Malarial Pathogenesis
By: Kareem Waleed Hamimy
6th Year Medical Student
Kasr Al Ainy - Cairo University
A short introduction
Malaria
Why?
What?
How?
Who?
Where?
Pathogenesis
Clinical picture
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.
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.
How?
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.
Where?
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).
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
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.
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.
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
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
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 )
Pathogenesis of clinical picture
CVS
Anemia leads to
○ Hypotension
○ Tachycardia
○ Muffled heart sounds
Kidney
Immune complexes Nephrotic syndrome
○ Albuminuria
○ Edema
○ hypertension
Malarial
Infections
High
Secondary Clinical Grade
Infection
Picture Fever
Anti
Malarial
Drugs
Any Questions ?
THANK YOU