Tropical Medicine and International Health

doi:10.1111/j.1365-3156.2007.01891.x

volume 12 no 9 pp 10871095 september 2007

Atypical manifestations of dengue

Sameer Gulati and Anu Maheshwari
Maulana Azad Medical College, New Delhi, India

Summary

As the spread of dengue and dengue haemorrhagic fever is increasing, atypical manifestations are also on
the rise, although they may be under reported because of lack of awareness. This review compiles
descriptions of atypical manifestations of dengue, such as dengue encephalitis, dengue myocarditis,
dengue hepatitis and dengue cholecystitis.
keywords dengue fever, dengue haemorrhagic fever, dengue encephalitis, dengue myocarditis, dengue
hepatitis, dengue cholecystitis

Introduction
Dengue, the most common arboviral disease transmitted
globally, is caused by four antigenically distinct dengue
virus serotypes (DEN 1, DEN 2, DEN 3 and DEN 4). The
dengue virus, a member of flavivirus group in the family
Flaviviridae, is a single stranded enveloped RNA virus,
30 nm in diameter, which can grow in a variety of
mosquitoes and tissue cultures. The four serotypes possess
antigens that cross-react with Yellow Fever, Japanese
encephalitis and West Nile viruses. The infection is
transmitted by infected female Aedes mosquitoes. Dengue
is a worldwide condition spread throughout the tropical
and subtropical zones between 30 N and 40 S. It is
endemic in South-East Asia, the Pacific, East and West
Africa, the Caribbean and the Americas (Gubler & Clark
1995; Gubler 1997). Dengue haemorrhagic fever (DHF)
epidemics occur annually with major outbreaks occurring
every 3 years. Factors responsible for dengues spread
include explosive population growth, unplanned urban
overpopulation with inadequate public health systems,
poor vector control and increased international recreational, business and military travel to endemic areas.
Indeed dengue and DHF is fast emerging as a global health
problem.
Dengue infections (Tables 1 and 2) may be asymptomatic, may lead to undifferentiated fever (or viral syndromes), dengue fever or DHF (World Health
Organization, 1997). Mild dengue disease is characterized
by biphasic fever, several types of skin rash, headache,
retro orbital pain, photophobia, cough, vomiting, myalgia,
arthralgia, leukopenia, thrombocytopenia and lymphadenopathy, while DHF is an often fatal disease characterized by haemorrhages and shock syndrome. Other
common symptoms include sore throat, altered taste
sensation, colicky pain and abdominal tenderness, consti-

2007 Blackwell Publishing Ltd

pation, dragging pain in the inguinal region and general

depression (Table 3).
Classical dengue fever is rare among indigenous people
as most of the adults are immune. In these areas both mild
dengue illness and DHF occur mainly in children, but cases
in young as well as older adults have been reported. DHF is
usually associated with secondary dengue infection but can
appear during a primary infection, especially in infants
who possess maternal IgG dengue antibody. With
increasing reports of dengue in adults, neonatal dengue
including DHF because of vertical transmission have been
reported (Chye et al. 1997). A second attack of DHF is
very rare: it has been shown to occur in about 0.5% of
cases in a study over a 16-year period at Childrens
Hospital in Bangkok (Nimmannitya et al. 1990). As
dengue and DHF are assuming global proportions, more
and more atypical presentations appear, which might be
under reported because of lack of awareness. The present
review briefly consolidates the atypical manifestations of
dengue (Figure 1).
Atypical manifestations of dengue
The endothelium is the target of the immunopathological
mechanisms in dengue and DHF. The hallmark is vascular
permeability and coagulation disorders. These mechanisms
can explain varied systemic involvement.
Atypical neurological manifestations of dengue
The relationship between DHF and neurological disturbances was first described in 1976 (Solomon et al. 2000;
Pancharoen & Thisyakorn 2001). Encephalopathy in
DHF is an atypical manifestation and may appear in
various forms, including depressed sensitivity, convulsions,
neck rigidity, pyramidal signs, headache, papilloedema,
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S. Gulati & A. Maheshwari Atypical manifestations of dengue

