logging in or signing up Malaria - A Review drmdsadiq Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 618 Category: Education License: All Rights Reserved Like it (0) Dislike it (0) Added: May 29, 2010 This Presentation is Public Favorites: 1 Presentation Description No description available. Comments Posting comment... By: krishnendhu (21 month(s) ago) this ppt is realy informative Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript In the Name of God, Most Gracious, Most Merciful : In the Name of God, Most Gracious, Most Merciful MALARIA : MALARIA Etiopathogenesis, Clinical features & Diagnosis - A Review - Dr. Mohammed Sadiq Azam PG – M : I ETIOLOGY : ETIOLOGY Vector: Female Anopheles mosquito Parasite: Genus Plasmodium Species: P.vivax, P.falciparum, P.ovale, P.malariae Slide 4: Picture Slide 5: P. ovale P. malariae P. falciparum P. vivax Who am I ?? PLASMODIUM: LIFE CYCLE : PLASMODIUM: LIFE CYCLE EPIDEMIOLOGY : EPIDEMIOLOGY Agent – Host – Environment P.falciparum: Africa, New Guinea, Haiti P.vivax: Central America Vivax=Falciparum: India, South America, Eastern Asia, Oceania P.malariae: Most endemic areas, sub-Saharan Africa P.ovale: < 1% isolates EPIDEMIOLOGY : EPIDEMIOLOGY Defined in terms of: Parasitemia rates Spleen palpable rates (children 2-9y) Hypoendemic (<10%) Mesoendemic (11-50%) Holoendemic (51-75%) Hyperendemic (>75%) EPIDEMIOLOGY - AGENT : EPIDEMIOLOGY - AGENT Stable Transmission Unstable Transmission Determinants of transmission: Number (= Density) Human biting habits (square of) Longevity of anopheline mosquitoes (10th power of 1 day survival) EPIDEMIOLOGY - AGENT : EPIDEMIOLOGY - AGENT Entomologic inoculation rate: No. of sporozoite positive mosquito bites per person per year Most common measure of malaria transmission Rate: <1 (Lat Am/SEAR) to >300 (trop Africa) ERYTHROCYTE CHANGES : ERYTHROCYTE CHANGES Degrades Hb – produces Haemozoin Alters RBC membrane – exposes cryptic surface Ag – inserts new proteins Irregular, more antigenic, less deformable RBCs Shorter RBC survival ERYTHROCYTE CHANGES : ERYTHROCYTE CHANGES P.falciparum: Membrane protuberances “Knobs” (12-15h) Strain spf erythrocyte membrane adhesie protein : Pf EMP1 – Cytoadherance ERYTHROCYTE CHANGES : ERYTHROCYTE CHANGES P.falciparum: Vascular receptors: ICAM -1 (Brain), Chondrotin sulfate B (Placenta) & CD36 Rosettes vs. Agglutination Sequestration – impede / escape / hideout HOST FACTORS : HOST FACTORS Non specific defense mechanisms Removal of RBC exaggerated Activation of macrophages, release of proinflammatory cytokines Temp ≥ 40oC damage mature parasites Effect to synchronize the cycle – spikes and rigors Characteristic periodicity – SEEN NO MORE. HOST FACTORS : HOST FACTORS Diseases decreasing risk: Sickle cell disease (6x risk) Ovalocytosis Thalassemia G6PD deficiency HOST FACTORS : HOST FACTORS Factors retarding development of CMI: Absence of MHC Ag on surface of infected RBC – no T cell recognition Malaria Ag specific immune unresponsiveness Enormous strain diversity VACCINE SOON??? : VACCINE SOON??? NO THANK U! Why?? Complexity of immune response Sophistication of parasite’s escape mechanisms Lack of a good in vitro correlate with clinical immunity CLINICAL FEATURES : CLINICAL FEATURES History: Non specific symptoms Nausea, vomiting, orthostatic hypotension. Malarial paroxysms : fever spikes, chills & rigors – if + ? P.vivax/ P.ovale Irregular fever / tachycardia / delirium Generalised seizures CLINICAL FEATURES : CLINICAL FEATURES Examination: Mild anaemia Palpable spleen Nonimmune individuals: several days Endemic areas: Healthy individuals Mild Hepatomegaly (esp. Children) Mild jaundice ( P.falcipaum, resolves in 1-3 wks) NO RASH (? Petechiae : rarely in severe falci. malaria) DIAGNOSIS : DIAGNOSIS Main stay: Demonstration of asexual forms of parasite in stained P/S. Stains: Giemsa (pH 7.2), Wright’s, Field’s or Leishman’s. Thin (fixed) smear / Thick (non-fixed) smear. DIAGNOSIS : DIAGNOSIS Labs: Normocytic normochromic anaemia WBC: Normal Slight monocytosis, lymphopaenia, eosinopaenia with reactive lymphocytosis & eosinophilia in wks following acute infection. ESR, plasma viscocity, CRP & other Acute phase proteins: DIAGNOSIS : DIAGNOSIS Labs: Platelet count: ~ 1,00,000/µl Severe infections: PT / PTT / severe thrombocytopaenia Antithrombin III: (even in mild infections) Electrolytes, BUN, Creatinine: Normal Hypergammaglobinemia: immune & semi-immune cases. CUE: Normal THE LAST WORD : THE LAST WORD Inspite of promising new control & research initiative, it remains today as it has forever been: A heavy burden on tropical communities A threat to non endemic countries A danger to travellers You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.
