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Yellow Fever

Clinical Course Of Yellow Fever




Once a mosquito has transmitted the yellow fever virus to a human, the likelihood of symptomatic disease development is about 5-20%. Some infections may be warded off by the host's immune system; others may be subclinical, meaning they lack the severity of symptoms that would usually result in the identification of infection.



After a human host has received the yellow fever virus, there are five distinct stages through which a classic yellow fever infection evolves. These have been termed the periods of incubation, invasion, remission, intoxication, and convalescence.

The incubation period is the amount of time between the introduction of the virus into the host and the development of symptoms. For yellow fever this period is three to six days. During this time there are generally no symptoms identifiable to the host.

The period of invasion lasts two to five days; it begins with an abrupt onset of symptoms, consisting of fever and chills, intense headache, lower backache, muscle aches, nausea, and extreme exhaustion. The patient's tongue shows a characteristic white furry coating in the center, surrounded by beefy red margins. While most other infections that cause an elevation in temperature also cause an increase in heart rate, yellow fever produces an unusual symptom, called Faget's sign—the simultaneous occurrence of a high fever with a slowed heart rate. Throughout the period of invasion, there are still viruses circulating in the patient's blood stream, so continued viral transmission through mosquito vectors is possible.

The next phase is called the period of remission. The fever falls, and symptoms decrease in severity for a period of several hours to several days. In some patients, this signals the end of the disease; in other patients, this proves to be only the calm before the storm.

The period of intoxication is the most severe and potentially fatal phase of the illness. During this time, lasting three to nine days, a type of degeneration, or tissue breakdown, of the internal organs—specifically the kidneys, liver, and heart—occurs. This fatty degeneration results in what is considered the classic triad of yellow fever symptoms: jaundice, black vomit, and the release of protein into the urine. Jaundice causes the skin and the whites of the patient's eyes to take on a distinctive yellow tint. This yellow color is due to liver damage, resulting in the accumulation of bilirubin normally processed by a healthy liver. The liver damage also results in a tendency toward bleeding; the patient's vomit appears black due to the presence of blood. Protein, which is normally kept out of the urine by healthy and intact kidneys, appears in the urine due to disruption of the kidneys' composition by fatty degeneration.

Patients who survive the period of intoxication enter into a relatively short period of convalescence, and recover with no long-term deficits related to the yellow fever infection. Further, infection with the yellow fever virus results in lifelong immunity against repeated infection with the virus.

Five to 10 percent of all diagnosed cases of yellow fever are fatal. The occurrence of jaundice during a yellow fever infection is an extremely grave predictor, with 20-50% of these patients dying from their infection. Death may occur due to hemorrhaging (massive bleeding), often following a lapse into a comatose state.


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