Table 1 Case definition of dengue fever (http://www.who.int/csr/resources/publications/dengue/Denguepublication/en/)

Probable case

Acute febrile illness with two or more of following

Headache, retro-orbital pain, myalgia, arthralgia, rash, hemorrhagic manifestations, leucopenia.
and
Supportive serology OR Occurrence at the same time and location as other confirmed cases of dengue fever
A case confirmed by laboratory criteria i.e.:
Isolation of dengue virus from serum or autopsy samples; or
Demonstration of fourfold or greater change in reciprocal IgG or IgM antibody titers to one or more dengue
virus antigens in paired serum samples; or
Demonstartion of dengue virus antigen in autopsy tissue, serum or cerebrospinal fluid samples by
immunohistochemistry, immunofluorescence or ELISA; or
Detection of dengue virus genomic sequences in autiopsy tissue, serum or cerebro spinal fluid by polymerase
chain reaction

Confirmed case

Table 2 WHO classification of dengue fever. (http://www.who.int/csr/resources/publications/dengue/Denguepublication/en/)

DF DHF

Grade

DF

DHF
DHF
DHF*

I
II
III

DHF*

IV

Symptoms

Laboratory

Fever with two or more of following:

Headache
Retro orbital pain
Myalgias
Arthralgias
Above signs plus positive tourniquet sign
Above signs plus spontaneous bleeding
Above signs plus circulatory failure
(weak pulse, hypotension, restlessness)
Profound shock with undetectable BP and pulse

Leucopenia, occasionally thrombocytopenia

may be present. No e o plasma loss.

Thrombocytopenia < 100 000; Hct rise 20%

Thrombocytopenia < 100 000; Hct rise 20%
Thrombocytopenia < 100 000; Hct rise 20%
Thrombocytopenia < 100 000; Hct rise 20%

DHF, dengue haemorrhagic fever; DF, dengue fever; DSS, dengue shock syndrome.
*DHF III and IV also called as DSS.

myoclonus and behavioural disorders. Post-infectious

sequelae are mainly amnesia, dementia, manic psychosis,
Reyes syndrome and meningo encephalitis. Neurological
involvement may occur because of intracranial haemorrhage, cerebral oedema, hyponatremia, cerebral anoxia,
fulminant hepatic failure with portosystemic encephalopathy, renal failure or release of toxic products. Pathophysiology of neurological involvement may include the
following factors: direct tissue lesion caused by the virus
because of its neurotropicity, capillary haemorrhage,
disseminated intravascular coagulation and metabolic
disorders (Lum et al. 1996).
A number of patients with DHF and concurrent neurological symptoms have been described as case reports or as
part of minor series of patients with unusual manifestations
(Kho et al. 1981; Nimmannitya et al. 1987; Patey et al.
1993; Row et al. 1996; Thakare et al. 1996; Hommel et al.
1998; Strobel et al. 1999; Solomon et al. 2000; Pancharoen & Thisyakorn 2001). During the 2-year study period
in a prospective casecontrol study carried out in a hospital
in Vietnam, patients with dengue-associated encephalo1088

pathy accounted for 0.5% of all patients admitted with

DHF (Cam et al. 2001). Another study from Vietnam
found dengue viruses in 4.2% of the patients with central
nervous system (CNS) infections (Solomon et al. 2000). In
one of the studies dengue virus was observed in the
cerebrospinal fluid (CSF) in five of six patients presenting
with encephalitis, indicating that the virus may cross the
bloodbrain barrier and directly invade the brain (Lum
et al. 1996). Studies in mice had already shown virusinduced cytokine mediated breakdown of bloodbrain
barrier. Dengue viral antigens have been demonstrated by
immunohistochemistry in CNS biopsies from five fatal
cases of dengue infection associated with encephalitis;
infiltration of infected macrophages could be one of the
pathways by which the virus may enter the brain in
dengue-induced encephalitis (Miagostovich et al. 1997).
Testing for both dengue and Japanese encephalitis antibodies should be carried out in areas endemic for either
because of antigenic cross reactivity (Innis et al. 1989).
Unfortunately, as yet there are no data to show dengue
viral replication in CNS of patients without neurological

