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Infectious Disease and Microbiology – Dengue
Dengue is a mosquito-borne viral illness that causes a severe flu-like disease and, in some cases, progresses to life-threatening dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS), with a fatality rate of approximately 1–5% in severe cases. It is caused by the dengue virus, a single-stranded RNA virus of the Flaviviridae family, with four antigenically distinct serotypes (types 1–4). Humans and nonhuman primates serve as reservoirs. Transmission occurs through the bite of infected Aedes aegypti and Aedes albopictus, which are predominantly day-biting mosquitoes.
Globally, about 2.5 billion people—nearly two-fifths of the world’s population—are at risk of infection. An estimated 50–100 million infections occur annually, including approximately 500,000 cases of DHF and hundreds of thousands of deaths worldwide. Transmission increases during the rainy season due to mosquito breeding in stagnant water. Dengue is endemic in around 100 countries across Asia, the Pacific, the Americas, Africa, and the Caribbean, primarily in tropical and subtropical urban and suburban areas.
The principal risk factor is travel to or residence in endemic regions. No genetic predisposition has been clearly identified. Prevention focuses on avoiding mosquito bites and vector control. Measures include using insect repellents containing at least 30% DEET, wearing long-sleeved clothing (preferably treated with permethrin), and eliminating mosquito breeding sites such as stagnant water. Indoor insecticide use and larvicidal agents may reduce mosquito populations. Bed nets are of limited value because Aedes mosquitoes bite during the daytime.
After inoculation, the incubation period ranges from 3 to 14 days, most commonly 4–7 days. The virus initially replicates in dendritic cells and then spreads to reticuloendothelial cells, hepatocytes, and endothelial cells. Immune mediators contribute to the acute febrile illness, which typically lasts 5–7 days, with full recovery within 7–10 days in uncomplicated cases. Prior infection with a different serotype increases the risk of DHF and DSS due to immune-mediated mechanisms.
DHF and DSS usually develop between days 3 and 7 of illness, often at the end of the febrile phase. Increased capillary permeability leads to plasma leakage, hemoconcentration, pleural effusions, and ascites. Thrombocytopenia, capillary fragility, and disseminated intravascular coagulation (DIC) can result in hemorrhage ranging from petechiae to life-threatening gastrointestinal bleeding. Liver involvement may cause hepatitis and coagulopathy, which can be fatal in severe cases. Mother-to-child transmission has been documented.
Clinically, patients present with fever, headache, chills, myalgias, bone pain, rash, nausea, vomiting, abdominal pain, and anorexia. Cutaneous hyperesthesia and changes in taste may occur. Hemorrhagic manifestations include bruising, epistaxis, gum bleeding, menorrhagia, and gastrointestinal bleeding. A careful travel history is essential.
On physical examination, fever is common. Rash may appear in two phases: an initial generalized blanching macular rash followed by a morbilliform maculopapular rash that typically spares the palms and soles. Conjunctival and pharyngeal injection are frequent findings. Signs of shock—tachycardia, hypotension, and delayed capillary refill—indicate severe disease. Hepatomegaly, lymphadenopathy, mucosal bleeding, and altered mental status (suggesting encephalopathy or intracranial hemorrhage) may also be present.
Laboratory evaluation often reveals leukopenia, lymphopenia, elevated hematocrit (reflecting hemoconcentration), and thrombocytopenia. Liver transaminases are commonly elevated, and albumin may be low. Electrolyte disturbances such as hyponatremia and metabolic acidosis may occur. Coagulation studies may show prolonged PT and APTT, low fibrinogen, and elevated fibrin degradation products in DIC. Serologic testing (ELISA for IgM and IgG) is commonly used for diagnosis. Imaging may demonstrate pleural or pericardial effusions and ascites. Head CT is indicated in patients with altered consciousness.
The differential diagnosis includes malaria, yellow fever, rickettsial infections, leptospirosis, typhoid fever, viral hepatitis, meningitis, bacterial sepsis, and other viral illnesses such as influenza or chikungunya.
There is no specific antiviral treatment for dengue, DHF, or DSS. Management is supportive. Aspirin and nonsteroidal anti-inflammatory drugs should be avoided due to bleeding risk. Adequate analgesia, antipyretics (such as acetaminophen), and careful fluid management are essential. In severe cases, aggressive fluid resuscitation using isotonic crystalloids or colloids is required to maintain adequate blood pressure and organ perfusion. Advanced life support protocols should be followed in patients with shock. Blood products may be necessary in cases of severe hemorrhage. Close monitoring of fluid balance, urine output, electrolytes, and coagulation status is critical.
Hospital admission is indicated for patients with hemodynamic instability, DHF, DSS, or significant bleeding. Intensive care is required for hypotension, DIC, or organ failure. Discharge is appropriate once the patient is hemodynamically stable and has recovered clinically.
Prognosis is generally excellent for uncomplicated dengue fever, with most patients recovering fully. Those who survive the critical phase of DHF or DSS usually recover without long-term sequelae. However, complications may include neurological manifestations (encephalopathy, seizures, Guillain–Barré syndrome, transverse myelitis), myocarditis, and liver failure. Cases should be reported to public health authorities, and patients should be informed that infection with a different serotype in the future increases the risk of severe disease.
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