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I. DEFINITION

Dengue fever (DF) is a worldwide infection caused by 4 related RNA viruses of the genus Flavivirus, dengue viruses (DENV) DENV-1, DENV-2, DENV-3, and DENV-4. DENV is primarily transmitted to humans through the bite of infected Aedes aegypti (and less commonly Aedes albopictus or Aedes polynesiensis) mosquitoes. DENV causes asymptomatic infection, DF, or a severe syndrome (dengue hemorrhagic fever [DHF]/dengue shock syndrome [DSS]). The latter is characterized by systemic capillary leakage, thrombocytopenia, and hypovolemic shock.

II. INCIDENCE

Dengue is a major public health problem in the tropics and subtropics; an estimated 50 to 100 million dengue cases occur annually in more than 100 countries, and 40% of the world’s population lives in areas with DENV transmission. In the United States, dengue is endemic in Puerto Rico, the Virgin Islands, and American Samoa. Additionally, limited outbreaks with local DENV transmission have occurred in Texas, Hawaii, and Florida in the past decade, but no neonatal cases have been reported from the United States. Millions of US travelers, including children, are at risk. Neonatal dengue has been described in case reports and case series from outside the United States; therefore, its true incidence worldwide is unknown.

III. PATHOPHYSIOLOGY

Viremia is usually detected about 6 to 18 hours before the onset of symptoms and ends as the fever resolves. Both innate and adaptive immune responses seem to play a role in the clearance of infection. Infection with 1 of the 4 DENVs (primary infection) provides long-lasting immunity to infection with a virus of the same serotype; however, immunity to the other dengue serotypes is transient. Individuals can subsequently be infected with another dengue serotype (secondary infection), often with more severe manifestations. DHF can develop with any of the 4 DENVs, but the risk is highest with DENV-2. DHF can usually be distinguished from DF as it progresses through 3 predictable pathophysiologic phases:

  1. Febrile phase: Viremia-driven high fevers.

  2. Critical/plasma leak phase: Sudden onset of varying degrees of plasma leak into the pleural and abdominal cavities. This phase probably occurs due to endothelial cell dysfunction rather than injury.

  3. Convalescence or reabsorption phase: Sudden arrest of plasma leak with concomitant reabsorption of extravasated plasma and fluids.

Neonates can be infected through mosquito bites but also as a vertical infection from the mother. The highest risk period is when the mother becomes acutely ill with dengue at or near the time of delivery. It has been hypothesized that there is an insufficient level of protective maternal antibodies (immunoglobulin [Ig] G) transferred to the fetus, and therefore, the newborn can manifest serious disease. Endothelial damage and plasma leakage may enable the virus an easy access across the placental barrier. Dengue virus has been identified in the breast milk of viremic mothers, and postnatal transmission through breast feeding has been documented, albeit this is rare. Bloodborne transmission is possible ...

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