2. Most rapidly spreading mosquito borne viral
disease.
Major public health concern throughout
tropical & subtropical regions of the world.
Global threat , with major brunt of the
disease in Asia Pacific region (75%).
3. The word ‘dengue’ is derived from the Swahili
phrase Ka-dinga pepo, meaning “cramp- like
seizure”, its origin is from spanish word dengue
meaning fastidious or careful gait due to bone
pains.
The first clinically recognized dengue epidemics
occurred almost simultaneously in Asia, Africa
and North America in the 1780s.
The first clinical case report (dates from 1789 of
1780 epidemic in Philadelphia )is by Benjamin
Rush, who coined the term ‘break bone fever’
because of the symptoms of myalgia and
arthralgia.
The term dengue fever came into use after 1828.
4. GLOBAL SCENARIO:
Global annual incidence: there are about 390
million cases, with(96) 50-100 million
symptomatic cases in recent years, 30 fold
increase in last 30 years
Predominantly dengue seen in Asia, followed
by Latin America & Africa, with clinical
cases likely to represent around 25% of all
dengue virus infections
In thousands of Severe cases 20,000
deaths/year are seen
5. Areas infested with Aedes aegypti
Areas with Aedes aegypti and recent epidemic dengue
5
6. 1.8 Billion population at risk for dengue lives in member
states of WHO South East Asia Region(SEAR) &
Western Pacific Region.
In SEAR 10 countries are endemic for dengue (over 2.2
million in 2010)
CATEGORY-A (THAILAND 30%, INDONESIA 29%,
MYANMAR, )
CATEGORY-B ( INDIA20%, BANGALADESH,
MALDIVES, SRILANKA )
CATEGORY-C (BHUTAN, NEPAL)
CATEGORY-D(DPR KOREA not endemic)
6
7. The annual number of dengue fever cases in India was
around 6 million between 2006 and 2012, about 282
times higher than average.
Of the 36 states/union territories, all 35 (except
Lakshdweep) have reported cases in period of july to
november, with disease peaks after monsoons.
Recurring outbreaks of DF/DHFseen in Andhra
pradesh,Chandigarh,Delhi,Goa,Haryana,Gujarat,
Karnatka,Kerala,Maharashtra,Rajasthan,UP,Puducherry,
Punjab,Tamilnadu, Westbengal.
With changing socioeconomic trends & man made
ecological changes dengue earlier was considered as a
disease of urban areas, has spreaded to rural areas as
well.
8.
9. YEAR CASES DEATHS
2010 28292 110
2011 18860 169
2012 50222 242
2013 75808 193
2014 40571 137
2015 99913 220
2016 129166 245
2017 20664 22 (till July)
NVBDCP DATA LAST FEW YEARS
India also saw a doubling up of cases of dengue
from 2014 to 2015 and the worst hit city was Delhi
with over 1800 cases of the fever.
12. Dengue virus belongs to the genus Flavivirus
in the family Flaviviridae.
Positively single stranded encapsulated
RNAvirus composed of 3 structural protein
genes that encode the nucleocapsid or core
protein, a membrane associated protein , an
enveloped glycoprotein & 7 nonstructural
proteins.
Four antigenically related but distinct
serotypes of the dengue virus :DENV-1,
DENV-2, DENV-3 & DENV-4.
13. All 4 serotypes can cause disease.
Each serotype has many genotypes.
In humans one serotype produces lifelong
immunity against reinfection but only partial &
temporary immunity against the other serotypes.
Each serotype has unique characteristics & can
present with severe manifestations in a particular
population depending upon its interaction with
the host response.
All 4 serotypes can cause severe disease &
epidemics.
14.
15. People of all ages & both genders are at risk of
being infeceted.
Humans are primary host.
Travel to dengue endemic areas is very important
risk factor in disease transmission.
Dengue is transmitted from an infected person to
other by the bite of the female Aedes aegypti
mosquito (urban vector) & the Aedes albopictus
mosquito, Aedes polynesiensis.
