DENGUE FEVER

JIANG YUANSEN

Part I.Dengue Fever(DF)

Ⅰ

. 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.

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 1979 GuangZhou 1980 1986 1988 1990 1991 Hainan Hainan Hainan GuangZhou GuangZhou type type type type type type type 4 1 3 2 2 4 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 rash, or scarletiniform 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 meningoencep halitis.

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, abnormal clotting time.

thrombocytopenia, 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 virus replication enhancing 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.