A tropical mosquito-borne viral hepatitis, due to yellow fever virus, a member of the family Flaviviridae, with an urban form transmitted by Aedes aegypti, and a rural, jungle, or sylvatic form from tree-dwelling mammals by various mosquitoes of the Haemagogus species complex; characterized clinically by fever, slow pulse, albuminuria, jaundice, congestion of the face, and hemorrhages, especially hematemesis; used to occur in epidemics mainly in port cities, especially in late summer, with 20-40% case fatality rates; immunity to reinfection accompanies recovery.
Also called as Bunyavirus Infection.
Yellow-fever, a flavivirus and member of the Arbovirus family, is an enveloped virus. It contains three structural proteins; the envelope (E) protein is the major component of the virion surface. The antigenic elements of this envelope protein inhibit red blood cell clotting, while other elements recognize and bind to host-cell receptors.
The yellow fever isolates appear to be genetically stable. Genetic drift occurs within each genotype; the envelope gene appears to mutate randomly at a rate of 2.2 bases per year,
Yellow fever is often called a classic hemorrhagic fever whose history is the history of the New World. Epidemics of this disease followed the trade ships from Africa to the Americas, and centuries of disease resulted. It is thought that the virus was brought to the New World via water casks and water barrels in which infected mosquitoes had laid their eggs.
Yellow fever is found only in parts of South America and Africa. There are two kinds of this disease, spread by two different cycles of infection.
1. Jungle yellow fever is mainly a disease of monkeys. It is spread from infected mosquitoes to monkeys in the tropical rain forest. People get jungle yellow fever when they put themselves in the middle of this natural cycle and are bitten by mosquitoes that have been infected by monkeys. Jungle yellow fever is rare and occurs mainly in persons who work in tropical rain forests.
2. Urban yellow fever is a disease of humans. It is spread by mosquitoes that have been infected by other people. Aedes aegypti is the type of mosquito that usually carries yellow fever from human to human. These mosquitoes have adapted to living among humans in cities, towns, and villages. They breed in discarded tires, flower pots, oil drums, and water storage containers close to human dwellings. Urban yellow fever is the cause of most yellow fever outbreaks and epidemics.
Yellow fever can be divided into three stages:
Early stage: Headache, muscle aches, fever, loss of appetite, vomiting, and jaundice are common. After approximately 3 to 4 days, victims often experience brief remission.
Period of remission: After a few days (3 to 4) fever and other symptoms go away. Most individuals will recover at this stage, but others may move onto the third, most dangerous stage (intoxication stage) within 24 hours.
Period of intoxication: Multi-organ dysfunction occurs. This includes liver and kidney failure, bleeding disorders/hemorrhage, brain dysfunction including delirium, seizures, coma, shock, and death.
Yellow fever is common in West and Central Africa and in parts of South America. Periodic epidemics in Africa lead to hundreds of thousands of cases. Yellow fever is a very rare cause of illness in U.S. travelers. There are between 50 and 300 cases of yellow fever reported annually in the Americas. Up to 5,000 cases are reported annually in Africa. However, epidemics are increasing in both size and frequency, and the actual number of cases in Africa can be as high as hundreds of thousands in a single year.
Yellow fever ranges in severity from a self-limited infection to hemorrhagic fever that carries a 50% mortality rate. Fatality rates are higher in the young. Early appearance of jaundice (day 3) indicates a poor prognosis. Transaminase elevations reflect the degree of hepatic injury and are prognostic. Individuals who survive the toxic phase may experience renal failure. Convalescence with symptoms of weakness and fatigue may last up to 3 months.
Following are the symptoms of yellow fever:
Recurrent muscle cramps and aches.
Nausea and vomiting.
High fever accompanied by chills.
Yellow fever symptoms are generally mild in the beginning, but they complicate themselves quite rapidly. The following are the important complications of yellow fever:-
Yellow fever infection can cause a severe disorder in the liver, which may cause the onset of jaundice-like conditions. This is accompanied by yellowing of the skin and the eyes.
There can be hemorrhage of the gastrointestinal tract. This causes vomiting. The vomitus is black in color and of the consistency of coffee-grind.
Proteinuria can occur (Proteinuria is a disorder of the kidney in which excess serum proteins are expelled through the urine making the urine frothy and foamy).
Prolonged affectation of the yellow fever can cause deliriums, which can be followed by strokes and comas. Such complications usually lead to death.
Other minor complications are low blood pressure and depression.
Causes and Risk Factors:
Yellow fever is a viral tropical disease that is spread to humans by infected mosquitoes. The disease is caused by a virus. Most yellow fever infections are mild. However, the disease can cause severe, life-threatening illness. Yellow fever is found only in parts of Africa and South America.
Humans and monkeys are most commonly infected with the yellow fever virus. Mosquitoes transmit the virus back and forth between monkeys, humans or both. When a mosquito bites a human or monkey infected with yellow fever, the virus enters the mosquito's bloodstream and circulates before settling in the salivary glands. When the infected mosquito then bites another monkey or human, the virus then enters the host's bloodstream, where it may cause illness.
