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Overview and Recommendations
Background
- •Recognize dengue as a systemic viral infection caused by four distinct serotypes (DENV-1, 2, 3, and 4), where DENV-2 is frequently associated with the highest virulence and risk of severe outbreaks.
- •Understand the transmission cycle involving female Aedes mosquitoes, which acquire the virus from viremic humans and can also transmit the virus vertically to their larvae, allowing environmental persistence during dry seasons.
- •Identify the primary risk factor for severe disease as secondary infection with a different serotype; this triggers antibody-dependent enhancement (ADE), where non-neutralizing antibodies facilitate viral entry into macrophages, causing a massive cytokine release.
- •Note the expanding geographic range of the vectors, with Aedes albopictus facilitating transmission in temperate regions like Southern Europe, while Aedes aegypti remains the dominant urban vector in tropical hyperendemic zones.
- •Consider the impact of comorbidities such as , , and , which significantly increase the risk of symptomatic presentation and progression to severe organ involvement.
Evaluation
- •Suspect dengue in any patient with acute high-grade fever (≥38°C) who has lived in or traveled to an endemic region (e.g., Southeast Asia, Puerto Rico, Mexico) within the last 14 days.
- •Ask about the classic triad of "breakbone fever": severe frontal headache, retro-orbital pain, and intense myalgias or arthralgias, often following a biphasic or "saddleback" fever pattern.
- •Examine the skin for the pathognomonic "isles of white in a sea of red" rash—a confluent erythematous exanthema with small circular areas of skin sparing—and check for petechiae on the extremities.
- •Perform the Tourniquet Test (TT) to assess capillary fragility: inflate a blood pressure cuff to the mean arterial pressure [(Systolic + Diastolic) / 2] for 5 minutes; a count of ≥10–20 petechiae per square inch on the ventral forearm is positive.
- •Monitor for "Warning Signs" during the transition from the febrile to the critical phase (typically days 3–7), including abdominal pain or tenderness, persistent vomiting, mucosal bleeding, and lethargy.
- •Order a (CBC) daily to track the characteristic progression of leukopenia (WBC <5,000 cells/mm³), followed by a rapid drop in platelet count and a rising hematocrit indicating plasma leakage.
- •Obtain NS1 antigen and/or RT-PCR for definitive diagnosis if the patient presents within the first 5 days of symptom onset (the viremic phase).
- •Order IgM and IgG serology if the patient presents after day 5 of illness; note that a four-fold rise in IgG titers in paired sera is diagnostic of recent infection.
- •Utilize bedside ultrasonography to detect subclinical plasma leakage, specifically looking for gallbladder wall thickening, , and pleural effusions (often appearing first on the right side).
- •Rule out co-infections such as , , and , particularly in regions where these pathogens overlap, as co-infection can exacerbate anemia and organ dysfunction.
- •Assess for neurological complications, including cerebellar , , or signs of if the patient exhibits motor weakness or altered consciousness.
- •Monitor respiratory mechanics closely if plasma leakage is suspected; an FVC < 15 mL/kg should prompt consideration for mechanical ventilation due to massive effusions or pulmonary edema.
Management
- •Administer Acetaminophen (Paracetamol) for fever and pain control, maintaining a maximum dose of 4g/day in adults; strictly avoid Aspirin and NSAIDs (e.g., Ibuprofen) due to the risk of gastritis and platelet dysfunction.
- •Encourage aggressive oral hydration in the ambulatory setting, aiming for approximately 2 liters of fluid per day (e.g., oral rehydration salts, fruit juices) to reduce the risk of hospitalization.
- •Initiate IV fluid therapy with isotonic crystalloids (e.g., Lactated Ringer's or Normal Saline) at 5–7 mL/kg/hour for patients with warning signs who cannot maintain oral intake.
- •Manage (DSS) with an immediate IV bolus of isotonic crystalloid at 10–20 mL/kg over 15–30 minutes, followed by reassessment of hemodynamic status.
- •Consider colloid boluses (e.g., 5% albumin) in patients with refractory shock or those with massive where crystalloids may worsen extravascular fluid accumulation.
- •Monitor hematocrit every 6–12 hours during the critical phase; a rising hematocrit despite fluid resuscitation suggests ongoing plasma leakage and requires an increase in fluid rate.
- •Avoid prophylactic platelet transfusions even in cases of severe thrombocytopenia; reserve transfusions for patients with clinically significant, life-threatening hemorrhage.
- •Delay elective surgeries or delivery in pregnant patients until the critical phase has passed to minimize the risk of massive maternal hemorrhage.
- •Administer IVIG 2 g/kg as a single infusion in pediatric patients who develop -like features (e.g., coronary artery aneurysms) post-dengue.
- •Refer patients to intensive care if they exhibit severe plasma leakage leading to respiratory distress, severe organ impairment (AST/ALT ≥1000 U/L), or impaired consciousness.
- •Monitor for fluid overload during the recovery phase; as third-spaced fluid is reabsorbed, decrease IV fluids and watch for signs of pulmonary edema or heart failure.
- •Discharge patients only when they have been afebrile for 48 hours without antipyretics, show a rising platelet count, and have stable hematocrit levels with improving clinical symptoms.
- •Counsel patients on the use of the Dengvaxia vaccine only if they have laboratory-confirmed prior dengue infection, as it may increase the risk of severe disease in seronegative individuals.
Board Review — High Yield
- •Breakbone fever — Common name for dengue due to severe myalgia and arthralgia.
- •Isles of white in a sea of red — Classic description of the confluent erythematous rash with skin sparing.
