30 January 1899 – 11 August 1972) was a South African-American virologist and physician. He was awarded the Nobel Prize in Physiology or Medicine in 1951 for developing a vaccine against yellow fever in 1937, becoming the first African-born Nobel laureate.Born in Pretoria, Theiler was educated in South Africa through completion of his degree in medical school. He went to London for postgraduate work at St Thomas's Hospital Medical School, King's College London, and at the London School of Hygiene and Tropical Medicine, earning a 1922 diploma in tropical medicine and hygiene. That year, he moved to the United States to do research at the Harvard University School of Tropical Medicine. He lived and worked in that nation the rest of his life. In 1930, he moved to the Rockefeller Foundation in New York, becoming director of the Virus Laboratory.

Mosquito-borne disease

Mosquito-borne diseases or mosquito-borne illnesses are diseases caused by bacteria, viruses or parasites transmitted by mosquitoes. They can transmit disease without being affected themselves. Nearly 700 million people get a mosquito-borne illness each year resulting in over one million deaths.Diseases transmitted by mosquitoes include: malaria, dengue, West Nile virus, chikungunya, yellow fever, filariasis, tularemia, dirofilariasis, Japanese encephalitis, Saint Louis encephalitis, Western equine encephalitis, Eastern equine encephalitis, Venezuelan equine encephalitis, Ross River fever, Barmah Forest fever, La Crosse encephalitis, and Zika fever, as well as newly detected Keystone virus and Rift Valley fever.

Visa policy of Singapore

Visitors to Singapore can either enter the country without a visa or in some cases they must first obtain a visa. Citizens of almost 80% of the world's countries may travel to Singapore for a period of 30 days or 90 days without a visa, depending on their nationality. Countries requiring visas are categorized into countries eligible to apply for an electronic visa and countries whose citizens need a visa vignette.

All visitors to Singapore must:

hold a passport or a travel document valid for more than 6 months at the time of departure,

hold an onward or return ticket,

have sufficient funds to stay in Singapore,

have entry documents (including a visa) to their next destination, if required,

have a completed Disembarkation/Embarkation Card, and,

have a visa and/or a yellow fever vaccination certificate for entry into Singapore (if applicable).

Walter Reed

Major Walter Reed, M.D., U.S. Army, (September 13, 1851 – November 22, 1902) was a U.S. Army physician who in 1901 led the team that postulated and confirmed the theory that yellow fever is transmitted by a particular mosquito species, rather than by direct contact. This insight gave impetus to the new fields of epidemiology and biomedicine, and most immediately allowed the resumption and completion of work on the Panama Canal (1904–1914) by the United States. Reed followed work started by Carlos Finlay and directed by George Miller Sternberg who has been called the "first U.S. bacteriologist".

Wellington Phoenix FC

Wellington Phoenix Football Club is a New Zealand professional football club based in Wellington. It competes in the Australian A-League, under licence from Football Federation Australia. Phoenix entered the competition in the 2007–08 season after its formation in March 2007, by New Zealand Football to replace New Zealand Knights as a New Zealand-based club in the Australian A-League competition. The club is one of the few clubs in the world to compete in a league of a different confederation (AFC) from that of the country where it is based (OFC).

Ernie Merrick was the head coach following the resignation of founding coach Ricki Herbert late in the 2012–13 season, until his own resignation on 5 December 2016. Andrew Durante has been the club captain since the 2008–09 season succeeding from the inaugural captain, Ross Aloisi. The club's highest achievement is reaching the A-League Preliminary Final in 2010. The club plays matches at Westpac Stadium, a 34,500-seat multi-purpose venue in Wellington. Their home kit consists of black and yellow stripes.

Yellow Fever (album)

Yellow Fever is the sixth album by the American blues rock band Hot Tuna, recorded and released in 1975 as Grunt BFL1-1238. The album was also released in Quadraphonic as Grunt BFD1-1238. The album rose to #97 on the Billboard charts.

Yellow fever vaccine

Yellow fever vaccine is a vaccine that protects against yellow fever. Yellow fever is a viral infection that occurs in Africa and South America. Most people begin to develop immunity within ten days and 99 percent are protected within one month of vaccination, and this appears to be lifelong. The vaccine can be used to control outbreaks of disease. It is given either by injection into a muscle or just under the skin.The World Health Organization (WHO) recommends routine immunization in all countries where the disease is common. This should typically occur between nine and twelve months of age. Those travelling to areas where the disease occurs should also be immunized. Additional doses after the first are generally not needed.Yellow fever vaccine is generally safe. This includes in those with HIV infection but without symptoms. Mild side effects may include headache, muscle pains, pain at the injection site, fever, and rash. Severe allergies occur in about eight per million doses, serious neurological problems occur in about four per million doses, and organ failure occurs in about three per million doses. It is likely safe in pregnancy and therefore recommended among those who will be potentially exposed. It should not be given to those with very poor immune function.Yellow fever vaccine came into use in 1938. It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system. The wholesale price in the developing world is between US$4.30 and US$21.30 per dose as of 2014. In the United States it costs between US$50 and US$100. The vaccine is made from weakened yellow fever virus. Some countries require a yellow fever vaccination certificate before entry from a country where the disease is common.

Arthropod-borne
Mammal-borne

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