Aedes mosquitoes, including A. aegypti, A. africanus, A. simpsoni, A. furcifer, A. luteocephalus, and A. albopictus (Asian tiger mosquito). Urban yellow fever is transmitted by the Aedes aegypti mosquito. A. aegypti becomes infectious 2 weeks after feeding on a viremic host. Jungle or sylvatic, yellow fever is transmitted by Haemagogus and other mosquitoes (such as Masoni africana) of the forest canopy (tree-hole breeding mosquitoes). These mosquitoes acquire the virus from viremic primates. The yellow-fever virus can also be passed from one mosquito generation to another via the mosquito eggs.
Yellow fever virus has been isolated from other insect vectors, such asphlebotomine flies, horse mosquitoes (Brazil), common ticks (Amblyomma variegatum) in West Africa, and other parasitic arthropods.
A secondary vector is nosocomial transmission in laboratories and hospitals.
The natural yellow-fever cycle is mosquito-monkey-mosquito. The virus is taken up by the mosquito which feeds on viremic monkeys. When the mosquito bites another host, the virus is transferred to the new host via the mosquito's saliva. The shift from jungle yellow fever to urban yellow fever is thought to be the result of humans entering the sylvan setting and becoming part of the yellow-fever cycle: Initially, wood cutters and other forest workers were bitten by forest-canopy mosquitoes carrying the yellow-fever virus. The humans then returned to the urban settings. The A. aegypti mosquito, which breeds in standing water such as water barrels, shallow basins, and so on; lived in the urban setting and fed on viremic humans in towns and villages. A. aegypti then became a vector for the transmission of yellow fever within urban populations. However, Haemagogus mosquitoes have also been discovered biting humans inside dwellings near forests.
Because of mosquito breeding cycles, yellow fever occurs most often during months with high rainfall, humidity, and temperature. In Africa, the incidence of disease is greatest at the end of the rainy season and early into the dry season.
There are three types of transmission cycle for yellow fever: sylvatic, intermediate, and urban. All three cycles exist in Africa, but in South America, only sylvatic and urban yellow fever occur.
Intermediate yellow fever: In humid or semi-humid savannahs of Africa, small-scale epidemics occur. These behave differently from urban epidemics; many separate villages in an area suffer cases simultaneously, but fewer people die from infection. Semi-domestic mosquitoes infect both monkey and human hosts. This area is often called the "zone of emergence", where increased contact between man and infected mosquito leads to disease. This is the most common type of outbreak seen in recent decades in Africa. It can shift to a more severe urban-type epidemic if the infection is carried into a suitable environment (with the presence of domestic mosquitoes and unvaccinated humans).
Urban yellow fever: Large epidemics can occur when migrants introduce the virus into areas with high human population density. Domestic mosquitoes (of one species, Aedes aegypti) carry the virus from person to person; no monkeys are involved in transmission. These outbreaks tend to spread outwards from one source to cover a wide area.
Sylvatic (or jungle) yellow fever: In tropical rainforests, yellow fever occurs in monkeys that are infected by wild mosquitoes. The infected monkeys can then pass the virus onto other mosquitoes that feed on them. These infected wild mosquitoes bite humans entering the forest resulting in sporadic cases of yellow fever. The majority of cases are young men working in the forest (logging, etc). On occasion, the virus spreads beyond the affected individual.
Risk Factors: Anyone can be infected with the yellow fever virus, but older adults are at greater risk of getting seriously ill.
Mild cases of yellow fever are nonspecific enough that they cannot be distinguished from a variety of other conditions. Severe cases can still be confused with other diseases which cause jaundice, such as: viral hepatitis, falciparum malaria, Rift Valley fever, typhoid, Q fever, typhus, and so on. Specific diagnosis can be confirmed by isolating the virus or demonstrating the viral antigen or a specific antibody response. The virus is best isolated from serum taken during the first 4 days of illness. However, the virus can still be detected from serum obtained up to 14 days after onset of symptoms.
Diagnostic tests for yellow fever include:
HI, CF, and neutralization tests for antibodies. The HI and neutralization antibodies appear with 7 days of onset of symptoms; the CF antibodies appear later in the course of the disease.
ELISA, which is sensitive enough that it may be able to detect antigen even in poorly handled or contaminated samples.
PCR, which can detect the viral genome in serum.
No specific antiviral therapy is available for yellow fever. Specific chemotherapies under investigation include interferon and ribavirin. Dehydration and fever can be corrected with oral rehydration salts and paracetamol. Any superimposed bacterial infection should be treated with an appropriate antibiotic. Intensive supportive care may improve the outcome for seriously ill patients, but is rarely available in poorer, developing countries.
Vaccination is the single most important measure for preventing yellow fever. In populations where vaccination coverage is low, vigilant surveillance is critical for prompt recognition and rapid control of outbreaks. Mosquito control measures can be used to prevent virus transmission until vaccination has taken effect.
Histamine H2 antagonists.
Note: The following drugs and medications are in some way related to, or used in the treatment. This service should be used as a supplement to, and NOT a substitute for, the expertise, skill, knowledge and judgment of healthcare practitioners.
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