malarial pathogenesis
TRANSCRIPT
Malarial Pathogenesis
By: Kareem Waleed Hamimy
6th Year Medical Student
Kasr Al Ainy - Cairo University
A short introduction
MalariaWhy?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 phaseSporozoites 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 merozoitesThey develop first to Hypnozoites (dormant
form) for 6-12 month leading to long incubation and late relapses
Malarial Pathogenesis
PfEMP1Plasmodium falciparum erythrocyte
membrane protein 1Adhesion (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 & toxinsRelease of cytokines such as TNF and
interleukin-1 from macrophages, resulting in chills and high grade fever.
Pathogenesis of clinical picture
AnemiaFebrile paroxysmal hemolysisImmune & Non Immune hemolysisIncreased splenic clearanceDyserythropoeisis in BMDrug induced hemolysis
Bone marrow Iron sequestration DyserythropoeisisDysthrombopoeisis
Pathogenesis of clinical picture
SpleenSplenomegaly
○ Edema of the pulp○ RES hyperplasia○ Increased phagocytic function○ New guinea “Tropical splenomegaly syndrome”
LiverHepatomegaly (hepatic phase)Malarial pigments greyish blackFalciparum malarial hepatitis
Pathogenesis of clinical picture
Due to adherence factor of falciparum blocking of venules of organs lead to a lot of manifestations asCerebral 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
CVSAnemia leads to
○ Hypotension○ Tachycardia○ Muffled heart sounds
KidneyImmune complexes Nephrotic syndrome
○ Albuminuria○ Edema○ hypertension
Clinical Picture
Malarial Infections
High Grade Fever
Anti Malarial Drugs
Secondary Infection
Any Questions ?
THANK YOU