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Table of Contents
Year : 2022  |  Volume : 10  |  Issue : 3  |  Page : 146-152

Atypical manifestations of dengue

Department of Medicine, MVJMC and RH, Bengaluru Rural, Karnataka, India

Date of Submission09-Jul-2021
Date of Decision08-Aug-2021
Date of Acceptance16-Aug-2021
Date of Web Publication12-Jul-2022

Correspondence Address:
Dr. Vasantha Kamath
Department of Medicine, MVJMC and RH, Hoskote, Bengaluru Rural - 562 114, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ajim.ajim_71_21

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Dengue is a major concern in India. It has a diverse spectrum of atypical manifestations across the various systems of the human body with significant mortality and morbidity rates. The following review emphasizes on the various systemic manifestations, including the need for their early recognition and treatment.

Keywords: Atypical, dengue, morbidity

How to cite this article:
Kamath V, Radhakrishnan B, Markanday K. Atypical manifestations of dengue. APIK J Int Med 2022;10:146-52

How to cite this URL:
Kamath V, Radhakrishnan B, Markanday K. Atypical manifestations of dengue. APIK J Int Med [serial online] 2022 [cited 2022 Nov 28];10:146-52. Available from: https://www.ajim.in/text.asp?2022/10/3/146/350749

  Introduction Top

Dengue fever is the most widely distributed mosquito-borne viral infection prevalent in most Indian states. It is chiefly transmitted by Aedes aegpti with peaks in incidence in and around monsoon.[1],[2],[3]

The World Health Organization reports a significant increase in incidence in the past five decades with nearly 100 million cases clinically reported annually. It is currently re-emerging in many countries showing endemicity mostly in South East Asian countries with a drop in the gender differentiation and resilience to eradication.[2],[4]

The estimated annual incidence of dengue in India is around 7.5–32.5 million leading to significant morbidity in endemic regions. It is caused by dengue virus (DENV), an arbovirus with 4 serotypes: DENV 1–4, found generally in tropical and subtropical regions. Initially affecting urban areas, it is spreading in rural areas as well owing to the rapid urbanization occurring together with a lack of hygiene. The serotypes currently prevalent in the country DENV 2 and DENV 4 have been reported to cause the more serious forms of dengue.[1],[2],[3],[4]

The presentation of dengue can differ broadly ranging from asymptomatic infection to life-threatening disease ending in shock. Dengue shock syndrome (DSS) is characterized by hemodynamic compromise with plasma leakage, hemorrhagic complications, and thrombocytopenia, associated with high morbidity and mortality.[5],[6]

With the increase in the incidence of infectious diseases, particularly the vector-borne diseases, especially in the endemic regions around the world, there is an increasing incidence of two or more than two infections occurring in one individual at the same time. Such conditions often pose a challenge to the treatment offered and have a higher incidence of complications thus adding up the morbidity and mortality caused by that particular disease. Dengue has been globally reported to occur along with a number of co-infections, especially rickettsial infections, malarial disease, chikungunya, and COVID-19. In the recent times of ongoing pandemic, dengue with COVID-19 is being increasingly reported.[2] The stark differences between the two are listed in [Table 1].[7],[8],[9]
Table 1: Salient differences between COVID-19 and dengue

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Dengue usually manifests as an acute febrile illness, its symptomatology consisting of body ache, retroorbital pain, and generalized rashes. Supportive management, including fluid replacement and treatment of secondary complications, comprises the majority of the treatment. However, as the incidence of dengue increases, atypical manifestations of dengue are on the rise, and these are likely to go underreported [Figure 1]. Failure to recognize these may result in a delay in the diagnosis and initiation of appropriate treatment.[3],[4]
Figure 1: Atypical manifestations of dengue

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  Gastrointestinal and Hepatic Manifestations Top