- •Antibody-Dependent Enhancement (ADE) — Mechanism where secondary infection with a different serotype leads to more severe disease.
- •Tourniquet Test — Bedside marker for capillary fragility; positive if ≥10-20 petechiae per square inch.
- •Critical Phase — Occurs at the time of defervescence (fever drop), which is when plasma leakage and shock are most likely.
- •NS1 Antigen — Viral protein detectable in the blood from day 1 of symptoms, used for early rapid diagnosis.
- •Hematocrit/Platelet Divergence — A rising hematocrit with a falling platelet count is a hallmark of the critical phase.
- •Dengvaxia — Vaccine only recommended for those with evidence of prior dengue infection to prevent ADE-like reactions.
Deep Dive — Evidence Details
Etiology and Triggering Factors
- ▸Dengue is caused by four DENV serotypes transmitted primarily by Aedes mosquitoes. [105][174]
- ▸Serotype and genotype turnover, secondary infection, prior vaccination, and population immunity shape outbreak risk and disease expression. [107][108][109][111]
- ▸Imported infections can initiate local outbreaks when competent vectors and susceptible populations are present. [103]
- ▸Climate variability, vector expansion, globalization, El Niño, and altered seasonality can increase or prolong transmission. [112][173][175][172]
- ▸DENV commonly co-circulates with CHIKV and ZIKV, creating shared-vector transmission and diagnostic challenges. [105][173]
Etiologic agent and transmission
Dengue is caused by dengue virus (DENV), an enveloped flavivirus comprising four antigenically distinct serotypes—DENV-1, DENV-2, DENV-3, and DENV-4—that are transmitted primarily by Aedes mosquitoes. [105][174]D The principal epidemiologic mechanism is human–mosquito–human transmission; detection of acute DENV infection together with Aedes aegypti surveillance has documented this vector–pathogen association in both endemic and highland settings. [115] DENV circulation is frequently accompanied by other Aedes-borne arboviruses, especially chikungunya virus (CHIKV) and Zika virus, which share vectors and may produce overlapping illness or dual infection. [105][173]D
Serotype circulation and population immunity
Outbreak risk is influenced by which serotypes circulate and by the level and distribution of pre-existing population immunity. [112]C[172]D Sequential outbreaks can progressively reshape immunity, increasing the proportion of secondary infections and complicating interpretation of clinical and laboratory findings. [109] Antibody responses may differ according to the infecting serotype and genotype; in Myanmar, DENV-3 genotype III predominated before 2017, whereas genotype I emerged thereafter, with evidence of altered neutralization and in-vitro antibody-dependent enhancement (ADE) patterns in previously collected pediatric sera. [107] These findings support genotype-specific immune interactions, but they do not establish that ADE alone determines severe disease in individual patients. [107]
DENV serotype predominance changes geographically and over time. [106][112]C[172]D In Mexico, DENV-2 predominated until 2022, DENV-1 peaked in 2021, and DENV-3 increased subsequently; national surveillance also documented a nearly fivefold rise in reported cases from 2020 to 2024 and more than 123,000 confirmed infections with 426 deaths in 2024. [172]D In Thailand, DENV-4 re-emerged amid cyclical shifts in serotype predominance and continued co-circulation with other serotypes during 2018–2024. [176]D Molecular and serological surveillance in Saudi Arabia likewise indicates long-term variation in circulating serotypes and viral lineages over approximately three decades. [106] In China, imported infections have repeatedly preceded local outbreaks, although the country had not established stable nationwide local transmission through the period assessed. [103]
A first infection generally establishes serotype-specific immune experience, whereas subsequent infection with another serotype occurs in a population whose antibody profile has been altered by prior infection or vaccination. [107][109][108] Vaccination can further modify population immunity; long-term follow-up of CYD-TDV recipients in Indonesia assessed neutralizing antibodies against all four serotypes 10 years after vaccination, illustrating the importance of durability and serotype-specific protection when evaluating future transmission risk. [111] Because a validated correlate of protection remains unavailable, vaccine safety and efficacy—particularly in DENV-naive people and across individual serotypes—remain dependent on complex field and immunogenicity assessments. [108]
Environmental, climatic, and seasonal drivers
Transmission is promoted by the presence and abundance of competent Aedes vectors, suitable environmental conditions, and human exposure. [115][173]D Vector expansion, globalization, and climate change are recognized drivers of the growing global arboviral threat and may increase opportunities for DENV introduction and spread. [173]D Climate variability can modify transmission intensity and season length; modelling in Mexico specifically evaluated year-to-year changes in force of infection and the possibility that changing climate conditions may enhance future transmission. [112]C Mexico experienced sustained transmission extending into unusual winter months from late 2023, demonstrating that seasonal risk is not fixed. [172]D A strong El Niño episode was identified as a preparedness concern for Latin America because it coincided with limited DENV-3 immunity and was expected to narrow the window for preventing transmission and health-system overload. [175]D
Seasonal and geographic heterogeneity is also evident elsewhere. [103][170] Chinese outbreaks showed distinct monthly and regional distributions, while Caribbean surveillance from 2018–2024 evaluated temporal trends and seasonality in laboratory-tested arboviral infections. [103][170] In Saudi Arabia, dengue was documented in highland governorates of Jazan alongside A. aegypti surveillance, indicating that elevated or previously less-characterized areas may still support transmission. [115] Population-level serologic evidence from Guinea and multi-region surveillance in Burkina Faso confirms that DENV exposure and acute infection are distributed across multiple geographic settings rather than being confined to a single urban focus. [169][168]
