Post on 15-Jun-2015
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- 1. By: Kareem Waleed Hamimy6th Year Medical StudentKasr Al Ainy - Cairo University
2. A short introduction Malaria Why? What? How? Who? Where? Pathogenesis Clinical picture 3. Why Malaria ? One of the most common infectiousdiseases & an enormous public-healthproblem. Each year, it causes disease inapproximately 650 million people & kills1-3 million, most of them young childrenin Africa. At least one death every 30 seconds. 4. What is Malaria ? Malaria is a vector-borne infectiousdisease caused by protozoan parasitesof the genus plasmodium. The most serious forms of the diseaseare caused by Plasmodium falciparumand Plasmodium vivax. 5. How? 6. Who? Malaria is a disease whichcan be transmitted topeople of all ages, bittenby a vector Young children andpregnant women in hightransmission areas are ata large risk. 7. Where? 8. Malarial Pathogenesis Hepatic phase Sporozoites infect hepatocytes, multiplyingasexually & asymptomatically for a period of615 days. Then they differentiate into merozoites rupture the hepatocytes escape to bloodstream undetected (wrapping itself in the cellmembrane of the infected host liver cell). 9. Malarial Pathogenesis Erythrocytic phase Within the red blood cells the parasites multiply further, again asexually, periodically breaking out of their hosts to invade fresh red blood cells. p.vivax and p.ovale do not immediately develop into merozoites They develop first to Hypnozoites (dormant form) for 6-12 month leading to long incubation and late relapses 10. Malarial Pathogenesis PfEMP1 Plasmodium falciparum erythrocytemembrane protein 1 Adhesion (protective) protein produced byp.falciparum expressed on surface of RBCscausing it to stick to the walls slowing itslysis in spleen. Block endothelial venules cerebral &placental malaria. Extreme diversity not a good immunetargets. 11. Pathogenesis of clinical picture Prodromal symptoms (influenza like) Hepatic phase where the parasite asexually and asymtomatically multiply. Malarial paroxysms Decreased osmotic fragility rupture ofRBCs Release of metabolites & toxins Release of cytokines such as TNF andinterleukin-1 from macrophages, resulting inchills and high grade fever. 12. Pathogenesis of clinical picture Anemia Febrile paroxysmal hemolysis Immune & Non Immune hemolysis Increased splenic clearance Dyserythropoeisis in BM Drug induced hemolysis Bone marrow Iron sequestration Dyserythropoeisis Dysthrombopoeisis 13. Pathogenesis of clinical picture Spleen Splenomegaly Edema of the pulp RES hyperplasia Increased phagocytic function New guinea Tropical splenomegaly syndrome Liver Hepatomegaly (hepatic phase) Malarial pigments greyish black Falciparum malarial hepatitis 14. Pathogenesis of clinical picture Due to adherence factor of falciparum blocking of venules of organs lead toa lot of manifestations as Cerebral malaria (severeheadache, drowsiness, confusion, coma) Placental malaria (prematuredelivery, intrauterine growth retardationiURD) Dysenteric malaria (abdominalpain, vomiting, GIT bleeding ) 15. Pathogenesis of clinical picture CVS Anemia leads to Hypotension Tachycardia Muffled heart sounds Kidney Immune complexes Nephrotic syndrome Albuminuria Edema hypertension 16. Malarial InfectionsHighSecondaryClinical Grade Infection PictureFever AntiMalarialDrugs 17. Any Questions ?