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Dengue fever -more than enough information and what you need to know
- 3. Why ???? • Breakbone fever • Biphasic fever
- 4. She is theculprit……
- 6. • Female Aedesaegypti mosquito • Extrinsic incubation period – 10 to 14 days • Temperature may alter the extrinsic incubation period • Remains infective till it dies
- 7.
- 8. TYPES OF STRAINS •DENV 1 • DENV 2 • DENV 3 • DENV 4
- 10. PATHOGENESIS • Primary • Secondary(anamnestic)
- 11. PRIMARY INFECTION • AntiDengue Ig M appears within 2- 3days of defervescence peaking at 2 weeks after the onset of symptoms • Anti Dengue Ig G appears afterwards
- 12. SECONDARY INFECTION • IgG -dominant • Ig M – much lower • No protection against different strain of virus
- 15.
- 16. PATHOPHYSIOLOGY- ADE Activation Heterotypic antibodies -Low concentration - Partial neutralization Main Result: Increase in virus replication and numbers
- 17. PATHOPHYSIOLOGY- ADE Activation Heterotypic antibodies -Low concentration - Partial neutralization Virus uptake - Delivery to Fcɣ receptor cells Main Result: Increase in virus replication and numbers
- 18. ADE Activation Heterotypic antibodies - Low concentration -Partial neutralization Virus uptake - Delivery to Fcɣ receptor cells Replication - Increased viral replication compared to virus alone Main Result: Increase in virus replication and numbers
- 19. Complement Activation byNS1 antigens Anaphylatoxins • NS1- Glycoprotein secreted by dengue infected cells • Activation of innate immune system on endothelial cell surface 1) Classical complement 2) Alternative complement Result: 1) Apoptosis of endothelial cell 2) Inflammation = CYTOKINES!
- 20. COAGULOPATHY due toNS1 Autoantibodies Loss of Plasma Components - Platelets Immune- mediated Destruction of Platelets Glycocalyx Damage
- 21. T-Lymphocyte Pathogenesis Primary Infection DENV- 1 T-cell selection
- 22. T-Lymphocyte Pathogenesis Primary Infection Secondary Infection DENV- 1 T-cell selection DENV- 2 Clonal Expansion Cross- Reaction
- 23. T-Lymphocyte Pathogenesis Primary Infection Secondary Infection DENV- 1 T-cell selection DENV- 2 Clonal Expansion Cross- Reaction TNF-α IFN-ɣ IL-2 CYTOKINE TSUNAMI
- 24.
- 30. Warning signs Abdominalpain Persistent vomiting Clinical fluid accumulation Mucosal bleeds Lethargy/ Restlessness Liver enlargement > 2 cm Laboratory Increased Hematocrit Decreased platelet count
- 33.
- 34. HEMATOCRIT • Hematocrit >20% • Should be monitored every 24hrs.
- 35. THROMBOCYTOPENIA • Less than1lakh cells / cu.mm in onset of critical phase. • Platelet level should be monitored every 24hrs.
- 36. Biochemical profile • PTprolonged • aPTT prolonged • Hyponatremia in critical phase • Low serum albumin levels indicates hemoconcentration
- 37. SERODIAGNOSIS • NS1 viralprotein detection • Four-fold rise in Ig G • Ig M detection
- 38.
- 39. GENERAL MEASURES • Increaseoral fluid intake • Supplementation with IV fluids • Paracetamol • Monitor Platelet count & HCT level daily
- 40. STEPS INVOLVED • Step1:Overall assessment • Step 2:Diagnosis & severity assessment • Step 3:Categorizing into group A,B,C
- 41. STEP 1 • Warningsigns assessment • Physical examination on haemodynamics • Investigations: Haematocrit Platelet count WBC count • Additional test: LFT & RFT X-ray USG abdomen
- 42. STEP 2 Admission Criteria: Any warning sign Hypotension symptoms Bleeding from any site Renal ,Hepatic or CNS involvement Pleural effusion or Ascites Hematocrit rise Platelet count < 50,000 / cu.mm
- 43. STEP 3 • Categorisinginto groups: Group A Group B Group C
- 44. GROUP A –OPD •Encourage fluid intake • Paracetamol • Monitor fluid intake , urine output , fever , bleeding & altered sensorium • Bring back if any of the warning signs present
- 45. GROUP B-INPATIENT • Obtainbase line Haematocrit • Start isotonic fluids • Reassess Clinical status • Repeat HCT • Review Fluid infusion rates till the child is better
- 46. GROUP C -ICU •HCT , Blood Count & Organ function test • Compensated Shock Management • Hypotensive Shock Management
- 49. GROUP C -ICU •Packed cell transfusion if Indicated • Monitor vital signs 4 hrs once • Monitor HCT before & after fluid replacement • Monitor temp,HR,BP,PR.