Malaria - A Review drmdsadiq Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 618 Category: Education License: All Rights Reserved Like it (0) Dislike it (0) Added: May 29, 2010 This Presentation is Public Favorites: 1 Presentation Description No description available. Comments Posting comment... By: krishnendhu (21 month(s) ago) this ppt is realy informative Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript In the Name of God, Most Gracious, Most Merciful : In the Name of God, Most Gracious, Most Merciful MALARIA : MALARIA Etiopathogenesis, Clinical features & Diagnosis - A Review - Dr. Mohammed Sadiq Azam PG – M : I ETIOLOGY : ETIOLOGY Vector: Female Anopheles mosquito Parasite: Genus Plasmodium Species: P.vivax, P.falciparum, P.ovale, P.malariae Slide 4: Picture Slide 5: P. ovale P. malariae P. falciparum P. vivax Who am I ?? PLASMODIUM: LIFE CYCLE : PLASMODIUM: LIFE CYCLE EPIDEMIOLOGY : EPIDEMIOLOGY Agent – Host – Environment P.falciparum: Africa, New Guinea, Haiti P.vivax: Central America Vivax=Falciparum: India, South America, Eastern Asia, Oceania P.malariae: Most endemic areas, sub-Saharan Africa P.ovale: < 1% isolates EPIDEMIOLOGY : EPIDEMIOLOGY Defined in terms of: Parasitemia rates Spleen palpable rates (children 2-9y) Hypoendemic (<10%) Mesoendemic (11-50%) Holoendemic (51-75%) Hyperendemic (>75%) EPIDEMIOLOGY - AGENT : EPIDEMIOLOGY - AGENT Stable Transmission Unstable Transmission Determinants of transmission: Number (= Density) Human biting habits (square of) Longevity of anopheline mosquitoes (10th power of 1 day survival) EPIDEMIOLOGY - AGENT : EPIDEMIOLOGY - AGENT Entomologic inoculation rate: No. of sporozoite positive mosquito bites per person per year Most common measure of malaria transmission Rate: <1 (Lat Am/SEAR) to >300 (trop Africa) ERYTHROCYTE CHANGES : ERYTHROCYTE CHANGES Degrades Hb – produces Haemozoin Alters RBC membrane – exposes cryptic surface Ag – inserts new proteins Irregular, more antigenic, less deformable RBCs Shorter RBC survival ERYTHROCYTE CHANGES : ERYTHROCYTE CHANGES P.falciparum: Membrane protuberances “Knobs” (12-15h) Strain spf erythrocyte membrane adhesie protein : Pf EMP1 – Cytoadherance ERYTHROCYTE CHANGES : ERYTHROCYTE CHANGES P.falciparum: Vascular receptors: ICAM -1 (Brain), Chondrotin sulfate B (Placenta) & CD36 Rosettes vs. Agglutination Sequestration – impede / escape / hideout HOST FACTORS : HOST FACTORS Non specific defense mechanisms Removal of RBC exaggerated Activation of macrophages, release of proinflammatory cytokines Temp ≥ 40oC damage mature parasites Effect to synchronize the cycle – spikes and rigors Characteristic periodicity – SEEN NO MORE. HOST FACTORS : HOST FACTORS Diseases decreasing risk: Sickle cell disease (6x risk) Ovalocytosis Thalassemia G6PD deficiency HOST FACTORS : HOST FACTORS Factors retarding development of CMI: Absence of MHC Ag on surface of infected RBC – no T cell recognition Malaria Ag specific immune unresponsiveness Enormous strain diversity VACCINE SOON??? : VACCINE SOON??? NO THANK U! Why?? Complexity of immune response Sophistication of parasite’s escape mechanisms Lack of a good in vitro correlate with clinical immunity CLINICAL FEATURES : CLINICAL FEATURES History: Non specific symptoms Nausea, vomiting, orthostatic hypotension. Malarial paroxysms : fever spikes, chills & rigors – if + ? P.vivax/ P.ovale Irregular fever / tachycardia / delirium Generalised seizures CLINICAL FEATURES : CLINICAL FEATURES Examination: Mild anaemia Palpable spleen Nonimmune individuals: several days Endemic areas: Healthy individuals Mild Hepatomegaly (esp. Children) Mild jaundice ( P.falcipaum, resolves in 1-3 wks) NO RASH (? Petechiae : rarely in severe falci. malaria) DIAGNOSIS : DIAGNOSIS Main stay: Demonstration of asexual forms of parasite in stained P/S. Stains: Giemsa (pH 7.2), Wright’s, Field’s or Leishman’s. Thin (fixed) smear / Thick (non-fixed) smear. DIAGNOSIS : DIAGNOSIS Labs: Normocytic normochromic anaemia WBC: Normal Slight monocytosis, lymphopaenia, eosinopaenia with reactive lymphocytosis & eosinophilia in wks following acute infection. ESR, plasma viscocity, CRP & other Acute phase proteins: DIAGNOSIS : DIAGNOSIS Labs: Platelet count: ~ 1,00,000/µl Severe infections: PT / PTT / severe thrombocytopaenia Antithrombin III: (even in mild infections) Electrolytes, BUN, Creatinine: Normal Hypergammaglobinemia: immune & semi-immune cases. CUE: Normal THE LAST WORD : THE LAST WORD Inspite of promising new control & research initiative, it remains today as it has forever been: A heavy burden on tropical communities A threat to non endemic countries A danger to travellers