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S. Gulati & A. Maheshwari Atypical manifestations of dengue

Table 3 Atypical manifestations of dengue

System

Manifestations

Refrences

Neurological

Encephalopathy

Kho et al. (1981), Row et al. (1996), Thakare et al. (1996),

Cam et al. (2001)
Lum et al. (1996), Hommel et al. (1998)
Luiz Jose de Souza et al. Brazilian Journal of Infectious
Diseases vol.9 no.3 Salvador June 2005
Soares et al. (2006)

Encephalitis aseptic meningitis

Intracranial haemorrhages thrombosis

Gastrointestinal Hepatic

Renal
Cardiac

Respiratory
Musculoskeletal
Lymphoreticular

Mononeuropathies polyneuropathies
GuillaneBarre Syndrome
Myelitis
Hepatitis fulminant hepatic failure
Acalculous cholecystitis
Acute pancreatitis
Febrile diarrhea
Acute parotitis
Hemolytic uremic syndrome
Renal failure
Myocarditis
Conduction abnormalities
Pericarditis
ARDS
Pulmonary hemorrhage
Myositis
Rhabdomyolysis
Spontaneous splenic rupture
Lymph node infarction

Leao et al. (2002)

Lawn et al. (2003)
Sharma et al. (2006), Goh & Tan (2006), Wu et al. (2003)
Jusuf et al. (1998), Chen et al. (2004)
Helbok et al. (2004)
Torres et al. (2000)
Wiersinga et al. (2006)
Hommel et al. (1999), Wiwanitkit (2005a,b)
Promphan W et al. (Promphan et al. 2004)
Veloso et al. (2003), Khongphatthallayothin et al. (2000),
Chuah (1987)
Nagaratnam et al. (1973)
Sen et al. (1999), Thong (1998), Lum et al. (1995)
Setlik et al. (2004), Liam et al. (1993)
Kalita et al. (2005)
Gunasekera et al. (2000), Davis & Bourke (2004)
Imbert et al. (1993), Redondo et al. (1997),
Miranda et al. (2003)
Rao et al. (2005)

Figure 1 Clinical spectrum of dengue

fever (http://www.who.int/csr/resources/
publications/dengue/Denguepublication/
en/)

involvement. The severity of neurological disease caused by

different dengue serotypes has been examined in a number
of studies. Dengue serotypes 2 and 3 have been primarily
reported to cause neurological symptoms (Lum et al. 1996;
Row et al. 1996; Hommel et al. 1998).
Magnetic resonance imaging is superior to computed
tomography scans when demonstrating CNS lesions (Gilman 1998a,b). MRI in a cohort of patients with dengueassociated neurological involvement revealed cerebral

2007 Blackwell Publishing Ltd

oedema in most patients; encephalitis-like changes were

less common; and one patient had intracranial haemorrhage (Cam et al. 2001). Japanese encephalitis co-infection
had MRI findings consistent with this infection (Kalita &
Misra 2006). Globus pallidus involvement has also been
reported (Misra et al. 2006).
Strictly speaking, encephalitis can only be diagnosed on
histological confirmation. However, brain biopsy and
necropsy is not possible in many areas where dengue
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S. Gulati & A. Maheshwari Atypical manifestations of dengue

