1. By: Kareem Waleed Hamimy
6th 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?

7. 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.

8. Where?

9. 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).

10. 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

11. 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.

13. 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.

14. 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

15. 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

16. 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 )

17. Pathogenesis of clinical picture
 CVS
 Anemia leads to
○ Hypotension
○ Tachycardia
○ Muffled heart sounds
 Kidney
 Immune complexes  Nephrotic syndrome
○ Albuminuria
○ Edema
○ hypertension

18. Malarial
Infections
High
Secondary Clinical Grade
Infection
Picture Fever
Anti
Malarial
Drugs

19. Any Questions ?