my presentation on dengue fever for pediatric seminar.

1. PRESENTED BY: SITI NUR HAMIZAH HAMIDON
DENGUE FEVER

2. INTRODUCTION
 Ac. Febrile illness
 Viruses belonging to Flaviviridae family
 Characterized by:
 Biphasic fever
 Myalgia
 Arthralgia
 Rash

3. EPIDEMIOLOGY
 Endemic in Africa, America, Eastern
Mediterranean, SEAR, & Western Pacific.
 During epidemics- attack rates may reach
80-90%.
 Est 500000 cases of DHF requires
hospitalization each year.
 With modern intensive support therapy DHF
case fatality rate are reduced to <1%.

5. SCENARIO IN MALAYSIA
 Increasing trend of DF&DHF.
 Incidence rate in 1999 = 44.3 cases/100000 population
 Incidence rate in 2007 = 181 cases/100000 population.
 National target = <50cases/100000 population
 Incidence rate is higher in age group >15 yrs. Highest
among working & school going age group.
 Case fatality rate both DF&DHF remain well below 0.3%
since 2002.
 70-80% cases were reported from urban areas prob due
to high density of population and rapid development
activities which favour transmission.

7. VIRUS
 4 serotypes of dengue viruses
 DENV-1
 DENV-2
 DENV-3
 DENV-4
 Arbovirus-from family Flaviviridae.
 Single stranded RNA virus. Spherical, 50nm
diameter, envelop protein bears epitopes that
are unique to serotype.

8. All four serotypes can be isolated at any one time but the predominant circulating
dengue virus will show sinusoidal pattern.

9. TRANSMISSION
 Transmitted to humans through bites of
infective female Aedes mosquitoes.
 Aedes aegypti
 Aedes albopictus
 Humans are the main amplifying host.
 Incubation period 5-8 days.
 The virus circulates in the blood of infected
humans for 2-7 days, at approximately the
same time they have fever.

10. Aedes aegypti
Aedes albopictus

11. PATHOPHYSIOLOGY OF INFECTION & ITS
CONSEQUENCES.
 Dengue viral infection asso with
thrombocytopenia, the cause is molecular
mimicry b/w dengue virus proteins &
endogenous self-proteins.
 Generation of antibodies against dengue virus
proteins which cross-react with platelet surface
proteins and thus cause thrombocytopenia.
 There is activation of blood clotting and
fibrinolytic pathways.
 Mild DIC, liver injury & thrombocytopenia
together contribute to hemorrhagic tendency.

12.  DHF
 Sequential infection with any 2 of the 4 serotpes
og dengue virus result in DHF/DSS in endemic
area.
 How 2nd dengue infection causes severe disease
and why only some patients get severe disease
remains unclear.
 Suggested that residual Ab produced during 1st
infection are able to neutralize a second viral
infection with the same serotype.
 When no neutralizing Ab are present (i.e:
infection due to other serotype), the second
infection is under the influence of enhancing Ab
& the resulting infection and disease are severe.

13.  Serotype cross reactive antibodies generated from
previous primary infection with particular dengue
viral serotype are not highly specific for the other
serotypes involve in secondary infections.
 Hence, the bind to virion but do not neutralize them,
and instead increase their uptake by cells like tissue
dendritic cells, monocytes and macrophages leading
to more rapid activation and proliferation of memory
T-cells
 Cytokines produces by activated T-cells lead to
pathogenesis of DHF/DSS.
 Cytokines causes vascular compromise and
hemorrhage. The endothelial cell dysfunction is
manifested by diffuse increase in capillary
permeability microvascular
leakage,hemoconcentration, and circulatory
insufficientcy.

14. CLINICAL COURSE OF DENGUE INFECTION
 After the incubation period, the illness begins
abruptly and will be followed by 3 phases.
 Febrile phase
 Critical phase
 Recovery phase.