Human movement, co-circulating infections, and outbreak amplification
Imported infections are an important trigger for local transmission where competent vectors and susceptible people are present. [103] International travel and population movement can introduce DENV into receptive areas, while recurrent outbreaks can alter local immunity and change the serotypes or genotypes encountered in subsequent waves. [103][109] In Peru, recurrent outbreaks were associated with marked variability in clinical presentation, consistent with changing epidemiologic and immune contexts, although clinical heterogeneity alone does not identify a single causal trigger. [104]
Co-circulation with CHIKV, ZIKV, and other arboviruses can amplify diagnostic uncertainty and obscure recognition of DENV outbreaks. [105][173]D DENV–CHIKV dual positivity or co-infection has been reported across clinical, surveillance, and community populations, and the shared vector ecology creates opportunities for simultaneous transmission. [105] COVID-19-era public-health interventions may have affected dengue detection, transmission, and serotype dynamics in Thailand, including the observed DENV-4 resurgence. [176]D Finally, alternative or concurrent infections must be considered in atypical fatal cases: one traveler returning from Saudi Arabia had low-level DENV RNA and positive NS1 antigen but also extremely high-titer disseminated avian orthoavulavirus 1 infection, showing that DENV detection may coexist with another severe pathogen and should not automatically be assumed to explain the entire clinical syndrome. [171]C
| Factor | Relevance to dengue transmission or outbreaks | Evidence |
|---|---|---|
| DENV serotypes and genotypes | Serotype predominance and genotype emergence change over time and influence population immunity and antibody interactions. | [106][107][112]C[172]D[176]D |
| Prior infection or vaccination | Sequential infection and vaccine-derived immunity alter susceptibility, neutralization, and interpretation of future outbreaks. | [107][108][109][111] |
| Aedes vectors | Vector presence, including A. aegypti in highland settings, permits transmission. | [115][173]D |
| Human movement | Imported cases can seed local epidemics in receptive areas. | [103] |
| Climate and seasonality | Climate variability, El Niño, vector expansion, and extended seasonal transmission can increase exposure opportunities. | [103][112]C[172]D[173]D[175]D |
| Arboviral co-circulation | CHIKV and ZIKV share vectors and clinical overlap, producing co-infection and diagnostic uncertainty. | [105][173]D |
History and Physical Examination
- ▸Define fever onset precisely; surveillance protocols used **≥38 °C on two of three consecutive days**, with molecular sampling preferably within **5 days** of onset. [26]
- ▸Repeat examination through defervescence because dengue manifestations vary substantially and deterioration may occur after the initial febrile phase. [104] [130]
- ▸Assess hydration, perfusion, bleeding, abdominal findings, respiratory status, mental status, urine output, and evidence of fluid accumulation at every clinical review. [131] [45]
- ▸Do not attribute every acute fever to dengue or malaria; consider co-infections and alternative diagnoses, especially in children and travellers. [124] [41] [110] [133] [134]
- ▸Atypical or severe presentations may include pulmonary involvement, seizures, myocarditis, transverse myelitis, polyserositis, renal dysfunction, and severe disease without marked thrombocytopenia. [45] [122] [129] [131]
- ▸Older adults may have attenuated clinical findings despite severe laboratory evolution, requiring careful serial assessment. [127]
Clinical context and initial history
Dengue should be considered in any patient with an acute febrile illness who lives in, or has recently travelled to, a dengue-endemic area, particularly during an outbreak. In returning travellers, dengue was among the confirmed diagnoses in a hospital-based fever cohort, although malaria and other infections were also identified; therefore, travel history should include destinations, dates of travel, mosquito exposure, outbreak activity, and malaria prophylaxis. [134] Dengue may be under-recognized in settings where acute fever is routinely attributed to malaria, including parts of sub-Saharan Africa. [110]C [125] [133]
Document the exact date and time of fever onset, daily temperature pattern, antipyretic use, oral intake, urine output, vomiting, abdominal pain, bleeding, rash, headache, retro-orbital pain, myalgia, arthralgia, lethargy, dyspnea, chest discomfort, and neurological symptoms. In vaccine-surveillance practice, fever was defined as ≥38 °C on two of three consecutive days, and evaluation and blood collection were preferably performed within 5 days of fever onset, when molecular testing is most useful. [26] Prolonged fever is clinically relevant: in a pediatric hospitalized cohort, fever >38.3 °C beyond illness day 7 occurred in 11.06% of patients and was associated with warning signs or severe dengue. [130]
Ask about previous dengue infection, dengue vaccination, pregnancy, infancy or advanced age, and comorbidities that may increase the consequences of dehydration, bleeding, capillary leakage, or organ dysfunction. Prior exposure to SARS-CoV-2 may be relevant in regions where dengue and COVID-19 co-circulate, although evidence linking this history to altered dengue pathogenesis remains exploratory and based on a small pilot study. [43]D Ask specifically about nonsteroidal anti-inflammatory drugs, aspirin, anticoagulants, antiplatelet drugs, and other medications; a retrospective study examined low-dose ibuprofen exposure in initially non-severe dengue, but this does not establish safety for all patients or clinical circumstances. [132]
General and systemic examination
Assess mental status, appearance, hydration, perfusion, respiratory effort, pulse, blood pressure, pulse pressure, temperature, oxygen saturation, capillary refill, and urine output. Examine the skin and mucosa for flushing, maculopapular or petechial rash, bruising, ecchymoses, mucosal bleeding, and signs of dehydration. The tourniquet test, where used locally, should not replace direct assessment for bleeding or hemodynamic compromise. The clinical spectrum is variable across populations and outbreaks; a Peruvian systematic review and meta-analysis specifically identified substantial variability in dengue manifestations, supporting repeated examination rather than reliance on a single presenting phenotype. [104]