occurs. Most published postmortem series are on patients

who died from DHF rather than from CNS afflictions and
the lesions have been rather non-specific (oedema, vascular
congestions and focal haemorrhages) (Burke 1968). Dengue virus serotype 4 has been detected by immunohistochemistry and by RT-PCR in inferior olivary nucleus of
medulla and granular layers of cerebellum. Immunoreactivity has been observed in endothelial cells, astrocytes,
neurones and microglia. Extended immunohistochemical
studies have shown the virus positive cells located mostly
with Virchow Robin space of medium size and small veins,
infiltrating the white and grey matter are often close to
neurones displaying cytopathic features (Ramos et al.
1998).
Reported neurological manifestations other than
encephalitis encephalopathy include mononeuropathies,
polyneuropathies, GuillainBarre Syndrome and transverse
myelitis (Patey et al. 1993; Soares et al. 2006). Spinal cord
involvement due to dengue virus including transverse
myelitis (Solomon et al. 2000; Leao et al. 2002), postinfectious myelopathy (Fraser et al. 1978) and acute
disseminated encephalomyelitis (Yamamoto et al. 2002)
are rare. Preferential grey matter involvement was found in
a patient with dengue myelitis (Kunishige et al. 2004). This
grey matter involvement preferentially corresponded to
anterior horn cell involvement similar to poliomyelitis.
However, the findings with sensory levels in this patient
were unlikely to be poliomyelitis. CSFblood barrier
dysfunction has been shown in patients with myelitis and
GuillainBarre Syndrome (Soares et al. 2006).
Atypical gastrointestinal manifestations of dengue
Gastrointestinal manifestations of dengue are increasingly
being identified and reported, such as hepatitis, fulminant
hepatic failure, acalculous cholecystitis, acute pancreatitis,
acute parotitis and febrile diarrhoea. Any patient presenting with acute abdomen in dengue endemic areas should be
evaluated for dengue fever and dengue-related acute
acalculous cholecystitis; acute pancreatitis and acute
hepatitis should be promptly recognized.
Dengue virus antigen is found in Kupfer cells and
sinusoidal lining cells in the liver. Isolation of dengue virus
type I from the liver was made by Nogueira et al. (1988) in
Rio de Janeiro during the 1986 epidemic. Detection of
dengue antigen virus in hepatocytes suggests that such cells
can support viral replication (Miagostovich et al. 2002).
Hepatic manifestations can be characterized by manifestations of acute hepatitis with pain in the hypochondrium,
hepatomegaly, jaundice and raised aminotransferase levels.
In hepatitis the levels of these enzymes peak on the ninth
day after onset of symptoms and gradually return to
1090

normal levels within 3 weeks. Histopathological findings

include centrilobular necrosis, fatty alterations, hyperplasia
of the Kupfer cells, acidophil bodies and monocyte
alteration of the portal tracts. In most cases hepatic
involvement prolongs the clinical course of this selflimiting viral infection but it does not constitute a sign of
worse prognosis (Nimmannitya 1987; Miagostovich et al.
2002). The presence of jaundice in these patients is
multifactorial. It can be due to hepatic aggression caused
by the dengue virus and or hypoxia and tissue ischaemia in
cases of shock. Jaundice occurs in 1262% of patients with
dengue shock syndrome (Mohan et al. 2000). Increased
levels of alkaline phosphatase and bilirubin are found in a
smaller proportion of cases (Kuo et al. 1992). In a study,
1585 serologically confirmed cases of dengue were analysed for changes in aminotransferase levels (De Souza
et al. 2004) and showed that there was a greater elevation
in AST than ALT levels, which may be explained by AST
being released from the damaged monocytes (Chung et al.
1992). This information may be useful in differential
diagnosis of acute hepatitis especially in dengue endemic
areas. Liver damage, and consequently increases in aminotransferase levels, were more frequent among females and
in patients with DHF. Similar findings have been found in a
number of other studies also (Nimmannitya 1987; Kuo
et al. 1992; Mohan et al. 2000).
From 1973 to 1982, the observed hepatic involvement in
dengue infection in Thailand and Malaysia was mild and it
manifested solely as increase in aminotransferase levels.
But after this period several cases of fulminant hepatitis
with high mortality have been reported (Lawn et al. 2003).
Severe haemorrhage, shock, metabolic acidosis and disseminated intravascular coagulation may contribute to
severe changes in liver. It should be remembered that even
chronic liver disease, alcoholic steatonecrosis and hepatotoxic drug use (e.g. salicyclates, acetaminophen etc.) during
dengue infection may predispose to and may even increase
liver injury. Acute liver failure is a severe complicating
factor in dengue infection predisposing to life threatening
haemorrhage, disseminated intravascular coagulation and
encephalopathy. The increase in aminotransferases has
been associated with increased disease severity and might
serve as an early indicator of dengue infection.
Acute pancreatitis is a rare complication of dengue fever.
There are isolated case reports highlighting pancreatic
involvement in dengue fever (Jusuf et al. 1998; Chen et al.
2004). One hundred and forty-eight children with DHF
and abdominal pain were enrolled in a study to look for
sonographic evidence of pancreas involvement. Enlarged
pancreas and increase serum amylase and lipase levels were
found in 29% of the patients (Setiawan et al. 1998).
Pancreas involvement might be due to the direct viral

