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Understanding Dengue Pathophysiology

Dengue fever is caused by a virus transmitted through mosquito bites. During infection, the virus enters the bloodstream and infects cells, triggering an immune response and release of cytokines. For some patients, a second infection with a different virus strain can cause more severe dengue hemorrhagic fever or dengue shock syndrome due to antibody-dependent enhancement. This occurs when non-neutralizing antibodies from the first infection facilitate greater virus replication. The increased viral load triggers a massive 'cytokine storm' and systemic inflammatory response. Platelet-activating factor may also be involved, causing effects like vascular leakage, hemoconcentration, and hypotension seen in severe cases. Treatment for dengue fever and its severe

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122 views3 pages

Understanding Dengue Pathophysiology

Dengue fever is caused by a virus transmitted through mosquito bites. During infection, the virus enters the bloodstream and infects cells, triggering an immune response and release of cytokines. For some patients, a second infection with a different virus strain can cause more severe dengue hemorrhagic fever or dengue shock syndrome due to antibody-dependent enhancement. This occurs when non-neutralizing antibodies from the first infection facilitate greater virus replication. The increased viral load triggers a massive 'cytokine storm' and systemic inflammatory response. Platelet-activating factor may also be involved, causing effects like vascular leakage, hemoconcentration, and hypotension seen in severe cases. Treatment for dengue fever and its severe

Uploaded by

gizelle
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOCX, PDF, TXT or read online on Scribd

PATHOPHYSIOLOGY

Predisposing Precipitating
-Geographical area – tropical -Environmental conditions (open spaces
islands in the Pacific (Philippines) with water pots, and plants)
and Asia -Mosquito carrying dengue virus

Bite of a virus carrying aedes mosquito Redness & itchiness


in the area
Mosquito injects fluid to victim’s skin

Virus enters blood stream

Infects cell and generate cellular response

Initiates immune response (stimulates


release of cytokines)

Cytokines destroys cell membrane and cell wall


(viral antigens found in monocytes)

Dengue infection

Fever hemorrhagic hepatomegaly thrombocytopenia


anorexia manifestations
Increased vascular
permeability

Positive
tourniquet test
A B C D
A B C D
Hemoconcentration

hypoproteinemia

Pleural effusion Leakage of plasma Bleeding

(Dehydration)

hypovolemia

shock hypotension

(GI bleeding) Anoxia (Acidosis)

Intravascular
clot
DEATH
Coagulation
defect

The pathogenesis of dengue haemorrhagic fever and dengue shock syndrome remain unclear. The
requirement for a second infection with a different serotype of the virus suggested that antibody-
dependent enhancement is involved in these more serious conditions. After an initial period of protection,
antibodies from the primary infection can cross-react with other dengue virus serotypes but have waned to
non-neutralizing levels. These non-neutralizing antibodies could then mediate an increased uptake of
virus into monocyte/macrophage cells via Fc receptors, leading to increased virus replication and immune
activation including massive cytokine release (known as a “cytokine storm”). An alternative theory
involves reactivation of cross-reactive memory T cells specific for the previous rather than the current
virus strain, resulting in delayed virus clearance and/or increased cytokine secretion along with increased
apoptosis of both infected and uninfected bystander cells (known as “original antigenic sin”).

Platelet-activating factor (PAF) is a potent and versatile mediator of inflammation that is produced by


numerous cell types and tissues, and particularly by leukocytes. PAF acts on a single receptor (PAFR)
that may be expressed on the plasma membrane or the outer leaflet of the nucleus of various cell types,
but especially leukocytes, platelets, and endothelial cells. The endogenous release of PAF may account
for several of the manifestations of acute inflammation. The administration of PAF to rodents or humans
reproduces many features of the systemic inflammatory response syndrome, including hypotension,
increased vascular permeability, hemoconcentration, cytokine release, and shock.

Dengue fever and dengue shock or hemorrhagic syndromes (DSS) are mosquito-borne diseases caused by
1 of 4 serotypes of Dengue virus (DEN 1–4). Treatment of dengue fever and of the severe forms of
dengue infection is supportive only.

DSS is defined as fever with hemorrhage manifestations, thrombocytopenia, and hemoconcentration or


other signs of plasma leakage. Severe dengue infection is characterized by increased vascular
permeability, altered number of leucocytes, increased hematocrit, thrombocytopenia, and varying degree
of hemorrhage. The extensive plasma leakage in various serous cavities of the body may result in
profound and intractable shock. Hemorrhage, when it occurs, may contribute to hypotension.

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