Gastrointestinal manifestations include hepatitis, fulminant hepatic failure, acalculous cholecystitis, acute pancreatitis, acute parotitis, and febrile diarrhea. DENV antigen has been demonstrated in Kupfer cells and sinusoidal lining cells in the liver, suggesting that viral replication can occur in hepatocytes. Hepatic manifestations include acute hepatitis with pain in the right hypochondrium, hepatomegaly, jaundice as well as raised aminotransferase levels which peak on the 9th day after the onset of symptoms and gradually return to normal within 3 weeks. Histopathology shows centrilobular necrosis, fatty alterations, hyperplasia of the Kupfer cells, acidophil bodies, and monocyte alteration of the portal tracts. Hepatic involvement prolongs the natural course but does not indicate worse prognosis. The jaundice is multifactorial and can be due to hepatic aggression caused by the virus and/or tissue hypoxia with ischemia caused by shock. Alkaline phosphatase and bilirubin may be raised. Studies show a greater elevation in aspartate transaminase (AST) than alanine aminotransferase levels, which may be attributed AST being released from damaged monocytes. This comparison may be beneficial in differential diagnosis of acute hepatitis in endemic areas. Predominance is seen in females and dengue hemorrhagic fever (DHF) patients. Fulminant hepatitis with high mortality also has been reported. Severe hemorrhage, shock, metabolic acidosis, and disseminated intravascular coagulation may lead to severe changes in the liver. Chronic liver disease, alcoholic steatonecrosis, and hepatotoxic drug use (such as salicylates and paracetamol) may predispose to or escalate liver injury. Acute liver failure is a severe complication predisposing to life-threatening hemorrhage, disseminated intravascular coagulation, and encephalopathy. Raise in aminotransferases has been correlated with disease severity and might be an early indicator of dengue infection.[10],[11],[12]

Acute pancreatitis is a rare complication. Enlarged pancreas, and increased serum amylase and lipase levels and echocardiogram (ECHO) evidence of enlargement of head of pancreas have been found in patients with dengue. Pathogenesis may involve direct viral invasion or hypotension due to DHF.[10],[11],[12]

Acalculous cholecystitis is rare, presenting with right upper quadrant abdominal pain, fever, positive Murphy sign, abnormal liver function tests, and thickened gall bladder wall without stones on ultrasonography. Factors hypothesized in pathogenesis include prolonged fasting, spasms of ampulla of Vater, infection, endotoxemia, microangiopathy, and ischemia reperfusion injury-causing cholestasis and increased bile viscosity, as well as increased vascular permeability causing plasma leakage and serous effusion with high protein content causing thickening of gall bladder wall. This wall thickening has been correlated with the severity and progression of dengue fever. The course is generally self-limiting, and wall thickness returns to normal. Hence cholecystectomy is not typically advised. Rapid progression of cholecystitis to gangrene and perforation can occur where prompt recognition and intervention are required. Surgical intervention is needed in cases with diffuse peritonitis.[10],[11],[12]

Other presentations include “febrile diarrhea” followed by hemorrhagic skin lesions, bilateral parotid gland enlargement, and subacute intestinal obstruction.

Hence, patients presenting with acute abdomen in endemic areas should be evaluated for dengue fever, acute acalculous cholecystitis, pancreatitis, and hepatitis.[10],[11],[12]

  Cardiac Manifestations Top

Clinically cardiac manifestations can vary across a wide spectrum from subclinical to severe myocarditis which can be fatal. Myocardial involvement may occur owing to direct viral invasion or cytokine-induced immune damage, or both. Myopericarditis and myocarditis are usually subtle but may rarely be life-threatening and may correlate to the severity of the disease. Studies have attributed the increased resting diastolic myocardial calcium ion levels and elevated CPK-MB levels to the arrhythmia and diminished left ventricular function.[3],[4]

Investigations reveal electrocardiography (ECG) changes (encompassing sinus tachycardia, sinus bradycardia, T wave inversions, heart block), two-dimensional ECHO changes (including systolic and diastolic dysfunction), and elevated cardiac enzymes (e.g., troponin T, CPK-MB). Rhythm abnormalities are common, manifesting in a majority of patients as asymptomatic bradycardia.[3],[4]

Less common manifestations include mild pericardial effusion due to serositis or pericarditis. They are generally mild and not clinically significant but rapidly accumulating pericardial effusion compromises cardiac function. It is important to recognize this as patients present with sudden onset of hypotension and features of shock, which must be differentiated from DSS occurring because of increased vascular permeability. To conclude, although a significant proportion of dengue patients present with cardiac manifestations, most findings are subclinical and do not require further clinical interventions. The high incidence of cardiac involvement in dengue patients advocates for cardiac screening in all patients with dengue infection with ECG, ECHO, and CPK-MB levels.[3],[4]

