Dengue shock syndrome occurs due to -

Macrophage/monocyte infection is central to the pathogenesis of dengue fever and to the origin of DHF/DSS. Previous infection with a heterologous dengue-virus serotype may result in the production of nonprotective antiviral antibodies that neveheless bind to the virion's surface and through interaction with the Fc receptor focus secondary dengue viruses on the target cell, the result being enhanced infection. The host is also primed for a secondary antibody response when viral antigens are released and immune complexes lead to activation of the classic complement pathway, with consequent phlogistic effects. Cross-reactivity at the T cell level results in the release of physiologically active cytokines, including interferon g and tumor necrosis factor a. The induction of vascular permeability and shock depends on multiple factors, Dengue HF is identified by the detection of bleeding tendencies (tourniquet test, petechiae) or ove bleeding in the absence of underlying causes such as preexisting lesions. Dengue shock syndrome, usually accompanied by hemorrhagic signs, is much more serious and results from increased vascular permeability leading to shock. In mild DHF/DSS, restlessness, lethargy, thrombocytopenia (<100,000/mL), and hemoconcentration are detected 2-5 days after the onset of typical dengue fever, usually at the time of defervescence. The maculopapular rash that often develops in dengue fever may also appear in DHF/DSS. In more severe cases, frank shock is apparent, with low pulse pressure, cyanosis, hepatomegaly, pleural effusions, ascites, and in some cases severe ecchymoses and gastrointestinal bleeding. The period of shock lasts only 1 or 2 days, and most patients respond promptly to close monitoring, oxygen administration, and infusion of crystalloid or--in severe cases--colloid. ref:harrison&;s principles of internal medicine,ed 18,pg no 1913