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Yellow fever: causes and pathogenesis
Last reviewed: 23.04.2024
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Causes of yellow fever
The cause of yellow fever is RNA-containing virus Viceronhilus tropicus of Flavivirus family Flaviviridae, belonging to the group of arboviruses. The capsid has a spherical shape; dimensions of about 40 nm. In the environment, it is not very stable: it is rapidly inactivated at low pH values, by exposure to high temperatures and conventional disinfectants. Long lasts at low temperatures (in liquid nitrogen up to 12 years). An antigenic relationship with the viruses of dengue and Japanese encephalitis has been established. The yellow fever virus agglutinates the erythrocytes of geese, causes a cytopathic effect in Hela, KB, Detroit-6 cells.
The yellow fever virus is cultivated on chick embryos and in the cultures of cells of warm-blooded animals. It is also possible to use the cells of some arthropods, in particular Aedes aegypti mosquitoes .
It is shown that, with prolonged passages in cell culture and chick embryos, the pathogenicity of the virus for monkeys is significantly reduced, which is used to prepare vaccines.
[Pathogenesis of yellow fever
Infection with yellow fever occurs when bitten by an infected mosquito. When infected, the virus enters the regional lymph nodes through lymphatic vessels, in which its replication takes place during the incubation period. After a few days, it enters the bloodstream and spreads throughout the body. The duration of the viremia period is 3-6 days. At this time the virus gets mainly into the endothelium of the vessels, the liver, kidneys, spleen, bone and brain. When the disease develops, a pronounced tropism of the pathogen to the circulatory system of these organs is revealed. As a result, there is an increased permeability of blood vessels, especially capillaries, precapillaries and venules. Dystrophy and necrosis of hepatocytes, defeat of the glomerular and tubular kidney systems develop. The development of thrombohemorrhagic syndrome is caused both by vascular damage and microcirculatory disorders, and by a violation of the synthesis in the liver of plasma factors of hemostasis.
Skin covers of deceased people are usually painted in yellow, often crimson due to venous hyperemia. On the skin and mucous membranes reveal a hemorrhagic rash. Characteristic are degenerative changes in the liver, kidneys, and heart. The liver and kidneys are significantly enlarged, with small-point hemorrhages. Fatty dystrophy, foci of necrosis (in severe cases of subtotal). Identify the characteristic changes in the liver, while detecting the body of Kaunsilmen. In addition to changes in the cytoplasm, in the nuclei of the liver cells, acidophilic inclusions (Torres calf) are found. They arise from the multiplication of the virus in the cells and changes in their nuclei. Despite significant changes in the liver, after recovery, restoration of its functions is observed without the development of cirrhosis.
In a number of cases, the cause of death is renal damage, characterized by swelling and fatty degeneration of the renal tubules right up to necrosis. In the tubules accumulate colloid masses, blood cylinders. Changes in the glomeruli of the kidneys are often insignificant. The spleen is full of blood, the reticular cells of the follicle are hyperplastic. Degenerative changes occur in the heart muscle; In the pericardium, hemorrhages are detected. Yellow fever is characterized by multiple hemorrhages in the stomach, intestine, lungs, pleura, and perivascular infiltrates in the brain.