  Neurological Manifestations Top

The neurological involvement is commonly encountered during epidemics, in DHF/DSS and in younger patients and forms an important cause of a fatal outcome. About 95% of these involve the central nervous system (CNS). Neurological involvement was first reported in 1976. Recent studies note an increasing incidence rates, varying from 0.5% to 20%, owing to the direct neurotropism and neurovirulence of DENV as evidenced by its demonstration in the CNS by detecting viral proteins, ribonucleic acid (RNA) and immunoglobulins, as well as damage to the blood–brain barrier.

The neurological manifestations can be grouped into three categories. First, mild nonspecific symptoms of headache, giddiness, inattention, slight alteration in sensorium, reduced sleep, and restlessness. Second, severe syndromes of altered sensorium, lethargy, confusion, seizures, meningismus, myelitis, encephalitis, or encephalopathy. Third, delayed syndromes of paralysis of extremities, Guillain–Barré syndrome (GBS), bulbar palsy, seizures, memory impairment, sensory loss, and various psychiatric manifestations. The median time of onset of symptoms range from 3 to 7 days from the start of fever. Factors postulated in the pathogenesis are direct invasion of the CNS, neuroinflammation, autoimmune reaction, and metabolic disturbances. The nonstructural 1 antigen, a glycoprotein, acts as a cofactor for viral RNA replication and triggers cytokine release. There is an early activation of natural killer cells and subsequently the T helper (Th) cells. Th cells further multiply to form Th17 and Th9 cells, and promote the release of pro-inflammatory cytokines including interferon gamma, interleukin (IL) 12, IL-4 and transforming growth factor-beta. These cytokines are responsible for the damage of the blood–brain barrier and the subsequent entry of other immune mediators into the brain causing neuroinflammation.[13],[14],[15]

Encephalopathy and encephalitis

Encephalopathy is the most common neurological manifestation. It comprises a clinical picture of reduced consciousness which may result from encephalitis, metabolic complications such as liver failure, renal impairment, electrolyte imbalance, hypoxia, and shock caused by coagulation disorders in dengue hemorrhagic fever and DSS. Coagulation and bleeding abnormality in dengue secondary to thrombocytopenia and platelet dysfunction can result in stroke in the forms of intracranial hemorrhages and ischemic infarcts. Hepatic encephalopathy is also a well-recognized complication of dengue infection. Up to 80% of neurological complications are due to encephalopathy. It can manifest as reduced sensitivity, cognitive impairment, seizures, and personality and behavior disorders, for example, acute mania, depression, emotional lability, anxiety, psychosis, and agoraphobia. Intracranial hematoma can present with altered sensorium and focal weakness.

In patients with serious DHF/DSS, encephalopathy commonly follows brain edema, anoxia, hemorrhage, intense hyponatremia, liver or kidney failure, release of toxic substances, metabolic acidosis, and direct organ invasion. Apart from hemorrhage, infarct, and edema (encephalitis), other forms of encephalopathy usually do not demonstrate significant radiological findings. Encephalopathy in dengue is usually very serious, with a fatal outcome in around 50% of the patients.

Encephalitis is a severe manifestation of dengue infection. It refers to brain parenchymal inflammation usually caused by infection. It is characterized by fever, headache, seizures, altered sensorium, focal neurological deficits on clinical examination, focal abnormalities in neuroimaging, or focal EEG abnormalities. It may be clinically indistinguishable from encephalopathy. Cerebrospinal fluid (CSF) may show the virus, antibody, or pleocytosis. Normal CSF cellularity cannot exclude dengue encephalitis. Dengue is a major reason for encephalitis with normal CSF cellularity in patients with viral meningitis and encephalitis in dengue-endemic regions. DEN-2 (demonstrated in CSF) and DEN-3 are the most common serotypes reported to cause encephalitis. DEN-4 virus has been isolated by immunohistochemistry from medulla and cerebellum. Magnetic resonance imaging (MRI) is preferred for imaging, although changes are generally nonspecific. In the initial stages of dengue encephalitis, MRI will be normal in most cases. However, as the disease progresses, it may show hyperintense areas in the globus pallidus and thalamic involvement as the one seen in Japanese encephalitis. Most patients respond to supportive and symptomatic care and usually recover in 3–4 weeks without any residual neurological deficit.[13],[14],[15]