Look for warning features including persistent vomiting, increasing abdominal pain or tenderness, clinical fluid accumulation, mucosal bleeding, lethargy or restlessness, hepatomegaly, postural dizziness, narrowing pulse pressure, hypotension, cool extremities, delayed capillary refill, oliguria, and progressive respiratory distress. Pleural effusion and ascites may accompany severe disease and polyserositis; in a Mexican DENV-3 outbreak, polyserositis was present in fatal cases despite the absence of severe thrombocytopenia. [131] Respiratory assessment should include work of breathing, auscultation, and oxygen saturation. During a DENV-4 outbreak, pulmonary symptoms occurred in 31.3% of hospitalized patients, including lower-respiratory symptoms, cough, and chest distress. [45]D
Neurological, cardiac, and organ-specific examination
Perform a focused neurological examination when there is headache with altered behavior, confusion, seizures, focal weakness, sensory loss, gait disturbance, sphincter dysfunction, or reduced consciousness. Generalized seizures were reported in all deaths in one DENV-3 hospitalized cohort, and dengue-associated transverse myelitis is a rare but potentially disabling neurological complication characterized by spinal-cord involvement and motor, sensory, or autonomic dysfunction. [131] [122]C
Assess for myocarditis or cardiac involvement when there is chest pain, dyspnea, palpitations, syncope, new tachycardia, hypotension, gallop rhythm, or signs of heart failure. Dengue-associated cardiac involvement may range from asymptomatic electrocardiographic abnormalities to fulminant myocarditis; in a Vietnamese study of non-severe dengue, ECG abnormalities and elevated CK-MB were observed, supporting targeted cardiac assessment when symptoms or clinical findings suggest involvement. [129]C
Examine the abdomen for tenderness, guarding, hepatomegaly, ascites, and gastrointestinal bleeding. Evaluate the kidneys and fluid balance through urine output, mucosal hydration, peripheral perfusion, and edema. Older adults may have less conspicuous or atypical symptoms despite more severe laboratory evolution and poorer outcomes, so examination should be repeated and interpreted alongside comorbidities and serial laboratory results. [127]
Differential diagnosis and follow-up
Dengue remains a clinical diagnosis to consider among acute undifferentiated fevers, but malaria, chikungunya, Zika, respiratory infections, leptospirosis, scrub typhus, typhoid fever, meningitis or encephalitis, and bacterial sepsis may present similarly. Molecular investigations in febrile children have demonstrated dengue–malaria and dengue–other arbovirus co-infections, while studies in Nepal, Gabon, Mali, India, and returning travellers show that fever frequently has alternative or multiple causes. [124]C [41]D [110]C [133] [134]
Reassess patients during defervescence and the subsequent critical period, because clinical deterioration may emerge after the initial febrile presentation. Document persistent fatigue, depression, reduced activity, or other post-acute symptoms at follow-up; systematic reviews and prospective traveller cohorts indicate that post-dengue symptoms may persist and impair quality of life for months. [123] [126] In resource-limited or climate-affected health systems, access to serial assessment, diagnostics, referral, and emergency care may be constrained, and this should lower the threshold for safety-net instructions and reassessment. [125] [128]
| Domain | Findings to seek | Supporting evidence |
|---|---|---|
| Fever course | Onset, daily pattern, antipyretics, fever >38.3 °C beyond day 7 | [26] [130] |
| Warning features | Vomiting, abdominal pain, bleeding, lethargy, dyspnea, oliguria, dizziness, hypotension | [104] [131] |
| Respiratory | Cough, chest distress, hypoxemia, pleural effusion, increased work of breathing | [45]D |
| Neurological | Confusion, seizures, weakness, sensory or autonomic deficits | [122]C [131] |
| Cardiac | Chest pain, palpitations, syncope, heart-failure signs, abnormal ECG findings | [129]C |
| Epidemiology and differential | Travel, outbreak exposure, malaria risk, vaccination, prior dengue, possible co-infection | [26] [41]D [110]C [124]C [134] |
Diagnosis and Workup
- ▸Use RT-PCR, NS1 antigen, and IgM/IgG serology as complementary tests whose interpretation depends on illness timing and prior dengue exposure. [138][109]
- ▸A negative NS1 or RT-PCR result does not exclude dengue when clinical suspicion remains high, particularly during sequential outbreaks or secondary infection. [109]
- ▸Perform serial blood counts and assess bleeding, plasma leakage, perfusion, renal function, hepatic function, and neurologic or cardiac complications when indicated. [135][140][141][143][148]
- ▸Consider chikungunya and SARS-CoV-2 coinfection or alternative infection in patients with overlapping or atypical presentations. [137][145]
- ▸Quantitative NS1, antibody titres, cytokines, inflammasome markers, and machine-learning models are promising but remain adjunctive or investigational for severity prediction. [139][149][150][152]
Diagnostic approach
Dengue should be considered in patients with an acute febrile illness in, or with recent travel to, a dengue-risk area, particularly when thrombocytopenia, leukopenia, bleeding, rash, myalgia, or plasma-leakage features are present. Clinical differentiation is difficult because dengue circulates with chikungunya and other arboviruses, and early dengue and chikungunya manifestations may overlap substantially. [139][145] SARS-CoV-2 coinfection can further complicate the clinical picture because dengue-like manifestations and laboratory abnormalities may occur in both infections. [137]
Laboratory confirmation may be obtained by direct detection of DENV RNA using reverse-transcription polymerase chain reaction (RT-PCR), detection of NS1 antigen, or serology for anti-DENV IgM and IgG. These methods are not interchangeable across all illness stages, and agreement between NS1 rapid tests and RT-PCR may be imperfect, particularly in samples that are negative by both or either direct method. [138][109] A negative direct test therefore should be interpreted with the timing of specimen collection, prior infection, serotype, and the clinical syndrome in mind. Sequential outbreaks and increasing secondary infections may alter both clinical severity markers and the performance or agreement of routine direct diagnostic methods. [109]
