This document provides information on the epidemiology of dengue fever. It discusses that dengue fever is caused by dengue viruses and transmitted by Aedes aegypti and Aedes albopictus mosquitoes. It outlines the clinical manifestations of dengue which can range from an asymptomatic infection to dengue fever and the more severe dengue hemorrhagic fever/dengue shock syndrome. Environmental factors like rainfall, temperature and poor sanitation can contribute to dengue outbreaks by influencing mosquito populations and transmission.
• Is asingle-stranded RNA viruses
that belong to the family
Flaviviridae and the genus
Flavivirus single-stranded RNA
viruses that belong to the family
Flaviviridae and the genus
Flavivirus
6.
THE VECTOR
• Aedesaegypti and Aedes
Albopictus are the two most
important vectors of dengue.
• The symptommay be
asymptomatic or may lead to
classical dengue fever or dengue
haemorrhagic fever with shock
or dengue haemorrhagic fever
without shock.
AGENT
• The denguevirus belongs to a
distinct complex within the
genus flavivirus based on
antigenic and biological
characteristics.
14.
• There arefour virus serotypes
types which are designated as
DENV-1, DENV-2, DENV-3 and
DENV-4.
• Infection with any one serotype
confers a life long immunity to
that serotype.
15.
VECTOR
• Aedes aegyptiand Aedes
Albopictus are the two most
important vectors of dengue.
16.
• Both themosquitoes carry
vectorial competency for dengue
virus (high susceptibility
toinfecting virus, ability to
replicate the virus and ability to
transmit the virus to another
host.
17.
• Aedes aegyptiis a highly
domesticated, strongly
anthropophilic, nervous feeder(it
bites more than one host to
complete one blood meal)
18.
• Also isa discordant species(it
needs more than one feed for
the completion of the genotropic
cycle).
• This habit results in the
generation of multiple cases in
the cities.
19.
TRANSMISSION
• Aedes aegyptimosquito
becomes infective by feeding on
a patient from the day before
onset of the fifth day (viraemia
stage) of illness.
20.
• After anextrinsic incubation
period of 8 to 10 days, the
mosquito becomes infective, and
is able to transmit the infection.
• Once the mosquito becomes
infective it remains so for life.
25.
• The genitaltract of the mosquito
gets infected and transovarian
transmission of dengue virus
occurs when enters fully
developed egg at the time of
oviposition.
• The failureof urban authorities
to provide civil amenities and
poor public health infrastructure
raises the potential for the
vector to breed at high level and
makes the environment
transmission conducive.
• Dengue virusinfection may be
asymptomatic or may cause
undifferentiated febrile illness
(viral syndrome), dengue fever
(DF), Dengue haemorrhagic
Fever(DHF) including Dengue
Shock Syndrome(DSS).
UNDIFFERENCIATED FEVER
• Infants,children and adults who
have been infected with dengue
virus, especially for the first time
may develop a simple
undistinguishable fever from
other viral infection.
50.
• Maculopapular rashesmay
accompany the fever or may
appear during defervescence.
• Upper respiratory and
gastrointestinal symptoms are
common.
51.
CLASSICAL DENGUE FEVER
•The illness is characterized by an
incubation period of 3 to 10 days
(commonly 5 to 6 days).
52.
• The onsetis sudden, with chills
and high fever, intense
headache, muscle and joint
pains which prevent all
movement.
53.
• Within 24hours retro-orbital
pain, particularly on eye
movements or eye pressure and
photophobia develops.
54.
• Other symptomsinclude
extreme weakness, anoroxia,
constipation, altered taste
sensation, colicky pain and
abdominal tenderness, dragging
pain in the inguinal region, sore
throat and general depression
55.
• Fever isusually between 39 and
40 degree C.
• Fever is typically but not
inevitably followed by a
remission of a few hours to 2
days. (Biphasic curve)
56.
• The skineruptions appear in 80%
of cases during the remission or
during the second febrile phase,
which lasts for 1- 2 days.