The DENV is rarely known to involve the peripheral nervous system. Motor weakness, sensory findings, or bladder complications serve as clues for suspicion in serologically proven patients. DENV has been associated with acute polyradiculopathy, lumbosacral plexopathy, GBS, Miller-Fisher syndrome, and mononeuropathies such as phrenic neuropathy, long thoracic neuropathy, isolated Bell's palsy, abducens nerve palsy, and oculomotor palsy.

Spinal cord can involvement is rare and may be confirmed by diffuse signal intensity on MRI. It may manifest as postinfectious myelopathy, acute disseminated encephalomyelitis (ADEM) or transverse myelitis. It may present as flaccidity in the acute phase of illness and spasticity in its delayed phase.

The pathogenesis is attributed to direct viral invasion and immune-mediated mechanisms as evidenced by intrathecal synthesis of dengue IgG antibodies.[13],[14],[15]

Acute disseminated encephalomyelitis

ADEM is an immune-mediated illness, its cause generally being viral infections or vaccination. It is rare in dengue infection. MRI can show hemorrhagic foci within demyelinating lesions, signal changes in white matter lesions in the centrum semiovale, corona radiata and thalamus, and demyelinating lesions in the spinal cord similar to that of ADEM due to other etiologies. Pathogenesis is likely to involve molecular mimicry leading to an autoimmune response towards myelin or other self-antigens.

Transverse myelitis occurs exceptionally implying an acute infectious myelopathy or an immune-mediated process where the virus triggers an inflammatory process that targets the myelin cells. In these cases, the spinal cord involvement could represent a partial manifestation of post-viral ADEM. It can also be due to intramedullary hemorrhages secondary to thrombocytopenia.[13],[14],[15]

GuillainBarré Syndrome

Seen during the recovery phase of illness, GBS is a postinfectious illness in which an acute infection leads to an aberrant immune response causing nerve damage. GBS is reported to be the most common manifestation of dengue in the peripheral nervous system. This can be attributed to molecular mimicry. Pro-inflammatory cytokines such as tumor necrosis factor, ILs, and the complement proteins play a significant role in damaging peripheral nerve constituents, including myelin or axon.[13],[14],[15]

Other neurological manifestations

Dengue may lead to various other neuropathies including isolated phrenic neuropathy resulting in diaphragmatic palsy, long thoracic neuropathy, and ophthalmoplegia due to the involvement of the oculomotor nerve. Brachial neuritis, acute cerebellitis and parkinsonism-like presentation have also been rarely reported. A rise in occurrence suggests the need for increased awareness and understanding of the neurological complications of dengue infection with physicians, especially neurologists, will continue playing a major role in its diagnosis and treatment.[13],[14],[15]

  Musculoskeletal Manifestations Top

Musculoskeletal manifestations encompass diffuse myalgia, myositis, arthritis/polyarthralgia, rhabdomyolysis and hypokalemic periodic paralysis. Diffuse myalgia, the most common and characteristic symptoms of dengue fever, is noted during its early phase and is characterized by pain, tenderness, and mild muscle swelling. It principally affects proximal muscles of the limb and the back. The pain may lead to difficulty in walking.

The pathogenesis is attributed to the diffuse viral invasion of muscles during viremia and subsequent inflammatory changes in the muscles resulting in muscle pain. Muscle biopsies have shown mild to moderate perivascular mononuclear infiltrate, lipid accumulation, mild mitochondrial proliferation, few central nuclei, foci of muscle necrosis, and fiber type-grouping. Myalgia is often transient and self-limiting. Paracetamol relieves severe pain.[16],[17],[18],[19],[20]


Characterized by diffuse inflammation of skeletal muscles, myositis manifests as pure motor weakness of all four limbs. It can range in severity from self-limiting mild muscle weakness to severe dengue myositis resulting in complete quadriplegia and rarely respiratory insufficiency. Concomitant myocarditis has also been reported.