Dengue may also get transmitted via infected
blood products and through organ donation.
Vertical transmission from mother to child can
also occur during pregnancy
18. Aedes aegypti mosquito breeds in domestic man
made water receptacles, clean water bodies
whereas Aedes albopictus prefers natural larval
habitats.
Aedes mosquitoes bite during the day and breed
in a wide variety of man-made containers which
are common around human dwellings.
An infection can occur with single bite , after a
blood meal virus infects gut cells of mosquito,
replicates & spread to body tissues ,salivary
gland in next 8-10 days
Seasonal variation in dengue transmission is due
to the survival characteristics of vectors , best
between 30°c at relative humidity of 60-80%.
19. The risk of dengue has increased in recent years due to rapid urbanization,
and deficient water management including improper water storage practices
in urban, peri-urban and rural areas, leading to proliferation of mosquito
breeding sites.
21. Epidemic
Hyperendemic
Epidemic dengue transmission occurs when
virus is introduced into a region as an isolated
event that involves a single viral strain.
Hyperendemic dengue transmission is
characterised by the continuous circulation of
multiple serotypes in an area where a large pool
of succeptible hosts & a competent vector are
constantly present (with/without seasonal
variation). Major risk for DHF.Adult population
usually has antibodies & is immune.
23. Viral isolation in cell culture ,nucleic acid
detection by PCR ,antigen detection &
specific antibodies.
NS1 Antigen :by ELISA & dot blot assays in
acute phase sera. Detected after onset of
illness up to 9 days [usually up to 5 days
have higher sensitivity, later it decreases]
Virus specific antibodies :IgM & IgG
antibodies produced after 5 days of onset
of illness.
24. IgM :undetected after 30 to 90 days
IgM is diagnostic of acute infection in presence of
symptoms [MAC-ELISA test after 5th day ]
IgG : CAN BE DETECTED UPTO 60 YRS.
Indicate past infection.
After primary infection peak levels in blood 14-21
days.
Reinfection levels will peak earlier & titers are
higher .
IgG +ve with 4 fold rising titers in two blood
samples taken 14 days apart is diagnostic
Primary infection : High IgM,Low IgG.
Secondary infection : Low IgM, High IgG
25. IgM
Infection
Virus
Onset of disease
Acute Phase Convalescent Phase
0-7Day 7Day 2~3Months
IgG
Life long
14Day
<ExpressionLevel>
<Time>
J Infect Dis, 1997; 176:322-30.
25
Immunopathogenesis in DF
26.
27. Mosquito bites, DENV penetrates skin of
human being & binds to Langerhans cells
[dendritic] cells in the skin that identifies
pathogen.
Dendritic cell membrane protein & viral
protein binding occurs, it moves to nearest
lymph nodes.
Replication of viral genome on ER forms new
viral proteins & viral RNA is copied.
28. Immature viral particles
are transported to golgi
apparatus & bind with
glycoproteins .
Newly formed virus are
released by exocytosis
from the infected cell &
then are able to enter
other WBC.
The infected cell produce
interferon , cytokines TNF-
a, IL-2, IL-6, IL-8 which leads
to symptoms of disease.
29. Interferons stimulate the immune system.
Antibodies are produced, targeted to
phagocytose the virus & destroy it .
Some non neutralising antibodies bind the
virus less well , deliver them to part of
phagocyte where they start replicating i.e.
termed antibody dependent enhancement.
This leads to DHF /DSS.
Endothelial dysfunction, capillary leakage,
leads to leakage of fluid from blood to body
cavities
Leads to increased viral production in the body
organs like liver & bone marrow
31. Transient increase in capillary permeability due to
endothelial cell dysfunction and widening of tight
junctions.
Cytokine release and complement activation.
Plasma levels of various cytokines are significantly
higher in DHF than in DF.
The cytokines elevated in DHF include TNF alpha,
IL-2, IL-6, IL-8, IL-10, IL-12 and IF-gamma.