16. NEW CLASSIFICATION OF DENGUE
Non-severe dengue Non-severe dengue with Severe dengue
without warning signs warning signs
Probable dengue •Abdominal pain/ •Severe plasma leakage
•Live in/travel to endemic tenderness leading to
area •Persistent vomiting •Circulatory compromise/
•Fever & 2 of the following •Clinical fluid accumulation shock /DSS
criteria: •Mucosal bleed (tachy,cold&clammy
•Nausea&vomiting •Lethargy & restlessness extremities, cap refill
•Rash •Liver enlargement >2cm time >3sec, undetectable
•Aches&pains •Lab: incrase haematocrit pulse, late phase:
•Tourniquet test concurrent with rapid unrecordable BP)
positive decrease in platelet count. •Fluid accumulation with/
•Leucopenia without respiratory
•No warning sign distress.
Laboratory-confirmed •Severe bleeding
dengue. •Severe organ involvement.
•Liver: AST/ALT >/= 1000
•CNS: impaired
consciousness
•Heart & other organs.

18. TOURNIQUET TEST

19. LABORATORY INVESTIGATIONS
 Disease monitoring lab test:
 White cell count
 Early febrile phase usually normal but decrease rapidly as disease
progresses.
 Haematocrit
 Rising HCT is a marker of plasma leakage and helps to differentiate
b/t DF & DHF.
 May be masked in patients with concurrent significant bleeding &
those who received fluid therapy.
 Setting pt’s baselineHCT in early febrile phase will be useful in
recognition of a rising HCT.
 Thrombocytopenia
 Early febrile phase- platelet count usually w/in normal range.
 Decrease repidly as disease progresses to late febrile phase.
 May remain low for first few days of recovery.
 LFT
 Greater elevation of AST as compared to ALT.
 Degree of elevation higher in DHF compared to DF.

20.  Diagnostic test:
 Antibody detection (serology)
 Haemagglutination Inhibition Test
 Dengue IgM test
 Indirect IgG ELISA test

21.  Virusisolation
 Detection of virus genetic materials (PCR)
 Detection of dengue virus protein (NS1 Antigen)
 False positive dengue serology :
 Cross reaction with:
 other flaviviris – Japanese Encephalitis
 non-flavivirus – malaria, leptospirosis, toxoplasmosis, syphilis
 Connective issue disease – rheumatoid arthritis.

22. STEPWISE APPROACH

25. CRITERIA FOR ADMISSION

26. TREATMENT
 Symptomatic treatment + aggressive,
supportive fluid therapy

27.  Fever (antipyretic; Paracetamol)
: Max dose: 60mg/kg daily in divided doses
oral or IV (15mg/kg every 6h)
Rectal: 20mg/kg every 8h
 Avoid salicylates & NSAIDs (bleeds)
 Monitoring.
 DIC: can give FFP, platelet concentrates

30. CLINICAL & LAB CRITERIA FOR PT WHO CAN BE
TREATED AT HOME.

35. DIFFERENTIAL DIAGNOSIS OF DENGUE FEVER

36. PROGNOSIS
 Left untreated: mortality rate can be upto 40-
50%
 Early recognition & appropriate fluid therapy
1-5%
 Early detection of shock → excellent
prognosis
 Prolonged shock + cold extremities,
unrecordable BP → difficult

37. PREVENTION
 No approved vaccines approach yet
 Integrated Vector Control programme
a. Advocacy, social mobilization, legislation to ensure
public health bodies & communities are strengthened
b. Collaboration of health & other sectors
c. Integrated approach to disease control with maximum
use of resources
d. Evidence-based decision making
e. Capacity building to ensure adequate response
 Eliminate its habitats (empty water container/ +
insecticides)
 Reducing open collection of water
 Environmental modification
 Mosquito netting & insect repellent

38. REFERENCE
 Ghai Essential Pediatrics, 7th Edition, CBS publication, page 196-
200.
 Medicine Prep Manual for Undergraduates, 4th Edition, Elsevier
Publication, page 751-755.
 Dengue haemorrhagic fever: diagnosis, treatment,
prevention and control. 2nd edition. Geneva : World Health
Organization. :
http://www.who.int/csr/resources/publications/dengue/Denguepub
lication/en/index.html
 Dengue- Guidelines for Diagnosis, Treatment, Prevention &
Control. New Edition 2009. world Health Organization:
http://whqlibdoc.who.int/publications/2009/9789241547871_eng.p
df
 http://www.who.int/csr/disease/dengue/en/
 Clinical Practice Guidelines- Management of Dengue Infection in
Adults. Revised 2nd Edition. Ministry of Health Malaysia.: http:
www.moh.gov.my