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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