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What is The Pathophysiology of Dengue Fever?


Breeding around dwellings in small amounts of stagnant water found in old tires or other small containers discarded by humans. Female Aedes mosquitoes are daytime feeders. They inflict an innocuous bite and are easily disturbed during a blood meal, causing them to move on to finish a meal on another individual, making them efficient vectors. Entire families who develop infection within a 24- to 36-hour period, presumably from the bites of a single infected vector, is not unusual.
Humans serve as the primary reservoir for dengue; however, certain nonhuman primates in Africa and Asia also serve as hosts. Mosquitoes acquire the virus when they feed on a carrier of the virus. The mosquito can transmit dengue if it immediately bites another host. In addition, transmission occurs after 8-12 days of viral replication in the mosquito’s salivary glands (extrinsic incubation period). The mosquito remains infected for the remainder of its 15- to 65-day lifespan. Vertical transmission of dengue virus in mosquitoes has been documented. The eggs of Aedes mosquitoes withstand long periods of desiccation, reportedly as long as 1 year, but are killed by temperatures of less than 10°C. Once inoculated into a human host, dengue has an incubation period of 3-14 days (average 4-7 d). Following incubation, a 5- to 7-day acute febrile illness ensues. Recovery is usually complete by 7-10 days. DHF or DSS usually develops around the third to seventh day of illness, approximately at the time of defervescence. The major pathophysiological abnormalities that occur inDHF and DSS are plasma leakage and bleeding. Plasma leakage is caused by increased capillary permeability and may be manifested by hemo- concentration, as well as pleural effusion and ascites. Bleeding is caused by capillary fragility and thrombocytopenia and may present various ways, ranging from political skin hemorrhages to life-threatening gastrointestinal bleeding.
Most patients who develop DHF or DSS have had prior infection with one or more dengue serotypes. In individuals with low levels of neutralizing antibodies, no neutralizing antibodies to one dengue serotype, when bound by macrophage and monocyte Fc receptors, have been proposed to result in increased viral entry and replication, and increased cytokine production and complement activation. This phenomenon is called antibody-dependent enhancement. In addition, certain dengue strains, particularly those of DEN-2, have been proposed to be more virulent, in part because more epidemics of DHF have been associated with DEN-2 than with the other stereotypes.

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