Other classical features include calf and thigh muscle tenderness on stretching, normal deep tendon reflexes, and an elevated CPK.

In pediatric age group, it may mimic other musculoskeletal disorders, including muscle and joint hematomas, traumatic muscle injuries, septic arthritis and osteomyelitis.

The release of cytokines during viremia, such as tumor necrosis factor, leads to intense inflammation and subsequent damage to muscle fibers. The resultant muscle edema, hemorrhage, metabolic alterations, and changes in vascular endothelial cells lead to muscle dysfunction. Muscle biopsy has revealed interstitial hemorrhage, myonecrosis, and myophagocytosis. Studies mention the role of viral invasion of muscles during the acute stage of the illness. Electron microscopic studies in mice show destruction of myofibrils, rarefaction of the sarcoplasmic reticulum network, changes in the mitochondria and aggregation of electron-dense material as well as glycogen particles in the cytoplasm. Myotubules in human myoblasts infected with DENV have shown increased expression of inflammatory genes and protein interferon-gamma-induced protein 10. In addition, the infected myotubes also had elevated intracellular calcium concentration. The virus may also infect muscle satellite cells which are cells responsible for muscle repair. These cells lose their ability to upregulate myosin heavy chain I protein levels, hinting towards an immune mechanism which may be responsible for the muscle damage.[16],[17],[18],[19],[20]

Hypokalemic periodic paralysis

Hypokalemic periodic paralysis following dengue infection, although exceptional, has been reported. Hypokalemia can occur due to redistribution of potassium in cells or increased renal potassium wasting due to renal tubular abnormalities. Also as a response to the stress of infection, catecholamine levels may raise, leading to secondary insulin release and intracellular shift of potassium. It has a good prognosis, with most patients recovering within 12 h of potassium correction and complete recovery occurring in a few days. The frequent occurrence of musculoskeletal manifestations warrants for alertness and their early recognition.[13]

  Ocular Manifestations Top

Ocular involvement is now being reported increasingly, with most conditions resolving spontaneously. Ocular findings encompass a spectrum from subconjunctival hemorrhage to complications such as optic neuropathy and panophthalmitis leading to permanent impairment of vision in certain cases. The pathogenesis may be attributed to virulence, serotypes, mutations, host susceptibility, and geographic factor. Ocular complications comprise dengue maculopathy, retinal edema, retinal hemorrhages, optic disc swelling, and vitreitis. It usually occurs bilaterally with macular involvement. When patients with severe episodes of hypotension or encephalopathy present with ocular symptoms anterior ischaemic optic neuropathy should be suspected.

Onset of ocular symptoms occurs 2–5 days after onset of fever, mostly occurring within 1 day after the peak of thrombocytopenia. Symptoms include eye pain, retroocular pain, blurring of vision, diplopia, foreign body sensation, photopsia, metamorphopsia, and floaters. Subconjunctival hemorrhage, uveitis, and vitreitis may be seen. Leukopenia and hypoalbuminemia may precede ocular symptoms. These may predispose patients to an opportunistic infection of ocular tissues and hyperpermeability. Dengue maculopathy is well recognized and has been reported to be serotype and geography-related. Its common findings include macular edema and macular hemorrhage. It has a favorable prognosis, except for rare neovascular complications. Visual acuity usually recovers in 2–4 weeks. Given the favorable prognosis of the vasculitis and neuroretinitis, the use of steroids is controversial. The time duration for lesions to appear (nearly 8 days) implies an immune mechanism rather than direct viral invasion. Isolated uveitis occurs between 1 week and 5 months after the onset of the disease. It may manifest as anterior uveitis, intermediate uveitis, or vasculitis and mostly presents with decreased visual acuity. Maculopathy is often associated with chorioretinitis, monofocal or multifocal. Involvement is of bilateral posterior poles with co-occurrence of retinal hemorrhages, periphlebitis, cotton wool spots, hard exudates, and macular edema. Deep, yellowish lesions, hypofluorescent in their early phases, and hyperfluorescent in the later phases are seen. Inconsistent findings include vitreous cells and optic disc edema. Decreased visual acuity may occur due to chorioretinal scarring. However, uveitis has a favorable course, responds well to local or systemic steroids, and does not recur. Other rare lesions include superficial punctate erosions, keratitis, scleritis, cotton wool spots, oculomotor palsies, optic neuropathies, neuromyelitis optica, neurogenic ptosis, and significant permanent visual deficits. Owing to their growing incidence, ocular manifestations are to be watched for in all dengue patients.[15],[21],[22],[23]

