DENGUE FEVER

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DENGUE FEVER
JIANG YUANSEN
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• Part I.Dengue Fever(DF)
• ?. Definition
• Acute, febrile infectious disease
• Caused by an Aedes mosquito-borne dengue
  virus
• Characterized by fever, pain in various
  parte of the body, rash, prostration,
  lymphadenopathy, and leukopenia.

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• ?. 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.

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Recomplication of dengue virus
x120,000
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• ?. Epidemiology
• A. Source of infection acute patients,
  individuals with subclinical infection
• B. Vector Aedes mosquitoes (Aedes aegypti,
  A. albopictus)

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• 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.

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• D.Geographic distribution
• Southeast Asia, the Caribbean,
• the Western Pacific Regions.
• E. Other epidemiological features
• High incidence in rainy season
• Spread rapidly
• High mobidity

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Distribution of Aedes aegypti (red shaded areas)
in the Americas in 1970,and in 1997
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American countries with laboratory-confirmed
hemorrhagic fever (red shaded areas), prior to
1981 and from 1981 to 1997
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• 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

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• 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.

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• ?. Pathogenesis and Pathology
• A. Dengue virus mononuclears
• initial viremia mononuclears
• secondary viremia.

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• B. Dengue virus
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  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.

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• V. Clinical manifestations
• A. Incubation period 58 days.
• B. Clinical forms.
• a. Typical form.
• Feversudden onset
• up to 40? within 24 hours
• accompanied by headache,
• myalgia, prostration
• fleeting erythema, and enlarged
• lymph nodes

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• lasting 57 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.

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• Hemorrhageintestinal tract, epistaxis, bloody
  sputum, skin petechiae, purpura, etc.
• Other symptomsanorexia, nausea, vomiting, sore
  throat,
• depression, abdominal
• tenderness, hepatomegaly.

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• b. Mild form
• Low-grade fever, myalgia (not severe),
  lymphadenopathy,
• absence or few skin rash, no hemorrhage, lasting
  14 days.
• some be ignored.

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• c. Severe form.
• 1. Similar to the typical form when onset,
  then sudden exacerbation.
• 2. Severe hemorrhage
• Syndrome of meningoencep-
• halitis.

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• ?. Complications
• A. Acute intra-vascular hemolysis.
• B. Myocarditis.
• C. Encephalopathy.
• D. Urinemia.

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• ?. 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.

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• 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.

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• ?. Differential diagnosis
• A. Measles.
• B. Influenza.
• C. Scarlet fever.
• D. Epidemic hemorrhagic
• fever.

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• ?. 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.

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• ?. Prevention
• 1. Isolation of patient.
• 2. Reducing Aedes vector population.
• 3. Protection of the susceptibles individual
  protection, community protection, no vaccine
  available yet.

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• Part ?. Dengue Hemorrhagic Fever
• (DHF)
• ?. General consideration.
• A. One of the most serious type of DF.
• B. High fever, hemorrhage,
• hepatomegaly, circulatory
• failure, thrombocytopenia, hemoconcentration.

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• C. Involved in children mainly.
• D. Usually observed during
• second dengue infections.
• E. Often caused by serotype 2.
• F. High mortality.

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• ?. Pathogenesis.
• Three hypotheses
• 1. Reinfection.
• Dengue virus
• IC activating
• Prior Ab complement.
• 2. Variation of the virus.
• Caused by a more violent viral strain.

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• 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.

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• ?. Clinical features.
• A. Symptoms acceleration
• 23 days after fever.
• B. Hemorrhage, shock.
• C. Very low platelet count.
• D. Hepatomegaly, observed
• in gt90.

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• ?. Diagnosis
• 1. Epidemiologic data.
• 2. Laboratory
• investigations.
• 3. Clinical manifestations.
• 4. WHO diagnosis criteria.

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• ?. Differential diagnosis
• 1. Malaria.
• 2. Bacterial sepsis.
• 3. Leptospirosis.
• 4. Epidemic hemorrhagic
• fever.

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• ?. Treatment
• A. Supportive measures.
• B. Symptomatic treatment
• high fever, hemorrhage,
• shock, dehydration,
• coagulation abnormalities,
• acidosis.
• C. No specific treatment
• available.

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