- 50. FLUID OVERLOAD TREATMENT •Oxygen therapy • Discontinue or reduce IV fluids • Furosemide
- 51. DISCHARGE CRITERIA • Afebrileatleast 24 hrs • Passing urine normally • Improved appetite • No respiratory distress • Platelet count > 50,000 / cu.mm
- 52.
Editor's Notes
- #17 Antibody- dependent enhacement of dengue virus Enhanced virus replication in monocytes in presence of subneutralizing levels IN asymptomatic dengue infection= host develops immunity to serotype of infecting strain Cross-protective antibodies don’t neutralize but help viral uptake with Fcgamma receptor (expressed on monocytes and macrophages) in monocytes (Textbook of critical care) After initial infection : homotypic and neterotypic neutralizing antibodies are produced Over time, heterotypic decrease and homotypic increase Production of heterotypic antibodies that neutralize virus partially Deliver virus to cells in the compartment where it is not destroyed, instead it replicates Response dominated by antibodies to structural precursor-membrane protein (prM) At high concentration, cannot neutralize and highly cross reactive (Cross-reacting antibodies enhance dengue firus infection in humans) (Intrinsic antibody-dependent ehancement of microbial infection in macrophages: disease regulation by immune complexes) (Enhancing cross-reactive anti-prM dominates the human antibody response in dengue infection)
- #18 Antibody- dependent enhacement of dengue virus Enhanced virus replication in monocytes in presence of subneutralizing levels IN asymptomatic dengue infection= host develops immunity to serotype of infecting strain Cross-protective antibodies don’t neutralize but help viral uptake with Fcgamma receptor (expressed on monocytes and macrophages) in monocytes (Textbook of critical care) After initial infection : homotypic and neterotypic neutralizing antibodies are produced Over time, heterotypic decrease and homotypic increase Production of heterotypic antibodies that neutralize virus partially Deliver virus to cells in the compartment where it is not destroyed, instead it replicates Response dominated by antibodies to structural precursor-membrane protein (prM) At high concentration, cannot neutralize and highly cross reactive (Cross-reacting antibodies enhance dengue firus infection in humans) (Intrinsic antibody-dependent ehancement of microbial infection in macrophages: disease regulation by immune complexes) (Enhancing cross-reactive anti-prM dominates the human antibody response in dengue infection)
- #19 Antibody- dependent enhacement of dengue virus Enhanced virus replication in monocytes in presence of subneutralizing levels IN asymptomatic dengue infection= host develops immunity to serotype of infecting strain Cross-protective antibodies don’t neutralize but help viral uptake with Fcgamma receptor (expressed on monocytes and macrophages) in monocytes (Textbook of critical care) After initial infection : homotypic and neterotypic neutralizing antibodies are produced Over time, heterotypic decrease and homotypic increase Production of heterotypic antibodies that neutralize virus partially Deliver virus to cells in the compartment where it is not destroyed, instead it replicates Response dominated by antibodies to structural precursor-membrane protein (prM) At high concentration, cannot neutralize and highly cross reactive (Cross-reacting antibodies enhance dengue firus infection in humans) (Intrinsic antibody-dependent ehancement of microbial infection in macrophages: disease regulation by immune complexes) (Enhancing cross-reactive anti-prM dominates the human antibody response in dengue infection)
- #20 NS1 antigen = glyprotein secreted from dengue-infected cells , necessary for viral replication NS1 binds to heparan sulphate on microvascular endothelial cell = facillitates immune complex formation and complement activation ( Secreted NS1 of dengue virus attaches to the surface of cells via interactions with heparan sulfate and chondroitin sulfate) (Vascular leakage in severe degue virus infections: a potential role for the nonstructural viral protein NS1 and complement) Cross-reactive antibodies to the dengue virus can acivate complement on the surface of endothelial cells Release of C3a and C5a anaphylatoxins has been associated with leakage and shock NS1 = disease severity Able to activate complement leading to local and systemic production of C5a and Sc5n-9 complexes Detected in patients with severe degue NS1= complement attenuation as well through classical and lectin pathways, reduce capacity of C$ = LOCAL activation of complement = activatin of endothelial cells = vascular leakage
