Yellow fever is a menacing disease which has caused the death of enormous numbers of people in the past. It has been known since 1648 among people living on the islands in the Caribbean Sea and along the coast of North, Central, and South America. From 1798 to 1900, five lakh people in America contracted the disease. Yellow fever caused 36,000 deaths in Havana between 1853 and 1900, 23,000 deaths in Rio de Janeiro between 1851 and 1883, and 22,000 deaths between 1881 and 1889 during the construction of the Panama Canal.

The viral theory of the origin of yellow fever was suggested by the Cuban scientist K. Finlay in 1881. The virus was discovered in 1901 by American investigators W. Reed, J. Carroll, J. Agramonte, and J. Lazear.

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The yellow fever virus belongs to the genus Flavivirus. It ranges from 12 to 40 nm in size and forms irregularly shaped inclusions within the nuclei of nerve and hepatic cells. The virus grows in the brain tissue of albino mice and Macaca rhesus monkeys. It also multiplies readily in ground mouse embryo tissue cultures, in developing chicken embryos, in mouse testicular tissue, and in monkey kidney tissue cultures.

In natural foci, the yellow fever virus lives in the bodies of more than 27 species of animals, such as monkeys, opossums, and armadillos. Among experimental animals susceptible to the disease are European hedgehogs, albino mice, Macaca rhesus monkeys, and others. The virus is transmitted from one animal to another by the Haemagogus mosquito, which breeds in the hollows of trees or on the soil surface in tropical forests. Within 4 to 18 days, the infected mosquitoes become capable of transmitting the infection and remain infective throughout their lifespan (70–116 days).

The virus is highly sensitive to high temperatures. It persists for three months in 50 per cent glycerin on ice, for over a year when frozen, and for up to 12 years in a dried state. It is sensitive to heat and is destroyed at 55-65 degrees Celsius within 10 minutes. It is rapidly killed by exposure to 0.5 per cent formalin and other disinfectants.

Yellow fever occurs in two forms. Urban yellow fever is transmitted from an infected person to a healthy one by Aëdes aegypti, Aëdes simpsoni, Aëdes calopus, Aëdes africons, and other mosquito species. The Aëdes aegypti, however, is the primary vector. Jungle yellow fever is transmitted to humans from wild animals and rodents through mosquito bites and primarily prevails among people working in forests.

The virus penetrates the reticular cells of the lymph nodes before spreading to the blood, liver, spleen and bone marrow. It remains in human blood for up to five days before localising in the lymph nodes. The virus causes necrosis and fatty degeneration of cells in the liver, kidneys, and spleen, leading to haemorrhages in internal organs such as the stomach, pleura, lungs, and intestinal mucosa. The main clinical symptoms of yellow fever include jaundice, haemorrhages, and intensive albuminuria.

The incubation period lasts three to six days. The disease is characterised by a sudden onset and occurs in cycles. The first (infectious) phase is manifested by a headache, pain at the back of the head and in the muscles of the back, and flushed skin, conjunctiva, and mucous membranes. Nausea, anorexia, thirst, and polyuria are common at the onset of the disease. In the second phase (the period of remission), by the end of the third day, there is a drop in temperature, sometimes below normal, and a relative sense of well-being sets in. In mild cases, the disease terminates in recovery during this phase. The third phase is characterised by intoxication, the disappearance of the virus from the peripheral blood, massive gastrointestinal haemorrhages, anuria (lack of urine production), and an increase in the amount of protein and hyaline and granular casts in the urine. In fulminant forms of the disease, hepatic or uraemic coma develops, often leading to death.

With regard to the degree of severity, asymptomatic, very mild, benign, malignant, and fulminant, forms of the disease are distinguished. Complications include abscesses, parotitis, pneumonia, multiple skin lesions, sometimes gangrene, and myocarditis. Immunity is associated with the presence of virus-neutralising antibodies in the blood, which form on the fifth day of the disease. These antibodies are produced over a period of several weeks. Over time, the antibody titre gradually diminishes and persists at a low level for many years following recovery.

The diagnosis of yellow fever is based on clinical, epidemiological, and laboratory data. Laboratory examination comprises the isolation of the virus from the patient, detection of specific antibodies in the blood of patients and convalescents, and a histological study of the liver in fatal cases. The virus is isolated by intracerebral inoculation of albino mice with the patient’s blood collected in the first five days of fever. If the virus is present in the blood, symptoms of encephalitis will develop in the animals within seven to twenty days following inoculation. The presence of virus-neutralising antibodies is detected by performing the neutralisation test, as well as the haemagglutination-inhibition and complement fixation reactions.

No specific therapy is known for the treatment of this fever. Bed rest, thorough nursing care, and symptomatic treatment (administration of glucose, calcium gluconate, alkaline solutions, vitamins, purgatives, and cardiac medications, as well as transfusion of blood and plasma) are recommended.

The general measures of control include the extermination of mosquitoes, protection from them, and disinsection of all transport arriving from endemic areas. Active immunisation with the live vaccine, however, has proved to be the most effective. Two vaccinal strains are used in vaccination: the American and the French. Due to the widespread use of the French vaccine, the disease has been almost completely eliminated in Equatorial Africa. However, despite the availability of a highly effective vaccine, there are still cases of yellow fever in South America and West Africa. The incidence of the disease is increasing. Between 1962 and 1969, five-lakh people contracted the disease, and 30,000 of them died. Europe, Asia, and Australia remain free from yellow fever.

The author is an associate professor (retd.) and former head of the department of botany at Ananda Mohan College.