Quantitative NS1 antigen and IgM/IgG titres have been investigated in children as potential indicators of severity and as aids to distinguishing primary from secondary infection; reported study outcomes included bleeding, third spacing, thrombocytopenia, hepatic and renal involvement, shock, and length of hospitalization. [152] However, these assays should be treated as adjunctive risk-stratification tools rather than standalone predictors until validated across settings and serotypes. Acute-phase antibody profiles may influence viremia and clinical manifestations, while neutralizing and potentially enhancing antibody activity can vary with prior exposure and viral genotype. [144]C[107]
Initial laboratory and clinical assessment
The initial workup should establish whether the patient has uncomplicated illness, warning signs, or organ dysfunction. A complete blood count with serial platelet and leukocyte assessment is central because thrombocytopenia is common and may form part of a severe-dengue phenotype. [141][142] The platelet count should be interpreted alongside bleeding, hemodynamics, hematocrit or other evidence of hemoconcentration, and suspected plasma leakage rather than used alone to define severity. Prophylactic platelet transfusion has been evaluated in dengue-associated thrombocytopenia, including the outcome of achieving a platelet count of ≥50 × 10³/µL; the systematic review evaluated mortality, bleeding, hospital stay, and time to platelet recovery. [142]
Serial assessment should include vital signs, perfusion, fluid accumulation or third spacing, urine output, mental status, and evidence of bleeding. Severe dengue may present with connected endothelial-barrier dysfunction, plasma leakage, thrombocytopenia, hemorrhage, and shock; current mechanistic evidence supports contributions from NS1-associated endothelial injury, glycocalyx disruption, inflammatory myeloid activation, and platelet/coagulation abnormalities, but does not establish a single diagnostic biomarker. [135] Severe-dengue phenotypes are heterogeneous: an ICU cohort identified distinct organ-failure patterns, including a thrombocytopenia-predominant phenotype, indicating that evaluation should not focus exclusively on shock. [141]
Obtain liver and renal biochemical testing when clinically indicated and repeat testing in patients with warning signs or abnormal results. Liver failure has been specifically associated with routine laboratory abnormalities in hospitalized dengue patients, and machine-learning analysis has been used to corroborate candidate predictors in a non-endemic setting. [140] Biomarker research has also evaluated serial IL-6, IL-8, dengue serotype, and other clinical variables for severity prediction, but these findings remain investigational and are not substitutes for bedside monitoring. [149] NLRP3-inflammasome and autophagy-related gene, protein, and cytokine measurements have been associated with disease-severity research, but are research assays rather than routine diagnostic tests. [150]
Differential diagnosis and additional testing
Where chikungunya is circulating, test for CHIKV when the clinical presentation is compatible or dengue testing is negative or inconclusive. A retrospective hospital study found previously unrecognized chikungunya exposure among patients initially managed as suspected dengue, supporting consideration of dual or alternative arboviral infection. [145] A multiplex RT-MIRA platform has been developed for simultaneous DENV and CHIKV detection, with nested amplification for DENV-1 through DENV-4 serotyping and readout by portable fluorescence or lateral-flow dipstick at 39°C; this remains a diagnostic-platform development rather than a universally established standard. [146]
Consider SARS-CoV-2 testing when respiratory symptoms, epidemiologic exposure, or atypical features are present because documented DENV/SARS-CoV-2 coinfection can produce overlapping clinical and laboratory findings. [137] Serotype identification may be useful for surveillance and epidemiologic interpretation, but serotype alone should not determine individual risk because antibody history, genotype, and host response also influence disease expression. [107][109][144]C
Neurologic symptoms require targeted neurologic examination and appropriate neuroimaging or cerebrospinal-fluid evaluation according to the syndrome; dengue-associated spinal-cord involvement is uncommon, and published evidence consists largely of case reports, case series, and small cohorts. [143] Palpitations, syncope, chest discomfort, or hemodynamic instability warrant electrocardiography and cardiac assessment because dengue-associated arrhythmias and cardio-hemodynamic dysfunction have been specifically reported. [148] T-cell assays and other immune-profiling methods have described dengue-specific cellular memory, including in people living with HIV, but they are not part of routine diagnosis. [147]C
Interpretation and follow-up
A confirmed dengue diagnosis does not by itself predict an uncomplicated course. Patients with warning signs or evolving laboratory abnormalities require reassessment because deterioration may reflect plasma leakage, bleeding, liver or kidney injury, neurologic disease, or cardiac involvement. [135][140][141][143][148] Machine-learning models using routine clinical data may help distinguish dengue from chikungunya or identify organ-risk patterns, but they require external validation and should complement—not replace—clinical examination, serial laboratory testing, and direct pathogen testing. [139][140]
| Clinical question | Suggested evidence-based evaluation |
|---|---|
| Is DENV infection present? | RT-PCR, NS1 antigen, and/or anti-DENV IgM/IgG, interpreted according to illness stage and prior exposure. [138][109] |
| Is the patient worsening? | Serial platelet and leukocyte counts; assessment of bleeding, plasma leakage, perfusion, urine output, and organ function. [135][141] |
| Is there liver or kidney involvement? | Repeat hepatic and renal biochemical testing when warning signs, abnormal results, or clinical deterioration are present. [140][152] |
| Could this be another or concurrent infection? | Evaluate for CHIKV and SARS-CoV-2 when epidemiology or clinical features overlap; multiplex molecular testing is an emerging option. [137][145][146] |