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S. Gulati & A. Maheshwari Atypical manifestations of dengue

invasion or might be due to hypotension in DHF. We could

not find any case series or report investigating the pancreatic histological findings in dengue to document direct viral
invasion. This might be due to difficulty in obtaining
samples. Thus more definitive studies are required to
determine pathogenesis and which subset of dengue
patients develops pancreatitis.
Acalculous cholecystitis is equally rare in dengue fever
(Beniwal et al. 2000; Wu et al. 2003; Goh & Tan 2006;
Sharma et al. 2006). Patients present with right upper
quadrant abdominal pain, fever, positive Murphy sign,
abnormal liver function tests and thickened gall bladder
wall without stones on abdominal ultrasonography. Differential diagnosis of acalculous cholecystitis other than
dengue fever includes burns, trauma, vasculitis, postsurgical conditions and certain infections such as salmonellosis, leptospirosis, rickettsiosis and cytomegalovirus
infections in immunocompromised patients. The exact
pathogenesis of acalculous cholecystitis is not known, but
prolonged fasting, spasms of ampulla of vater, infection,
endotoxemia, microangiopathy and ischaemia reperfusion
injury have been suggested as possible causes of cholestasis
and increased bile viscosity. The main pathophysiological
changes in dengue fever could be due to increased vascular
permeability causing plasma leakage and serous effusion
with high protein content which causes thickening of gall
bladder wall (Gubler et al. 1998). There is a significant
association between thickening of gall bladder wall and
severity as well as progression of dengue fever (Setiawan
et al. 1995). The course of the disease is usually selflimiting and the gall bladder wall thickness usually returns
to normal. Thus cholecystectomy is usually not advised in
dengue patients unlike other subsets of patients. Rapid
progression of acalculous cholecystitis to gangrene and
perforation has been reported and therefore prompt
recognition and intervention are required for these complications. Surgical intervention is reserved for patients
with diffuse peritonitis.
Two dengue patients have been reported to present with
febrile diarrhoea followed by haemorrhagic skin lesions
(Helbok et al. 2004). Dengue fever was suspected early
mainly because of characteristic accompanying leucopenia
and thrombocytopenia. Both patients had a benign clinical
course. Bilateral parotid gland enlargement in an immunocompetent patient with dengue infection and evidence of
dengue virus in saliva has been described as a unique case
(Torres et al. 2000).
Atypical cardiovascular manifestations of dengue fever
Cardiac manifestations of dengue are uncommon but
cardiac rhythm disorders such as atrioventricular blocks,