• The rash is accompanied by
similar but milder symptoms.
57.
• The rashmay be diffuse,
flushing, mottling or fleeting pin
– point eruptions on the face,
neck and chest during the first
half of the febrile period and a
conspicuous rash, that may be
maculopapular or
scarlantiniform on the third or
the fourth day.
58.
• It startson the chest and trunk and
may spread to the extremities rarely
to the face.
• It may be accompanied by itching
and hyperaesthesia.
59.
• The rashlasts for 2 hours to
several days and may be
followed by desquamation.
• Fever lasts for about 5 days,
rarely more than a week after
which recovery is usually
complete although
convalescence may be
protracted.
61.
• Fever lastsfor about 5 days,
rarely more than a week after
which recovery is usually
complete although
convalescence may be
protracted.
65.
DHF
• DHF isa severe form of dengue
fever.
• The course of dengue illness can
be divided into three febrile
phases
FEBRILE PHASE
• Followingan incubation of 4 to 6
days, the illness commonly
begins abruptly with a high fever
accompanied by facial flushing
and headache.
68.
• Anorexia, vomiting,epigastric
discomfort, tenderness at the
right costal margin and
generalized abdominal pain are
common.
69.
• During thefirst phase of the
illness usually resembles classical
DF, but maculopapular rash
usually rubelliform type,is less
common.
• It mayappear early or late in the
course of illness.
• Occasionally, the temperature
may be 40 degree to 41 degree C
and febrile convulsions may
occur particularly in infants.
72.
• A positivetournicate test is the
most common haemorrhagic
phenomenon.
• The test is performed by inflating
a blood pressure cuff to a mid
point between systolic and
diastolic pressure for 5 min.
73.
• The testis considered positive
when 10 or more petechiae per
2.5 x 2.5 cm -1 inch square) are
observed.
• In DHF, the test usually gives a
definite positive with 20
petechiae or more.
74.
CRITICAL PHASE
• Aroundthe time of defervescence,
when the temperature drops to
37.5-38 degree C or less, and
remains below this level, usually
on days 3-7 days of illness, an
increase in capillary permeability in
parallel with increasing
haematocrit levels may occur.
75.
• This marksthe beginning of the
critical phase.
• The period of clinically
significant plasma leakage
usually lasts 24-48 hours.
76.
• Progressive leukopeniafollowed
by a rapid decrease in platelet
count usually precedes plasma
leakage.
77.
• At thispoint patients without an
increase in capillary permeability
will improve, while those with
an increase in capillary
permeability may become worse
as a result of lose of plasma
volume.
78.
• The degreeof plasma loss varies.
• Pleural effusion, mostly on the
right side and ascitis may be
clinically detectable depending
on the degree of plasma leakage
and the volume of fluid therapy.
79.
• Gall bladderoedema has been
found to precede plasma
leakage.
• Hence chest X ray and abdominal
ultrasound can be useful tools
for diagnosis.
80.
• Shock occurswhen a critical
volume of plasma is lost through
leakage.
81.
• It isoften precede by warning
signs of abdominal pain or
tenderness, persistent vomiting,
clinical fluid accumulation,
mucosal bleeding, lethargy and
restlessness, liver enlargement
more than 2 cm and oliguria.
• The bodytemperature may be
subnormal when shock occurs.
• With prolonged shock, the
consequent organ hypo
perfusion results in progressive
organ impairment, metabolic
acidosis and DIV.
85.
• This inturn leads to severe
haemorrhage causing the
haematocrit to decrease in
severe shock.
86.
• Instead ofleucopenia usually
seen during this phase of
dengue, the total white cell
count may increase in patients
with severe bleeding.
87.
• In additionto severe organ
impairment such as severe
hepatitis, encephalitis or
myocarditis and or severe
bleeding may also develop
without obvious plasma leakage
or shock.
88.
• Those whoimprove after
defervescence are said to have
non severe dengue.