| Is there an organ-specific complication? | Neurologic assessment and targeted imaging or cerebrospinal-fluid studies for spinal-cord syndromes; ECG and cardiac evaluation for suspected arrhythmia or hemodynamic dysfunction. [143][148] |
Special Populations
- ▸Children and adolescents have substantial dengue burden, and severe disease risk requires serial assessment rather than reliance on a single biomarker. [70][130][152]
- ▸Fever **>38.3°C beyond day 7** occurred in **11.06%** of a hospitalized Colombian pediatric cohort and was associated with greater severity. [130]
- ▸Dengue during pregnancy has been associated with reported maternal mortality, pregnancy loss, and preterm birth, but estimates are heterogeneous and evidence certainty varies. [46][154]
- ▸Dengue-associated GBS and hemophagocytic lymphohistiocytosis are uncommon but serious complications requiring specialist evaluation. [153][177]
- ▸In children with fever, dengue may coexist with malaria or be confused with bacterial infection; molecular and syndromic testing can improve diagnostic characterization. [41][124][158]
Children and adolescents
Children and adolescents represent an important dengue-risk population. A 2025 systematic review and meta-analysis of 158 studies found substantial geographic variation in incidence and seroprevalence, with incidence proportions reported across the Americas, Africa, and Asia; pooled analyses also examined age- and sex-related differences in infection risk. [70] Hospital-based data from Puducherry, India, described 632 pediatric dengue admissions during 2017–2022 and documented changes in clinical and epidemiological patterns before and during the COVID-19 pandemic. [84]D Pediatric dengue may be difficult to distinguish from other febrile illnesses, particularly in settings where malaria and arboviral infections coexist. [41]D[124]C
Children with warning signs or severe dengue require close observation because deterioration may occur with plasma leakage, thrombocytopenia, bleeding, hepatic or renal involvement, and shock. A prospective South Indian study of laboratory-confirmed patients aged 1 month to 18 years evaluated quantitative NS1 antigen, IgM, and IgG titres against these severity outcomes; it also assessed whether the IgM/IgG ratio could reliably distinguish primary from secondary infection. [152] However, these biomarkers should be interpreted with clinical findings because the study was conducted at a single tertiary center and did not establish universal thresholds for management. [152]
Persistent fever may identify a higher-risk pediatric subgroup. In a prospective Colombian study of 253 hospitalized children with dengue warning signs or severe dengue, fever >38.3°C beyond illness day 7 occurred in 11.06%; prolonged fever was associated with a higher proportion of severe dengue and immune dysregulation. [130] Hyperferritinemia has also been investigated as a marker of inflammation and severity in hospitalized children with dengue warning signs or severe dengue, including associations with organ dysfunction, new-onset multiple-organ dysfunction, thrombocytopenia, and respiratory-ventilation requirements. [159] These findings support serial clinical and laboratory assessment rather than reliance on a single measurement. [130][159]
Young infants and diagnostic uncertainty
Febrile young infants in dengue-hyperendemic regions require a broad evaluation because bacterial and viral infections can present similarly. A 13-year retrospective Colombian cohort included 4,671 admissions in patients younger than 18 years and developed an internally validated XGBoost model using nine clinical and laboratory variables to differentiate bacterial from viral infection; the model was compared with penalized logistic regression and single-marker rules. [158] The study supports risk-stratified decision-making but was internally validated, so external validation is required before routine adoption. [158]
In Nepal, a prospective cohort of children under 14 years used routine assessment, NS1 antigen testing, and expanded molecular panels during a dengue outbreak to identify infectious causes of fever. [124]C In malaria-endemic settings, dengue can be missed or misclassified: molecular testing in febrile children in Libreville, Gabon, demonstrated circulation of multiple dengue serotypes and dengue–malaria coinfection. [41]D A study of acute undifferentiated fever in Mali likewise evaluated dengue and other arboviruses from 2016–2024, highlighting the potential for dengue burden to be obscured when fever is attributed primarily to malaria. [110]C
Pregnancy
Pregnancy is associated with clinically important maternal and fetal considerations, although the certainty of evidence remains limited. A systematic review of 23 studies published from 2010 onward found that dengue during pregnancy was most frequently acquired in the third trimester; reported maternal mortality ranged from 0–21.7%, pregnancy loss from 0–11.6%, and preterm birth from 4.3–37.5%. [154] Interpretation is constrained by heterogeneous study designs, incomplete quantitative comparisons with dengue-negative pregnant individuals, and limited evidence quality. [154]
An umbrella review of systematic reviews and meta-analyses found that evidence concerning dengue and adverse pregnancy or fetal outcomes varied in credibility; the review assessed three dengue meta-analyses alongside evidence for Zika and chikungunya and graded certainty according to precision, consistency, small-study effects, and AMSTAR 2 quality ratings. [46] Accordingly, dengue in pregnancy warrants careful maternal assessment, fetal monitoring when clinically indicated, and attention to bleeding, plasma leakage, organ dysfunction, and obstetric complications, while recognizing that precise excess risks cannot be inferred consistently from the available literature. [46][154]
Neurological and hyperinflammatory complications
Guillain–Barré syndrome (GBS) is an uncommon but recognized neurological complication associated with dengue. A systematic review identified 56 patients from 36 publications across Asia, Latin America, and other endemic regions; cases generally followed laboratory-confirmed or clinically diagnosed dengue, and the review examined clinical characteristics, outcomes, and predictors of severity. [153] Because the evidence consisted primarily of case reports and case series, the frequency of dengue-associated GBS and comparative prognosis remain uncertain. [153]