- #22 Monocytes – most susceptible cell population to dengue virus infection Production of TNF alpha resulting in endothelial cell activation PRODUCTION OF VASOACTIVE FACTORS T lymphocytes may also exacerbate tissue injury (relevant during secondary dengue infection Found that T cross-reactive memory T lympcytes induced by primary dengue virus infection proliferate more rapidly during secondary exposure to dengue virus (can react to many flavivirus epitopes and other straings of degue) Activation of dengue specific T lymphocytes = increased permeability 1) CD4+ T cell = IFN-gamma, IL2, TNF alpha, TNF B TNF alpha =plasmal leakge and shock IL-2 = induce plasma leakage IFN- gamma = increase TNF alpha production by activating monocytes, interacts with TNF alpha to activate endo cells, enhance the presentation of viral antigens to T cells (in crease expression of II HLA antigens and increased expression of IGG receptors augments uptake of virus in monocytes) Activated T cells – target cell lysis, able to lyse dengue virus-infected cells, lysed infected autologous cells, also lyse uninfected cells by interaction between FasL on T cell and Fas on target cell) TNF alpha with more severe disease IFN-gamma elevation more frequently seen in DHF Soluable CD4, CD8, and IL2 receptors and TNF receptors in plasma = immune activation Saw elevation two days before plasma leakage
- #23 Monocytes – most susceptible cell population to dengue virus infection Production of TNF alpha resulting in endothelial cell activation PRODUCTION OF VASOACTIVE FACTORS T lymphocytes may also exacerbate tissue injury (relevant during secondary dengue infection Found that T cross-reactive memory T lympcytes induced by primary dengue virus infection proliferate more rapidly during secondary exposure to dengue virus (can react to many flavivirus epitopes and other straings of degue) Activation of dengue specific T lymphocytes = increased permeability 1) CD4+ T cell = IFN-gamma, IL2, TNF alpha, TNF B TNF alpha =plasmal leakge and shock IL-2 = induce plasma leakage IFN- gamma = increase TNF alpha production by activating monocytes, interacts with TNF alpha to activate endo cells, enhance the presentation of viral antigens to T cells (in crease expression of II HLA antigens and increased expression of IGG receptors augments uptake of virus in monocytes) Activated T cells – target cell lysis, able to lyse dengue virus-infected cells, lysed infected autologous cells, also lyse uninfected cells by interaction between FasL on T cell and Fas on target cell) TNF alpha with more severe disease IFN-gamma elevation more frequently seen in DHF Soluable CD4, CD8, and IL2 receptors and TNF receptors in plasma = immune activation Saw elevation two days before plasma leakage
- #24 (Original antigenic sin in dengue revisited) Monocytes – most susceptible cell population to dengue virus infection Production of TNF alpha resulting in endothelial cell activation PRODUCTION OF VASOACTIVE FACTORS T lymphocytes may also exacerbate tissue injury (relevant during secondary dengue infection Found that T cross-reactive memory T lympcytes induced by primary dengue virus infection proliferate more rapidly during secondary exposure to dengue virus (can react to many flavivirus epitopes and other straings of degue) Activation of dengue specific T lymphocytes = increased permeability 1) CD4+ T cell = IFN-gamma, IL2, TNF alpha, TNF B TNF alpha =plasmal leakge and shock IL-2 = induce plasma leakage IFN- gamma = increase TNF alpha production by activating monocytes, interacts with TNF alpha to activate endo cells, enhance the presentation of viral antigens to T cells (in crease expression of II HLA antigens and increased expression of IGG receptors augments uptake of virus in monocytes) Activated T cells – target cell lysis, able to lyse dengue virus-infected cells, lysed infected autologous cells, also lyse uninfected cells by interaction between FasL on T cell and Fas on target cell) TNF alpha with more severe disease IFN-gamma elevation more frequently seen in DHF Soluable CD4, CD8, and IL2 receptors and TNF receptors in plasma = immune activation Saw elevation two days before plasma leakage