Bleeding diathesis
Circulating blood volume decreases, BP falls so
vital organs are affected.
32. Anti-platelet Autoantibodies are formed during
Dengue Virus Infection.
Most of anti-platelet antibodies are cross-
reactive with viral NS-1 protein due to
molecular mimicry between NS-1 and platelet.
It can be competitively inhibited by recombinant
NS-1 protein.
The binding to platelet would lyse the platelet in
the presence of complement or enhance the
ADP-induced platelet aggregation
33. Coagulopathy: decrease prothrombin
complex due to alteration of liver
functions.
Low platelets:
◦ Destruction by autoantibody
◦ Destruction by liver and spleen
◦ Platelet dysfunction
◦ Bonemarrow suppression (leucopenia,
thrombocytopenia)
◦ DIC
◦ Endothelial Platelet aggregation
33
36. DISEASE SPECTRUM : DF/DHF/DSS
ASYMPTOMATIC
SYMPTOMATIC:
Mild
Moderate
(a) with high risk & comorbid conditions
(b) with warning signs & symptoms
Severe
37. After the incubation period of 4 to10 days,
disease is followed by three phases −
febrile,
critical and
recovery
38. Onset of DF with sudden rise in temperature, lasts
for around 4-5 days and is usually associated with
severe frontal headache, myalgia, retro-orbital pain,
flushing and rash.
Rash may be maculopapular or scarlatiniform,
usually appears after 3rd/ 4th day of fever.
A second episode of fever and symptoms can arise,
called “saddleback” pattern.
Potential complications can include:
Dehydration due to decreased fluid intake,emesis,
and increased metabolic state.
Febrile convulsions
39. Occurs after 3-4 days after onset of fever. It is
characterized by hypovolemia and hemorrhagic
manifestations due to increased vascular
permeability and plasma leakage, which persists
for 36-48 hours.
Potential complications can include:
Unrecognized plasma leakage/ hemorrhage
leading to shock.
Pleural effusion
40. Usually occurs after 6-7 days of fever and lasts for
2-3 days.
ECF lost during capillary leakage returns to
circulatory system.
Clinical improvement is seen.
Potential complications can include:
Intravascular fluid overload due to continual
aggressive volume resuscitation during
convalescence
41.
42. DF
An acute febrile illness of 2-7 days duration with
two / more of the following manifestations:
Headache,
Retro-orbital pain,
Myalgia,
Arthralgia,
Rash
Haemorrhagic manifestations
This undifferentiated mild form of DF is without
complications like bleeding, hypotension, organ
involvment. Can give home management.
43. (a)A case with clinical criteria of DF plus:
(b) Haemorrhagic tendencies evidenced by
one or more of the following:
Positive tourniquet test.
Petechiae, ecchymoses, or purpura.
Bleeding from mucosa, gastrointestinal
tract, injection sites or other sites. Plus
(c)Thrombocytopenia (<1,00,000 cells/mm3)
plus
44. (d)Evidence of plasma leakage due to
increased vascular permeability, manifested
by one/more of the following:
a rise in average haematocrit for age & sex
>20%,
a more than 20% drop in haematocrit
following volume replacement treatment
compared to baseline,
signs of plasma leakage pleural effusion,
ascites, hypoproteinemia
47. All the criterias for DF & DHF with evidence
of circulatory failure manifested by rapid &
weak pulse & narrow pulse pressure or
hypotension for age , cold & clammy skin &
restlessness.
48.
49. Virus strain (genotype)
◦ Epidemic potential: viremia level, infectivity
Virus serotype
◦ DHF risk is greatest for DEN-2, followed by DEN-3, DEN-4
and DEN-1
49
Dengue-2 serotype most virulent
Increased severity with secondary infections
Increased risk in children <15 years and elderly.
Greatest risk of DHF in infants.
