Download Caused by an Aedes mosquito

DENGUE FEVER
JIANG YUANSEN
Part I.Dengue Fever(DF)
Ⅰ. Definition
Acute, febrile infectious disease;
Caused by an Aedes mosquitoborne dengue virus;
Characterized by fever, pain in
various parte of the body, rash,
prostration, lymphadenopathy, and
leukopenia.
Ⅱ. Etiology
Member of the family flavivirus;
Replication in a wide range of
host cells; C6/36 cell line
Low resistance;
Four serotypes;
Cross-immunity
among the four serotypes;
among dengue virus and other
flaviviruses.
Recomplication of dengue virus
x120，000
Ⅲ. Epidemiology
A. Source of infection; acute
patients, individuals with
subclinical infection
B. Vector: Aedes mosquitoes
(Aedes aegypti, A. albopictus)
C. Susceptibility and immunity:
Newly epidemic areas:
Susceptible in both sexes and all
ages.
Endemic areas: involved in
children mainly.
Long-lasting immunity against
the homologous virus infection.
Partial immunity against the
other subtypes.
D.Geographic distribution:
Southeast Asia, the Caribbean,
the Western Pacific Regions.
E. Other epidemiological features:
High incidence in rainy season;
Spread rapidly;
High mobidity;
Distribution of Aedes aegypti (red shaded areas)
in the Americas in 1970,and in 1997
American countries with laboratory-confirmed
hemorrhagic fever (red shaded areas), prior to 1981
and from 1981 to 1997
1978
Fushan
type
4
1979
GuangZhou
type
1
1980
Hainan
type
3
1986
Hainan
type
2
1988
Hainan
type
2
1990
GuangZhou
type
4
1991
GuangZhou
type
1
5.Seasonal distribution:
Guangdong: between May and
October
Hainan: between March and
October
Generally the disease firstly
appears in urban areas, then
rapldly spreads to rural areas
and smaller towns. Transported
by airplane travel.
Ⅳ. Pathogenesis and Pathology
A. Dengue virus
mononuclears
initial viremia
mononuclears
secondary viremia.
B. Dengue virus
IC
Anti-dengue virus Ab
anctivation of complement;
release of vasoactive amines;
increase of vascular permeability;
hemorrhagic spot, petechiae.
Infiltration of mononuclear cells.
edema of endothelial cells.
V. Clinical manifestations
A. Incubation period: 5～8 days.
B. Clinical forms.
a. Typical form.
Fever——sudden onset;
up to 40℃ within 24 hours;
accompanied by headache,
myalgia, prostration;
fleeting erythema, and enlarged
lymph nodes;
lasting 5～7 days;
sometimes saddle-back fever.
Rash ——appearance in the third or
fourth day,
maculopapular or scarletiniform
rash,
begin on the trunk, then spread to
the whole body,
lasting 3-4 days,
with itching, rare desquamation.
Hemorrhage——intestinal
tract,
epistaxis, bloody sputum, skin
petechiae, purpura, etc.
Other
symptoms——anorexia,
nausea, vomiting, sore throat,
depression, abdominal
tenderness, hepatomegaly.
b. Mild form
Low-grade fever, myalgia (not
severe), lymphadenopathy,
absence or few skin rash, no
hemorrhage, lasting 1～4 days.
some be ignored.
c. Severe form.
1. Similar to the typical
form when onset, then
sudden exacerbation.
2. Severe hemorrhage;
Syndrome of meningoencephalitis.
Ⅵ. Complications
A. Acute intra-vascular
hemolysis.
B. Myocarditis.
C. Encephalopathy.
D. Urinemia.
Ⅶ. Diagnosis
1. Epidemiological data.
History of living in or travelling
to epidemic areas; season.
2. Clinical manifestations.
Abrupt onset of fever, pain in
various parts of the body,
bleeding, lymphadenopathy, rash,
etc.
• 3. Laboratory investigations.
A. Leukocytopenia,
thrombocytopenia,
abnormal clotting time.
B. Serological tests: complement fixation
test, hemagglutination inhibition test,
neutralization test.
C. Isolation of virus. C6/36 cell line
D. Molecular biologic assays: nucleic
acid hybridization, polymerase chain
reaction.
Ⅷ. Differential diagnosis
A. Measles.
B. Influenza.
C. Scarlet fever.
D. Epidemic hemorrhagic
fever.
Ⅸ. Treatment and prognosis
1. No specific therapy.
2. Supportive treatment.
3. Symptomatic treatment: high
fever, hemorrhage, secondary
bacterial infection, dehydration.
4. Case fatality: 3/10000, no
sequelae observed.
Ⅹ. Prevention
1. Isolation of patient.
2. Reducing
population.
Aedes
vector
3. Protection of the susceptibles:
individual protection, community
protection, no vaccine available
yet.
Part Ⅱ. Dengue Hemorrhagic Fever
(DHF)
Ⅰ. General consideration.
A. One of the most serious type
of DF.
B. High fever, hemorrhage,
hepatomegaly, circulatory
failure,
thrombocytopenia,
hemoconcentration.
C. Involved in children mainly.
D. Usually observed during
second dengue infections.
E. Often caused by serotype 2.
F. High mortality.
Ⅱ. Pathogenesis.
Three hypotheses:
1. Reinfection.
Dengue virus
IC
activating
Prior Ab
complement.
2. Variation of the virus.
Caused by a more violent viral
strain.
3. Immune enhancement.
Anti-dengue virus Ab
enhancing
virus replication
Virus complexed
with pre-existing Ab
bound to
the Fc receptors of mononuclears
releasing proteases, lymphokines,
and vasoactive amines
activating
complement, coagulation cascade,
dvascular permeability factors
hemorrhage, shock.
Ⅲ. Clinical features.
A. Symptoms acceleration
2～3 days after fever.
B. Hemorrhage, shock.
C. Very low platelet count.
D. Hepatomegaly, observed
in >90%.
Ⅳ. Diagnosis
1. Epidemiologic data.
2. Laboratory
investigations.
3. Clinical manifestations.
4. WHO diagnosis criteria.
Ⅴ. Differential diagnosis
1. Malaria.
2. Bacterial sepsis.
3. Leptospirosis.
4. Epidemic hemorrhagic
fever.
Ⅵ. Treatment
A. Supportive measures.
B. Symptomatic treatment:
high fever, hemorrhage,
shock, dehydration,
coagulation abnormalities,
acidosis.
C. No specific treatment
available.