Synopsis
Dengue fever, also known as breakbone fever, is caused by an RNA-containing flavivirus transmitted to humans by day-biting mosquitoes, notably Aedes aegypti. It is endemic in tropical areas of the Caribbean, the Pacific Islands, Central America, South America, Southeast Asia, the Middle East, and Africa. Limited autochthonous outbreaks have occurred in Europe. Worldwide, there are estimated to be 400 million dengue virus infections each year, with 100 million cases of illness and 40 000 deaths. Approximately 4 billion people live in areas with a risk of dengue.
In 2024, there has been a surge of dengue virus infection in the Americas region, including in Brazil, Argentina, and Peru. In March 2024, Puerto Rico declared an outbreak. Local transmission has been reported in the US Virgin Islands.
Local spread has also occurred occasionally in the United States (in 2015-2016 in Hawaii; in 2023-2024 primarily in Florida, also in California). Most cases in the United States are travel related, and in 2024, there have been a higher-than-expected number of dengue cases identified among US travelers. Health care providers should be aware of an increased risk of dengue virus infections in the United States.
Travelers can present once home due to a 2- to 7-day incubation period. Clinical manifestations vary and include asymptomatic infection (75% of cases), mild dengue, classic dengue, and dengue hemorrhagic fever.
In classic dengue fever, there is a biphasic pattern to symptoms. During the first phase, there is an abrupt onset of fever for 2-5 days, malaise, chills, severe headache, myalgias, and retro-orbital and lumbosacral pain. The fever may climb as high as 41°C (105.8°F) but is not associated with an increased pulse. There can be a faint, transient diffuse morbilliform macular rash during the first few days.
During the next several days, there is defervescence despite the onset of nausea, vomiting, possible cough, rhinitis, and sore throat. Leukopenia, thrombocytopenia, and hemorrhagic manifestations are possible.
In young children with dengue fever, nonspecific symptoms such as refusing to accept oral fluids and foods, restlessness, abdominal pain, skin mottling, cold sweat, and low urine output may present early in the disease course.
Incidence is associated with increased urbanization in endemic areas. There is increased severity and 10%-30% mortality in children.
In October 2013, discovery of a new dengue virus serotype, dengue 5, was announced; it is thought to be phylogenetically distinct from the other 4 types.
Transmission of dengue virus via allogeneic blood cell transplantation has been documented, and patients with sickle cell disease or trait may be at increased risk of death from dengue.
The hemorrhagic form, dengue hemorrhagic fever (DHF), is believed to be more likely to occur during a second infection with the dengue virus, especially if the second infection involves a different serotype. DHF affects approximately 500 000 people annually and is most common in children younger than 15 years.
DHF typically begins with the abrupt onset of high fever (40°C-41°C [104°F-105.8°F]), facial flushing, circumoral cyanosis, and headache. Sore throat, anorexia, weakness, abdominal pain, nausea, and vomiting are common. This febrile phase lasts for 2-7 days and may be accompanied by a maculopapular rash, similar to dengue fever. DHF can be distinguished from dengue fever by accompanied petechiae and nonpalpable purpura present on the extremities, trunk, and face, as well as potential bleeding from the nose, gums, and gastrointestinal (GI) tract. Moderate cases will resolve after the fever subsides. However, after a few febrile days, the critical stage of plasma leakage may occur following a rapid drop in temperature. Circulatory failure accompanied by diaphoresis with cool extremities and shock may herald dengue shock syndrome (DSS). Death rates of up to 20% are reported and usually occur within 24 hours of DSS.
Look For:
Initially, look for transient facial flushing and blanchable erythematous mottling, which may occur before or during the first 1-2 days of fever. Then, 2-3 days after defervescence, look for a pruritic morbilliform rash that develops first on the trunk and then extends to the limbs and face. This can be a petechial / maculopapular eruption with islands of normal skin (“small islands in a sea of red”) and sometimes a scarlatiniform eruption that spares the palms and soles. The rash may be accentuated on the extremities. The rash can heal with desquamation.
In DHF, petechiae and nonpalpable purpura mostly on the extremities, axillae, trunk, and face can usually be seen. Bleeding from the nose, gums, and GI tract may be noted. A confluent petechial eruption with scattered pale macules of normal skin can be seen in the convalescent phase on the lower extremities. Hepatomegaly may be present.
Impact of skin color on clinical presentation: Erythema may be subtle in darker skin colors, or it may appear violaceous. Applying brief gentle pressure with a fingertip or microscope slide to blanch involved skin may accentuate subtle erythema as the pressure is withdrawn. Petechiae and purpura may also appear violaceous or brown and may be more difficult to discern. As these lesions may not be palpable, a careful and thorough skin examination under bright light would be beneficial in patients with darker skin colors.
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