More severe in females
Less common in malnourished children
50. Infants / old age
Diabetes
Hypertension
Pregnancy
CAD
Haemoglobinopathies
Immunocompromised host
Patients on steroid, anticoagulants, or
immunosupressants
51. Recurrent vomiting
Abdominal pain /tenderness
General weakness/letharginess/restlessness
Mild pleural effusion / ascites
Hepatomegaly
Increased haematocrit > 20%
DHF I & II with minor bleeds
Moderate DF cases need close monitoring
& possibly hospitalisation
52. DF/DHF with significant haemorrage
DHF with shock (DHF III & IV-DSS)
Severe organ involvement (expanded dengue
syndrome)
Severe metabolic disorder
Severe cases need tertiary level care
55. Gastrointestinal system :Acalculous cholecystitis,
Febrile diarrhea, Hepatitis/Fulminant hepatic
failure,acute pancreatitis,bleed from pre-
existing peptic ulcers, spontaneous splenic
rupture
Auto-immune Dysregulated immune response
leading to systemic lupus erythematosus
Kawasaki disease: Reported in a child with
mucocutaneous involvement
Haemophagocytic syndrome :Evidence of
pancytopenia with bone marrow
haemophagocytosis
56.
57. Excellent in DF, with complete recovery being
the norm.
Cases with DHF/DSS who do not die usually
recover without sequels.
58. 1. Assessment:
a. History
b. Examination
c. Investigations and Diagnosis
2. Grading of severity, case classification
3. Management and Disease Notification
4. Prevention of Dengue
59. Obtain complete history:
- Onset of fever/ illness,
- Associated symptoms: diarrhea, respiratory
- Fluid intake and Urine output
- Warning signs
- Prior episodes of dengue
- Travel history, Family history
- Presence of co-existing conditions: infancy,
pregnancy, obesity, diabetes mellitus,
hypertension
61. All patients:
i. Complete Blood count including Hematocrit Leucopenia at
the end of febrile illness. Lymphocytosis with atypical
lymphocytes seen before shock ,thrombocytopenia
ii. Dengue serology for diagnosis:
- NS1 Ag /IgM/IgG
-
iii. Specific tests:
- Blood Sugar Level
- Organ Function tests
- Coagulation profile: PT & APTT are prolonged, low
fibrinogen, elevated FDPs.
Blood culture
62. BP charting
ECG monitoring – if the admission ECG shows any
abnormality a repeat ECG should be conducted
daily to monitor the ongoing cardiac insult and
pulse chart to be maintained to know the rate and
rhythm abnormality.
Cardiac enzymes
- CK MB
- Troponin I
- Troponin T
Echocardiography – to rule out wall hypokinesia or
pericardial effusion
63. Virus isolation to determine serotype of the infecting virus
IgM ELISA test for serologic diagnosis
◦ Rapid test
◦ ELISA
Antigen test –NS1
◦ Rapid test
ELISA
Reverse transcriptase PCR (RTPCR) are being increasingly
used in diagnosis of DV infection.
A single tube nested PCR for detection and serotyping of DV
was developed and used for detection of an infection by two
viruses.
The NASBA (nucleic acid sequence based amplification) assay
is an isothermal RNAspecific amplification assay to dengue
virus detection with sensitivity near that of virus isolation in
cell cultures
64. A dengue virus E/M protein-specific IgM/IgG
ratio can be used to distinguish primary
from secondary dengue virus infections.
Dengue infection is defined as primary if the
IgM/IgG OD ratio is greater than 1.2 or 1.4
The infection is secondary if the ratio is less
than 1.2 or 1.4
65.
66.
67. 67
Epidemic Management
Space mobilization
Staff mobilization
Augmentation of Lab. Services
Diagnosis not required in all cases
Augmentation of blood bank services
increase of blood and blood component
Case management
Individual case management
Diagnosis
Severity assessment
Specific management
68. Currently no effective antiviral are available
for dengue so treatment is clinically
managed with supportive & symptomatic
therapy.