89.
• Some patientsprogress to
critical phase of plasma leakage
without defervescence and in
the patients, changes in full
blood count should be used to
guide the onset of the critical
phase and plasma leakage.
90.
• Those whodeteriorate will
manifest warning signs.
• This is called dengue warning
signs.
91.
• Cases withdengue warning signs
will probably recover with early
intravenous rehydration.
• Some cases will deteriorate to
severe dengue.
92.
RECOVERY PHASE
• Ifthe patient survives the 24-48
hour critical phase, a gradual re
absorption of extra vascular
compartment fluid takes place in
the following 48-72 hours.
93.
• General wellbeingimproves,
appetite returns, gastro
intestinal symptoms abate,
haemodynamic status stabilizes
and dieresis ensues.
94.
• Some patientsmay have a rash
of “isles of white in the sea of
red”.
• Some may experience
generalized pruritis.
95.
• Bradycardia andECG changes are
common during this stage.
• The haematocrit stabilizes or
may be lower due to the dilution
effect of reabsorbed fluid.
96.
• WBC countstarts to rise soon
after defervescence., but the
recovery of platelet count is
typically later than that of WBC
count.
97.
• Respiratory distressfrom
massive pleural effusion and
ascitis will occur any time if
excessive IV fluids have been
administered.
98.
• Often dueto fluid therapy
pulmonary oedema or
Congestive Heart Failure may be
reported during the treatment.
• 1. Plasmaleakage that may lead
to shock,
• 2. Severe bleeding and / or,
• 3. Severe organ impairment.
101.
• As denguevascular permeability
progresses, hypovolaemia
worsens and results in shock.
• It usually takes place during
defervescence usually on day 4
or 5 (range 3-7 days) of illness.
• During theinitial stage of shock, the
compensatory mechanism which
maintains a normal systolic pressure
also produces tachycardia and
peripheral vasoconstriction with
reduced skin perfusion, resulting in
cold extremities and delayed
capillary refill time.
104.
• Uniquely, thediastolic pressure
rises towards the systolic
pressure and the pulse pressure
narrows as the peripheral
vascular resistance increases.
105.
• Patients indengue shock often
remain conscious and lucid.
• Inexperienced health personnel
may measure a normal systolic
pressure and misjudge the
critical state of the patient.
106.
• Finally thereis decompensation
and both the disappear abruptly.
• Prolonged hypotensive shock
and hypoxia may lead to multi
organ failure and an extremely
difficult clinical course.
107.
• The patientis considered to have
shock if the pulse pressure is <
20 mm Hg in children or he/she
has signs of poor capillary
perfusion.
• In adults, the pulse pressure of <
20 mm Hg may indicate a more
severe shock.
108.
• Hypotension isusually
associated with prolonged shock
which is often complicated by
major bleeding.
109.
• Patients withsevere dengue may
have coagulation abnormalities,
but these are not sufficient to
cause bleeding.
And at leastone of the
following:
• Supportive serology on simple
serum sample : titre > 1280 with
haemagglutinin inhibition test,
• Comparable IgG titre with enzyme
linked immunosorbant assay ,
115.
• Or testingpositive in IgM
antibody test,
• Occurrence at the same location
and time as confirmed cases of
dengue fever.
116.
CONFIRMED DIAGNOSIS
• Aprobable case with at least one
of the following:
1. Isolation of dengue virus for
serum, CSF, or autopsy samples.
117.
2. Fourfold orgreater increase in
serum IgG (by
haemagglutination inhibition
test) in increase in IgM antibody
specific to dengue virus.
118.
3. Detection ofdengue virus or
antigen in the tissue, serum or
CSF by immunohistochemistry,
immunofluorescence or enzyme-
linked immunosorbant assay.
IS CHARATERRIZED BYALL OF
THE FOLLOWING :
• Acute onset of fever of two to seven
days duration.
123.