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atrial fibrillation, sinus node dysfunction and ectopic

ventricular beats have been reported during episodes of
DHF (Chuah 1987; Khongphatthallayothin et al. 2000;
Veloso et al. 2003; Promphan et al. 2004). Most are
asymptomatic and have a benign self limiting course with
resolution of infection. These arrythmias have been
attributed to viral myocarditis, but an exact mechanism
has not been elucidated. In most of the reported cases there
were no documented electrolyte disturbances or significant
Chest X ray or echocardiography findings. Pericardial
involvement has also been attributed to dengue infection
along with myocarditis (Nagaratnam et al. 1973).
Atypical renal manifestations of dengue
Acute renal failure is rare in dengue fever and it mainly
presents as shock induced acute tubular necrosis. It has
been observed as a complication of dengue fever in French
Guiana (Hommel et al. 1999) and was found to occur in
0.3% of cases in a series of 6154 patients with DHF
(Wiwanitkit 2005a). Descriptions of glomerular changes
observed in DHF are scarce. They include a variety of signs
including IgG, IgM and or C3 deposition and thickening
of the glomerular basement membrane (Boonpucknavig
et al. 1976). Acute renal failure and multiple organ failure
can also be a manifestation of rhabdomyolysis (Gunasekera et al. 2000). The role of immune complex in development of renal failure in dengue infection is still unclear.
Wiwanitkit discovered that the diameter of dengue virus
immunoglobulin complex is much smaller than the diameter of glomerulus. Thus he postulated that immune
complex can be entrapped only if a previous glomerular
lesion causes narrowing of the glomeruluss diameter, and
concluded that the immune complex does not play a
significant role in pathogenesis of renal failure in dengue
infection (Wiwanitkit 2005b). Renal failure because of
haemolytic uraemic syndrome has been described in an
isolated case report where renal biopsy revealed thrombotic microangiopathy with glomerular and arteriolar
microthrombi. Electron microscopy demonstrated presence
of microtubuloreticular structures suggesting a viral infection. This patient was treated with plasmapheresis, haemodialysis and anti-hypertensive drugs (Wiersinga et al.
2006).
Atypical respiratory manifestations of dengue
Dengue haemorrhagic fever can result in acute respiratory distress syndrome (ARDS) (Lum et al. 1995; Thong
1998; Sen et al. 1999). Dengue virus antigen is found in
alveolar lining cells of the lung. Increased permeability of
the alveolar-capillary membrane results in the oedema in
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S. Gulati & A. Maheshwari Atypical manifestations of dengue

the alveoli and interstitial spaces which lead to pulmonary dysfunction (Lum et al. 1995). Dengue shock
syndrome is reported to be third leading cause of ARDS
in the paediatric intensive care setting in a dengue
endemic area (Goh et al. 1998). Early restoration of
adequate tissue perfusion is critical to prevent progression of dengue shock syndrome to ARDS. However,
equal care must be exercised to avoid excessive fluid
infusion after adequate volume replacement because fluid
overload may result in ARDS. This complication requires
early recognition and management for good results.
Pulmonary haemorrhage with or without haemoptysis
has also been reported in DHF (Liam et al. 1993; Setlik
et al. 2004).
Lymphoreticular complications of dengue
Dengue virus antigen is found predominantly in cells of the
spleen, thymus and lymph nodes. In DHF, lymphadenopathy is observed in half of the cases and splenomegaly is
rarely observed in small infants. Splenic rupture and lymph
node infarction in DHF are rare. The spleen which is
frequently congestive, bears sub capsular hematomas in
15% of cases (Bhamarapravati et al. 1967). There are only
three reported cases of splenic rupture in DHF (Imbert
et al. 1993; Redondo et al. 1997; Miranda et al. 2003).
Physicians should be aware of this fatal complication in
areas endemic to dengue. A case of splenic rupture can be
misdiagnosed because of misinterpretation of the shock
syndrome as in a case of dengue shock syndrome dengue
shock syndrome. Splenectomy can be curative.
A case of lymph node infarction in association with
disseminated intravascular infarction in a serologically
proven case of dengue fever has been reported (Rao
et al. 2005). Multiple sections of the infarcted and the
surrounding non-infarcted lymph nodes failed to reveal
any predisposing condition. However the parahilar vessels showed thrombotic occlusion, which must have been
responsible for infarction. As malignant lymphoma is the
commonest cause of lymph node infarction, this disease
should be ruled out using immunohistochemistry. A
2-year follow up is required to rule out development
of malignant lymphoma beyond which the risk is
negligible.
Atypical musculoskeletal complications of dengue fever
Dengue fever has been described classically as break bone
fever as it causes severe muscle, joint and bone pain.
Rhabdomyolysis is not well characterized in DHF. There
are a handful of case reports recognizing this complication
(Gunasekera et al. 2000; Davis & Bourke 2004). Direct
1092