Dengue-associated hemophagocytic lymphohistiocytosis (DA-HLH) is a rare, severe hyperinflammatory complication that can clinically overlap with severe dengue and delay recognition. A Colombian retrospective cohort evaluated pediatric DA-HLH diagnosed using HLH-2004 criteria and supported by the HScore, including clinical features, laboratory findings, treatments, and mortality associations. [177]C Suspected DA-HLH should therefore be considered when inflammation, cytopenias, organ dysfunction, or clinical deterioration are disproportionate or persistent, while applying formal diagnostic criteria and specialist input. [177]C
Population-level prevention relevant to special populations
A cluster-randomized Singapore trial evaluated repeated releases of male Aedes aegypti carrying wAlbB Wolbachia, which produce nonviable offspring after mating with wild-type females through cytoplasmic incompatibility; the intervention was intended to suppress mosquito populations and reduce dengue infection risk. [2] This approach may provide indirect protection to populations at heightened clinical risk, including children and pregnant individuals, but it is a vector-control intervention rather than an individual treatment. [2]
In southern Brazil, a six-year population-based cohort evaluated Dengvaxia after a campaign offered in 30 municipalities, with approximately 300,000 people vaccinated and about 60% receiving at least one dose; probable dengue was the primary outcome, while laboratory-confirmed dengue, serotype, warning signs, and hospitalization were secondary outcomes. [74] Vaccine effectiveness estimates should be interpreted in the context of the studied population, vaccination coverage, and product-specific eligibility considerations. [74]
Epidemiological context
Global burden analyses indicate increasing dengue incidence and substantial variation by region, age, sex, and sociodemographic context, including in South Asia and China. [81]D[156] During the 2023–2024 Colombian outbreak, prospective hospital surveillance assessed virologically confirmed dengue across all ages and examined demographic, clinical, viral-serotype, and genotype-related factors associated with serious manifestations. [86]D In Brazil’s Espírito Santo epidemic, 127,070 cases were reported in 2023 and 131,170 in 2024; warning signs or severe dengue, hospitalization, and deaths were recorded, while genomic surveillance documented DENV-1 and DENV-2 cocirculation. [155] These findings reinforce the need to adapt surveillance and clinical triage to local transmission intensity, circulating serotypes, and the characteristics of vulnerable populations. [86]D[155]
| Population or complication | Evidence-based consideration |
|---|---|
| Children and adolescents | Monitor for warning signs, severe dengue, prolonged fever, organ dysfunction, and shock; pediatric biomarker thresholds remain context-dependent. [70][130][152] |
| Young infants | Maintain broad bacterial, viral, and arboviral differential diagnosis; internal prediction models require external validation. [124]C[158] |
| Pregnancy | Reported risks include maternal mortality, pregnancy loss, and preterm birth, but estimates are heterogeneous. [46][154] |
| Neurological disease | Consider GBS after dengue, recognizing that evidence is mainly from case reports and series. [153] |
| Hyperinflammation | Consider DA-HLH when inflammation, cytopenias, or organ dysfunction are disproportionate or persistent. [177]C |
| Malaria-endemic areas | Test for dengue and malaria when clinically appropriate because coinfection and diagnostic misclassification occur. [41]D[110]C |
Guidelines and Resources
- ▸Dengue classification should support triage but should not replace serial reassessment because clinical findings may correlate poorly with severity. [91][161]
- ▸NAAT is preferred for suspected dengue or Zika virus infection; IgM is useful but can be limited by cross-reactivity and uncertain timing. [87]
- ▸Non-febrile dengue can occur, so absence of fever should not automatically exclude the diagnosis. [93]
- ▸Warning-sign assessment and febrile-phase risk prediction are central to early detection of severe disease. [90][94]
- ▸CYD-TDV vaccination safety messaging requires evidence of prior dengue infection and adherence to current product information. [162]
- ▸Emerging biomarkers such as soluble HLA-G and complement measures remain investigational. [96][56]
Scope and use of dengue guidance
Dengue guidance should be applied as a continuum covering surveillance, laboratory confirmation, clinical classification, triage, supportive management, prevention, and outcome monitoring. Dengue surveillance is most effective when it involves relevant public-health, clinical, laboratory, vector-control, and community stakeholders and follows the pathway from mosquito exposure through case detection and reporting. [88] The Asia-Pacific and Americas Dengue Prevention Boards described surveillance methods and stakeholder responsibilities after reviewing international programs and expert experience from 22 countries. [88]
Clinical classification and triage
The revised WHO approach distinguishes dengue without warning signs, dengue with warning signs, and severe dengue, with classification intended to support decisions about the level of medical and nursing care required. [92] Prospective multicountry work in Southeast Asia and Latin America evaluated clinical and laboratory profiles against intervention needs and was undertaken to improve the evidence base for classification and warning signs. [92] Subsequent studies have found that clinical features may correlate poorly with severity categories under both the traditional 1997 and revised 2009 WHO systems, so classification should not replace repeated clinical assessment and laboratory monitoring. [91] The sensitivity of the traditional WHO definition for identifying severe illness has also been questioned in pediatric dengue, reinforcing the importance of early recognition and serial reassessment. [161]