• Haemorrhagic manifestations,
shownby any of the following:
Positive tourniquet test,
petechiae, ecchymoses or
purpura, or bleeding from
mucosa –GI tract/injection sites
or other locations.
124.
• Haemorrhagic manifestations,
shownby any of the following:
Positive tourniquet test,
petechiae, ecchymoses or
purpura, or bleeding from
mucosa –GI tract/injection sites
or other locations.
• Objective evidenceof plasma
leakage due to increased vascular
permeability shown by any of the
following: Rising
haematocrit/haemoconcentration >
20% from baseline or evidence of
plasma leakage such as pleural
effusion, ascitis or
hypoproteinaemia/albuminaemia.
128.
DENGUE SHOCK SYNDROME
•Includes al the symptoms of DSS
including:
• Tachycardia, cool extremities,
delayed capillary refill, weak pulse,
lethargy or restlessness, which may
be a sign of reduced brain
perfusion.
129.
• Pulse pressure< 20 mm Hg with
increased diastolic pressure, e.g.
100/80 mm Hg.
• Hypotension by age, defined as
systolic pressure < 80 mm Hg for
those aged < 5 years, 80 or 90
mm Hg for older children and
adults.
131.
LABORATORY DIAGNOSIS
• Rapidand accurate dengue
diagnosis is very important for
the following reasons.
1. Clinical management.
2. Epidemiological
surveillance.
VIRUS ISOLATION
• Isolationof dengue virus from
clinical specimens is possible
provided the specimen is taken
during the first six days of illness
and processed without delay.
138.
• Specimen thatare suitable for
virus isolation are- acute phase
serum, plasma or washed buffy
coat from the patient, autopsy
tissue from fatal case (liver,
spleen lymph nodes and
thymus), and mosquitoes
collected from affected area.
139.
VIRUS NUCLEIC ACID
DETECTION
•Dengue viral genome, which
consists of RNA, can be detected
by reverse transcriptase
polymerase chain reaction (RT-
PCR) assay.
140.
IMMUNOLOGICAL RESPONSE &
SEROLOGICALTESTS
• THE FOLLOWING TESTS ARE AVAILABLE
• Haemagglutination-Inhibition test
(HI).
• Complement Fixation(CF).
VIRAL ANTIGEN DETECTION
•Elisa and dot blot tests are
directed against the
envelop/membrane antigens
and nonstructural protein 1
(NS1) can be detected in both
patients with primary and
secondary dengue up to 6 days
after the onset of illness.
144.
RAPID DIAGNOSTIC TEST
(RDT)
•A number of commercial rapid
format serological test-kits for
anti-dengue IgM and IgG
antibodies are available in the
market.
• The presenceof thrombocytopenia
with concurrent haemoconcentration
differenciates grade I and grade II DHF
from DF.
149.
MANAGEMENT OF
DENGUE FEVER
•For the patients who are able to
tolerate adequate volumes of
oral fluids and pass urine every 6
hours, and do not have any
warning signs adhere to the
following plan.
150.
• Encourage intakeof ORS, fruit
juice and other fluids containing
electrolytes and sugar to replace
losses from fever and vomiting.
151.
• Adequate oralfluid intake may
be able to reduce the number of
hospitalizations.
152.
• Administer Paracetamolfor high
fever if the patient is
uncomfortable.
• The interval of Paracetamol
dosing should not be less than
six hours.
153.
• Tepid spongeif the patient still
has high fever.
• Do not give Asprin (Acetylsalicilic
acid), ibuprofen or other non
steroidal anti inflammatory agents
(NSAIDs) as these drugs may
aggravate gastritis or bleeding.
• Instruct thecare givers that the
patients should be brought to
hospital immediately if any of
the following occur:
1. No clinical improvement.
156.
• 2. Deteriorationaround the time
of defervescence.
• 3. Severe abdominal pain.
• 4.Persistent vomiting or cold and
clammy extremities.
157.
• 5. Lethargyor irritability,
restlessness, bleeding (black
stools or coffee-ground
vomiting).