No hemorrhagic manifestations/TT -ve and
patient is well-hydrated: home treatment
Hemorrhagic manifestations or hydration
borderline: outpatient observation center or
hospitalization
Warning signs (even without profound shock)
or DSS: hospitalize
68
69. HOME MANAGEMENT - symptomatic & supportive Rx
Bed rest in acute phase.
Cold sponging keep temperatures below 39* c
Antipyretics paracetamol is preferred [10mg/kg 4
to 6 hourly]. Avoid aspirin, NSAIDS .
Daily clinical Review for disease progression
Adequate oral fluid intake
Watch for Warning signs
Good urine output
Oral fluid & electrolytes in cases with excessive
sweating/ vomiting.
Monitor patient in DHF endemic zone by PC,
hematocrit & clinical improvement
70. Patients treated at home
◦ Instruction regarding danger signs
◦ Consider repeat clinical evaluation
Patients with bleeding manifestations
◦ Serial hematocrits and platelets at least daily
until temperature normal for 1 to 2 days
All patients
◦ If blood sample taken within first 5 days after
onset of fever, need convalescent sample
between days 6 - 30
◦ All hospitalized patients need samples on
admission and at discharge or death
70
71.
72. Treat febrile phase as above .Give IV fluids if
persistent vomiting /refusal to feed.
Critical period is during the transition from
the febrile to the afebrile stage & usually
occurs after the 3rd day of illness.
Rx is guided by serial hematocrits [every 3rd
day] it reflects plasma leakage ,plan iv fluids
accordingly.
73. Case of DF with PC decreased,
hemoconcentration, abdominal pain, black
tarry stools, infection, epistaxis, bleeding
gums should be hospitalized.
Monitor for shock. Hemoconcentration rises
give iv fluids.
In spite of Rx BP falls ,urine output falls,
shock treat as DHF GRADE 3 /4/DSS.
74. Regular & sustained monitoring of patient
needed for vitals, PC, hematocrit, urine
output .
Give 1litre iv fluid & change to colloids
like dextran.
Hematocrit is falling give fresh whole
blood transfusions 10ml/kg /dose given .
If no improvement suspect internal bleed
continue whole blood 10ml/kg/hr. Give
oxygen to all in shock.
75. IV fluids to restore intravascular volume: Ringer
lactate with isotonic saline 10-20ml/kg rapidly over
20 mts , assess case clinically .[caution for brain &
lung edema ]
Dextran40 :polymer of glucose @not to exceed
20ml/kg on day1 / 1oml/kg thereafter [caution for
hypersensitivity , pulmonary edema, glucose
intolerance.
Albumin: shifts fluid from extra cellular space into
circulation, decreases hemoconcentration. Dose 25gm
iv, not>250gm/48hrs.[caution pulmonary edema,
hypersensitivity, protein load]
76.
77.
78. No need to give platelet prophylactically even
at <20,000/cmm.
Prophylactic platelet given at
PC<10,000/cmm in absence of bleeding.
Bleeding present from natural orifices
Prolonged shock with coagulopathy .
Systemic bleeding .
Use FFP/Cryoprecipitate in coagulopathy with
bleeding.
79. Stabilization of dehydration : stop iv fluids
after 24-48 hrs.
IV fluids stopped when hematocrit levels fall
below 40%.
Reabsorption of extravasated fluid starts.
80. 1. Afebrile > 48 hours
2. Clinical improvement
3. Platelet count increasing(>50,000/mm3)
4. No Respiratory distress
5. Stable haematocrit without intravenous
fluids
6.Three days after recovery from shock
81. In immunocompromised patients the course is
usually prolonged. Principles of treatment
remain the same, although close monitoring is
preferrd.
Transplant and Dengue: In post-solid organ
transplant patients, dengue usually follows a
benign course with no evidence of longterm
damage/ rejection episodes.
Thrombocytopenia is more severe in patients
receiving steroids, azathioprine and cyclosporine
concomitantly.