Fever is the core feature in the 2009 revised WHO framework, but non-febrile dengue occurs and can complicate diagnosis. [93] A prospective study of 30,670 laboratory-confirmed cases evaluated the prognostic importance of fever and the relationship between fever, treatment timing, and disease risk. [93] During the febrile phase, clinicians should use validated clinical assessment together with laboratory findings and should not rely on a single symptom or sign to exclude future deterioration. [90] A systematic review and meta-analysis specifically examined predictors detectable during the febrile phase because early prediction of progression to severe dengue is central to triage and clinical management. [90]
Warning-sign assessment should include the features specified by the applicable WHO or national protocol, including abdominal symptoms, persistent vomiting, fluid accumulation, mucosal bleeding, lethargy or restlessness, liver enlargement, and changing hematocrit and platelet values. [94] Postural reduction in systolic blood pressure has been investigated as an additional marker of intravascular volume reduction and capillary leak, but it should be regarded as an adjunct rather than a replacement for established warning signs. [165] In adults, a locally derived dengue score using routine laboratory parameters was proposed to predict pleural effusion and/or ascites; such scores require external validation before generalized use. [160]
Diagnostic resources
For patients with a clinically compatible illness and risk of infection with dengue or Zika virus, nucleic acid amplification testing is the preferred diagnostic method. [87] Dengue NS1 antigen detection, reverse-transcription polymerase chain reaction, and enzyme-linked immunosorbent assay were used to confirm cases in major clinical studies. [93] IgM testing can identify additional infections, but interpretation is limited by antibody cross-reactivity and difficulty determining the precise timing of infection, particularly when distinguishing dengue from Zika virus infection. [87] Diagnostic interpretation should therefore account for illness timing, epidemiologic exposure, prior flavivirus infection, and the possibility of coinfection or cross-reactive results. [87]
A negative result from one test should not automatically terminate clinical surveillance when the presentation remains compatible with dengue, because diagnostic performance varies with the stage of illness and the test method used. [87] Non-febrile presentations may be overlooked if fever is treated as an absolute requirement for diagnosis. [93]
Supportive care and fluid-related resources
No antiviral treatment was identified in the 2009–2019 systematic review summarized by Wellekens and colleagues; management therefore remains supportive and depends on early recognition of deterioration. [164] Hydration and warning-sign assessment are relevant in ambulatory care, and a prospective primary-care study in Réunion measured reported fluid intake and warning signs in patients with dengue-like illness. [94] Fluid management should be individualized and closely monitored when plasma leakage, shock, ascites, or pleural effusion is suspected. [95]C Case reports of dengue shock syndrome with ascites and pleural effusions highlighted uncertainty about fluid selection and showed that third-space fluid loss may be present at shock, whether or not intravenous fluids had already been administered. [95]C
Vaccination and prevention resources
CYD-TDV (Dengvaxia) was the first dengue vaccine to receive marketing authorization, reported in a review of dengue prevention and management published before the WHO 2010–2020 goals. [164] Safety communications and prescriber education emphasized that vaccination should be restricted to individuals with evidence of prior dengue infection; a survey of 300 prescribers in Brazil and Thailand found that the educational risk-minimization measures did not consistently achieve the predefined knowledge and practice targets. [162] Vaccine policy should therefore follow the current product information and jurisdiction-specific recommendations rather than relying on historical schedules alone. [162]
Surveillance, quality improvement, and research
Surveillance systems should connect case finding, laboratory confirmation, clinical severity assessment, reporting, and vector-control response. [88] Audits of adherence to WHO-based protocols are useful because nonadherence has been associated with inappropriate use of blood products and increased hospitalization costs in Brazil. [163] Fatal dengue investigations in Puerto Rico demonstrated the value of linking surveillance records, death certificates, nucleic acid amplification, tissue immunohistochemistry, and IgM testing to identify determinants of death and improve clinical management. [167]C
Emerging biomarkers should not yet replace established clinical pathways. Elevated soluble HLA-G levels were associated with dengue severity in hospitalized Vietnamese patients classified as dengue without warning signs, dengue with warning signs, or severe dengue under WHO criteria. [96]D Complement and acute-phase response abnormalities have likewise been investigated in relation to varying dengue severity, but these findings remain research resources rather than routine triage standards. [56]D
Practical resource hierarchy
Use the applicable WHO or national dengue protocol for classification, warning signs, fluid management, and referral; use NAAT and appropriately timed serology for laboratory confirmation; use organized surveillance for population-level detection and response; and use vaccine product information and local policy for vaccination decisions. [87][88][92][162][164]
| Clinical or public-health need | Recommended resource or approach | Evidence |
|---|---|---|
| Surveillance | Integrated case detection, laboratory confirmation, reporting, stakeholder coordination, and vector-control response | [88] |
| Diagnosis | NAAT as preferred testing; IgM as an additional test with cross-reactivity limitations | [87] |
| Classification | Dengue without warning signs, dengue with warning signs, and severe dengue; reassess serially | [92][91][161] |
| Febrile-phase triage | Combine clinical evaluation with laboratory monitoring and risk predictors | [90] |
| Fluid-related care | Individualized monitoring when plasma leakage, shock, ascites, or pleural effusion is suspected | [95]C |
| Vaccination | Follow current product information and restrict CYD-TDV use to evidence-supported populations with prior dengue infection | [162][164] |
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