• 6. Not passing urine for more
than 4-6 hours.
158.
• Patients whoare discharged
should be monitored daily by the
health care providers for
temperature pattern.
• Paracetamol is administered to
keep the temperature below 39
degree celcius.
159.
• Copious amountof fluids should
be give to main fluid and
electrolyte imbalance.
• Patients should be monitored for
initial signs of shock.
160.
• The criticalperiod is during the
transition from the febrile to the
afebrile stage and usually occurs
after the third day of illness
161.
• Serial haematocritdeterminants
are essential guide for
treatment, since they reflect the
degree of plasma leakage and
need for IV therapy.
• A personwith dengue
haemorrhagic fever with
thrombocytopenia and
haemoconcentration presents
with abdominal pain, black tarry
stools, epistaxis, bleeding from
gums and infection.
167.
• All thesepatients should be
observed for signs of shock.
• The critical period for
development of shock is
transition from febrile to afebrile
phase of illness which usually
occurs in the third day of illness.
168.
• A riseof haemoconcentration
indicates the need for IV fluid
therapy.
• Despite this treatment, if the
patient’s Bp falls with a decrease
in urine output, the management
for Grade III/IV DHF/DSS should
be instituted.
169.
• Oral dehydrationshould be given
along with antipyrectics like
paracetamol, sponging.
• Common signsof complications
are observed during the afebrile
phase of DHF.
172.
• Following hospitalization,the
haematocrit, platelet count and
vital signs should be examined to
assess the patient’s condition
and intravenous fluid therapy
should be started.
173.
• The patientrequires a regular
and sustained monitoring.
• If the patient has already
received about 1000 ml of IV
fluid, it should be changed to
colloidal solution preferably.
174.
• Dextran 40/haemacceleor if
haematocrit is decreasing, fresh
whole blood transfusion
ml/kg/hour should be given.
175.
• In caseof persistent shock, after
initial fluid replacement and
resuscitation with plasma or
plasma expanders, the
haematocrit continues to
decline, internal bleeding should
be suspected.
176.
• It isthus recommended to give
fresh whole blood in small
volumes of 10ml/kg/hour for all
patients in shock as a routine
precaution.
• Oxygen should be given to all
patients in shock.
• Loss of(overt blood) blood-10 %
or more of total blood volume-
preferably give whole blood or
components to be used.
• Refractory shock despite
adequate fluid administration
and declining haematocrit.
179.
• Replacement volumeshould be
10ml/kg body weight at a time
and coagulogram should be
done.
• If fluid overload is present
packed cells are to be given.
• In generalthere is no need to
give prophylactic platelet even at
<,20,000cu.mm.
• Prophylactic platelet transfusion
may be given at level of <
10,000/cu.mm.
182.
• Prolonged shock,with
coagulopathy and abnormal
coagulogram.
• In case of systemic massive
bleeding, platelet transfusion
may be needed in addition to
red cell transfusion.
• Absence offever for at least
24 hours without use of anti-
pyretic drugs.
• Return of appetite.
• Visible clinical improvement.
185.
• Good urineoutput.
• Minimum of 2-3 days after
recovery from shock.
• No respiratory distress from pleural
effusion or ascitis.
• Platelet count > 50,000/cu.mm.
186.
DISEASE NOTIFICATION
• Indengue-endemic countries,
cases of suspected, probable and
confirmed dengue should be
notified as soon as possible so
that appropriate health
measures can be initiated.
MOSQUITO CONTROL
• Thevectors of DF and DHF
(A.aegypti) breed in and around
houses and in principle
controlled by individual and
community action, using
antiadult and antilarval
measures.
VACCINES
• So farthere is no satisfactory
vaccine and no immediate
prospect of preventing the
disease by immunization.
197.
OTHER MEASURES
• Isolationunder bed-nets during the
first few days; individual protection
against mosquitoes.
• Other personal prophylactic
measures.
• Environmental measures.