Tacrolimus is found to prolong duration of
thrombocytopenia.
Graft survival and outcome following dengue
fever was not affected in the studies.
82. In studies involving renal transplant recipients,
likelihood of developing severe forms of dengue
was found to be low, probably due to diminished
T-cell responses
dengue in stem cell recipients,sometimes donor-
derived.
Dengue fever complicating patients with aplastic
anemia have been salvaged with stem cell
therapy. However,this disease appears to be
more severe in this population and poor outcome
is reported
83. High index of suspicion for diagnosis is necessary as the
consequences due to dengue infection are multifold.
Complications ranging from miscarriages,
preterm births, haemorrhages in labour, perinatal
deaths, adverse maternal outcomes and vertical
transmission of infection to the fetus.
Serial Haematocrit measurement is crucial for disease
monitoring.
Unless imperative, to avoid induction of labour
/Caesarian section during critical phase, as risk of
bleeding is at its peak during that period.
Baby should be evaluated and monitored post- delivery
as vertical transmission of disease has been observed.
Breastfeeding has been shown to transmit dengue in
a case study, however there are no clear guidelines
on the same.
84.
85. Acalculous cholecystitis due to plasma leakage
leading to gall bladder wall edema is a clinical
manifestation of Dengue Fever. The patient
presents with right hypochondrial pain. The
course is usually self-limiting and surgery is not
warranted unless there is diffuse peritonitis.
There are no guidelines on management of
surgical patients with Dengue. Post-operative
bleeding from surgical sites should be closely
monitored.
86. : Diabetes Mellitus is an independent risk
factor for developing profound
thrombocytopenia and severe forms of
dengue infection.
Studies have shown DM to
be a predictor of mortality in dengue
87. HIV infection alters the natural history of other
infections, often leading to more severe
presentations and worse outcome.
Studies in asia have shown hiv dengue
coinfection had non severe dengue & no signs of
accelerated progression of hiv disease.
Due to transient reduction in hiv viral load during
acute dengue infection
Less hemorrhagic features with more other organ
involvment & severe plasma leakage was seen
88. Zika virus (ZIKV), an emerging arboviral
infection also transmitted by Aedes spp
belonging to genus Flavivirus is an important
public health issue
There is an interplay between host antibody
response to ZIKV and DENV, with concern of
DENV being a cofactor for increasing severity
of Zika infection.
89. WHO targets to reduce the overall dengue
mortality & morbidity by 50% & 25%
respectively, by 2020.
90.
91. Screen Outlets (use 18” screening/mesh wire)
Screen Down spouts from the roof
Seal points of entry of pipe into cistern
Place small fish in your cisterns for these eat
the mosquito larvae (wrigglers)
92. Ensure the cover fits tightly; this prevents
adult mosquitoes from entering and laying
eggs.
Repair broken manhole covers.
Plug overflow holes – located under the cover
of Black Rotoplastic tanks.
93. Change the water-pots holding your plants
or cut flowers at least once a week.
Drain flower pots – flowerpots should have
holes for drainage
Plants should ideally be grown in a mixture
of sand and water or...
Use damp soil instead of water for growing
plants.
Keep the saucers of flower pots dry
94. Throw out the water in your draining pan
under your refrigerator at least once per
week
Clean and scrub your dish drainers at least
once per week
Toilet flush tanks should be inspected and
cleaned at least once per week and always
kept tightly covered
Keep surroundings clean and get rid of
containers which may hold even the tiniest
amount of water e.g. tins, old tires, old
pans, bottles, etc.
95. Punch holes in tins before disposal
Get rid of derelict vehicles
Ornamental pools and fountains should be
regularly drained and scrubbed, chlorinated,
and/or stocked with guppies (fish).
Swimming pools should be kept clean,
filtered, and in good condition.
96. Community members can work together to:
Keep the environment clean e.g. de-bush
empty lots
Keep gullies/ghuts and drains clean
Monitor and destroy any other mosquito
breeding places.