  Respiratory Manifestations Top

Pulmonary manifestations comprise pleural effusion, pneumonitis, noncardiogenic pulmonary edema or acute respiratory distress syndrome (ARDS), and hemorrhage/hemoptysis. These coincide with capillary leak syndrome and thrombocytopenia. DSS is reported as the third leading cause of ARDS in endemic areas.[11],[24],[25],[26],[27]

DENV antigen has been demonstrated in alveolar lining cells. Pulmonary dysfunction results from increased permeability of the alveolar-capillary membrane leading to edema in the alveoli and interstitial spaces. Early restoration of adequate tissue perfusion is essential in preventing ARDS. However, the excessive fluid infusion should be avoided after adequate volume replacement as ARDS may occur due to fluid overload. DHF has also been known to cause pulmonary hemorrhage with or without hemoptysis. Thromboembolic events may also occur owing to increased levels of von Willebrand factor, tissue factor, tissue plasminogen activator, plasminogen activator inhibitor-1, and fractional catabolic rate of fibrinogen leading to pulmonary embolism.[11],[24],[25],[26],[27]

The most frequent imaging findings include bilateral areas of ground-glass opacity or consolidation and bilateral pleural effusions. Early recognition of these findings helps initiate prompt treatment and reduce mortality.[11],[24],[25],[26],[27]

  Renal Manifestations Top

Common renal manifestations include proteinuria, hematuria in the absence of thrombocytopenia, rhabdomyolysis, and acute kidney injury (AKI). AKI may significantly affect both morbidity and mortality. AKI may manifest with raised serum creatinine, proteinuria, glomerulonephritis, and hemolytic uremic syndrome (HUS). While a mild elevation of serum creatinine is common clinically significant AKI is less common in DHF. The incidence of AKI is variable. Predisposing factors include older age, male sex, previous history of stroke or chronic kidney disease, gastrointestinal bleeding, concurrent bacteremia, low hemoglobin and serum albumin levels, prolonged prothrombin time, and elevated liver enzymes. Etiopathogenesis may be attributed to acute glomerulonephritis, rhabdomyolysis, and HUS. Renal complications increase health-care burden that emphasizes the need for alertness for their optimal prevention and management.[28],[29]

  Lymphoreticular Manifestations Top

The antigen is chiefly found in cells of the spleen, thymus, and lymph nodes. In DHF, lymphadenopathy is commonly observed, and splenomegaly is rarely observed in infants. A congestive spleen may have subcapsular hematomas. Splenic rupture, a rare fatal complication, is to be watched for in endemic areas. It can be misdiagnosed as a case of DSS. Splenectomy can be curative.

Lymph node infarction is rare. Malignant lymphoma, being its most common cause, should be ruled out using immunohistochemistry and a 2-year follow-up.[10],[11],[30]

Hemophagocytic lymphohistiocytosis (HLH), an exceptional complication, is a group of clinical syndromes marked by activation and uncontrolled nonmalignant proliferation of T-lymphocytes and macrophages leading to a cytokine storm. The presentation includes fever, hepatosplenomegaly, multiorgan dysfunction, and fulminant pancytopenia resembling severe sepsis. Persistence of fever for more than 7 days, persistent progressive cytopenias, raised ferritin, and organomegaly in dengue patients raise a suspicion of HLH.[10],[11],[30]

  Conclusion Top

Atypical manifestations of dengue are being reported with an increasing frequency and have been shown to contribute to a significant increase in the mortality and morbidity. Hence, these should be included in the case definition of severe dengue. They require early recognition and aggressive treatment even in the absence of shock.

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Conflicts of interest

There are no conflicts of interest.

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