Malarial pathogenesis

1. Malaria l Pathogenesis By: Kareem Waleed Hamimy 6 th Year Medical Student Kasr 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 infectious diseases & an enormous public-health problem. Each year, it causes disease in approximately 650 million people & kills 1-3 million, most of them young children in Africa. At least one death every 30 seconds.

4. What is Malaria ? Malaria is a vector-borne infectious disease caused by protozoan parasites of the genus plasmodium. The most serious forms of the disease are caused by Plasmodium falciparum and Plasmodium vivax .

5. How?

6. Who? Malaria is a disease which can be transmitted to people of all ages, bitten by a vector Young children and pregnant women in high transmission areas are at a large risk.

7. Where?

8. Malarial Pathogenesis Hepatic phase Sporozoites infect hepatocytes, multiplying asexually & asymptomatically for a period of 6–15 days. Then they differentiate into merozoites  rupture the hepatocytes  escape to blood stream undetected (wrapping itself in the cell membrane 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 erythrocyte membrane protein 1 Adhesion (protective) protein produced by p.falciparum expressed on surface of RBCs causing it to stick to the walls slowing its lysis in spleen. Block endothelial venules cerebral & placental malaria. Extreme diversity  not a good immune targets.

11. Pathogenesis of clinical picture Prodromal symptoms (influenza like) Hepatic phase where the parasite asexually and asymtomatically multiply. Malarial paroxysms Decreased osmotic fragility  rupture of RBCs Release of metabolites & toxins Release of cytokines such as TNF and interleukin-1 from macrophages, resulting in chills 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 to a lot of manifestations as Cerebral malaria (severe headache, drowsiness, confusion, coma) Placental malaria (premature delivery, intrauterine growth retardation iURD ) Dysenteric malaria (abdominal pain, 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. Any Questions ?

17. Thank you