97. People can further protect themselves from
mosquito bites by using:
Mosquito coils
electric vapor mats
Mosquito repellent sprayed on skin
Screen windows and doors
sleep under mosquito proof bed nets
Close windows late evenings and early mornings
Wear protective clothing, such as long sleeve
shirts, long pants, and thick (bobby) socks during
day time. It is also advisable to avoid wearing dark
colours.
98. An ideal vaccine should be able to produce a
protective immune response which is
lifelong in the form of neutralising
antibodies.
It should be equally effective against all 4
serotypes.
99. Live attenuated vaccines , including live
chimeras based on attenuated DENV or
yellow fever virus backbones.
Recombinant vector vaccines , such as those
using adenoviruses.
DNA Vaccine
Inactivated vaccines or subunit proteins
used in combination with adjuvants.
Combination of several technologies
100. This is a live attenuated chimeric yellow fever –
dengue virus tetravalent dengue vaccine
Manufactured by Sanofi Pasteur
Used in dengue endemic countries
Composed of four CYD Vaccine viruses each of
which express the structural genes encoding the
membrane protein (prM) & envelope protein (E)
of the four DENV serotypes.
These structural genes are expressed using a
yellow fever virus strain17D(YFV17D) genetic
backbone, which is a well known live attenuated
flavivirus vaccine for which immunogenecity &
safety are well documented.
101. With 3 main clinical trials it has completed 3
phases globally in 15 countries on 40,000 people
of different ages, geographic & epidemiological
settings ,ethnic & socioeconomic backgrounds.
All these 3 trials have 4 years long follow up
period beyond the 25 mth surveillance period as
recommended by WHO
two phase III trials (Asian trial/CYD14 & Latin
American trial/CYD15), a phase llb (CYD23)trial
in Thai children assessed safety & efficacy
analysis of the vaccine
Vaccine was administered as a 0.5ml dose given
subcutaneously at 0,6 & 12 mths
102. It has demonstrated high levels of
protection against severe disease & DHF in
virologically confirmed cases of dengue
Lower hospitalisation rates for dengue
among participants in the vaccine group
The vaccine protects 2/3rd (65.6%) of the
vaccinated individuals above 9 yr of age
against dengue of any severity & due to any
serotype.
105. In India phase ll trial(CYD47) was conducted
in subjects from 18 – 45 yrs in 5 centres
Delhi, Pune,Ludhiana,Banglore,Kolkata
Vaccine was used in same dose as in global
trials & was well tolerated
It produced antibodies against all 4 serotypes
in both dengue sero+ve & sero-ve Indian
adults
During the trial no cases of severe dengue ,
no deaths & no adverse events were reported
106. In July 2016 WHO has recommended the
introduction of CYD-TDV vaccine in endemic
areas
All other comprehensive dengue control
measures & surveillance are to be continued
with vaccination
107. Vaccine is currently licensed in Mexico, the
Philippines, Brazil, El Salvador, Costa Rica ,
Guatemala, Peru, Paraguay, Indonesia, Thailand,
Singapore, Bolivia & Cambodia for the
prevention of dengue disease caused by all 4
serotypes in endemic areas
The vaccine dossier has been submitted to
various regulatory agencies for approval & use
The Philippines & Brazil have introduced a public
dengue vaccination programme in the dengue
endemic parts of their countries
108. Every government takes the responsibility for keeping public
places free of garbage and “junk” that can become mosquito-
breeding places. Your Government provides us with
information on how we can act to protect yourself, and assist
us as much as possible.
But, no Department of Health, no government, can come into
our homes and workplaces and stop mosquitoes from biting
us. Only we can do this. The government cannot stop the
mosquito from breeding in our flowerpots or debris left
strewn in our yards. Only we can do this.
If we are serious and determined, we can ensure that
mosquitoes have no place to breed more mosquitoes to bite
us and give us dengue fever.
So Search and Destroy mosquito breeding places at home and
work