invasion of muscle by virus has not been demonstrated and

the most likely cause appears to be myotoxic cytokines,
particularly TNF. Studies of muscle biopsy specimens have
revealed a range of findings from mild lymphocytic
infiltrate to foci of severe myonecrosis (Malheiros et al.
1993). Davis et al. suggest that urinalysis be performed in
all patients with severe DHF as a screening tool and that
serum creatinine phosphokinase levels be measured if
urinalysis is positive for haeme. This will go a long way in
recognizing this underreported entity. Rhabdomyolysis can
lead to acute renal failure and electrolyte disturbances, if
unrecognized. However, if recognized early, these complications can be easily prevented.
Patients with dengue might present with pure motor
weakness. Creatinine phosphokinase is elevated in most
and electromyography and muscle biopsy is consistent with
myositis. Patients usually show satisfactory improvement
(Misra et al. 2006). Kalita et al. (2005) have pointed out
that in an area endemic with dengue, dengue-related acute
pure motor quadriplegia because of myositis should be
considered in the differential diagnosis of acute flaccid
paralysis. Myalgias associated with dengue fever are
usually short lived, but prolonged myalgias after resolution
of infection have been reported (Finsterer & Konqchan
2006). These myalgias resolved with a course of corticosteroids.
Conclusion
Dengue can have varied and multisystemic presentations.
The atypical manifestations described here might be
unrecognized and underreported. However, it is imperative
to know all these manifestations for clinical diagnosis and
appropriate management, especially given the global health
problem which dengue presents.
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S. Gulati & A. Maheshwari Atypical manifestations of dengue

Corresponding Author: Sameer Gulati, Maulana Azad Medical College, New Delhi, India. E-mail: drsameergulati@gmail.com

Revue: Manifestations atypiques de la dengue

Alors que la propagation de la dengue et de la fie`vre hemorragique de la dengue saccrot, les manifestations atypiques sont egalement en augmentation
bien quelles pourraient etre encore sous rapportees a` cause du manque de prise de conscience. Cette revue compile des descriptions sur les
manifestations atypiques de la dengue, telles que: lencephalite de la dengue, la myocardite de la dengue, lhepatite de la dengue et la cholecystite de la
dengue.
mots cles fie`vre de la dengue, fie`vre hemorragique de la dengue, encephalite de la dengue, myocardite de la dengue, hepatite de la dengue, cholecystite
de la dengue

Revision: Manifestaciones atpicas del dengue

A medida que aumenta la dispersion del dengue y de la fiebre hemorragica del dengue, las manifestaciones atpicas tambien van en aumento, aunque
podran estar por debajo de la cifra real debido a una falta de concienciacion. Esta revision recoge descripciones de manifestaciones atpicas del
dengue, tales como la encefalitis, miocarditis, hepatitis o colecistitis por dengue.
palabras clave fiebre del dengue, dengue hemorragico, encefalitis por dengue, miocarditis por dengue, hepatitis por dengue, colecistitis por dengue

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