MALARIAL MICROBIOLOGY AND PATHOLOGY

1. CARDIOVASCULARAND
HAEMOPOETICSYSTEM
CORRELATION SEMINAR
TOPIC: MALARIA
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2. OBJECTIVE:
Describe
pathogenesis
of malaria.
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3. INTRODUCTION:
WHY MALARIA?
MAL=foul ; ARIA=air
One of the most common infectious disease
and enormous health problem.
It causes disease in approximately 219
million cases of malaria in 87 countries.
4,35,000 Malarial deaths worldwide in 2017.
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4. WHO ARE AT RISK?
Younger children, Pregnant women,
Immunocompromised patient and traveler.
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5. WHERE?
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6. MALARIAL PATHOGENESIS
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Paniker’s Textbook of Medical Parasitology

7. HEPATIC PHASE
Sporozoites attach to and invade liver cells by bind
ing to the hepatocyte receptor for the serum
proteins: Thrombospondin and Properdin.
Malaria parasites multiply,
releasing as many as
30,000 merozoites
(asexual, haploid forms)
infected hepatocyte
ruptures. 7
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Robbins and Cotran Pathologic Basis of
diseases SAE

8. HEPATIC PHASE
P. falciparum infection,
rupture usually occurs
within 8 to 12 weeks.
P. vivax and P. ovale form
latent hypnozoites in
hepatocytes, which cause
relapses of weeks to
months.
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A colour atlas of tropical medicine and
Parasitology 2nd E

9. ERYTHOCYTIC PHASE
Plasmodium merozoites use a lectin-like
molecule to bind to sialic acid residues on
glycophorin molecules on the surface of
RBCs and invade by active membrane penetration.
Schizogony in RBCs
Release of merozoites by
lysis of RBCs
Robbins and Cotran Pathologic Basis of diseases SAE
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10. ERYTHOCYTIC PHASE
Release of toxic waste products-RBC
membrane products, hemozoin pigment
Activate macrophages and endothelium
Release tumor necrosis factor alpha(TNF alpha)
& other cytokines(IL-1, IL-6, IL-8, etc.).
Fever, Chills and Rigors characteristic of malaria10
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11. HEPATIC & SPLENIC
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Paniker’s Textbook of Medical Parasitology

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Atlas of Medical Helminthology and Protozoology

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••Destruction of large number of
RBCs by complement mediated
and autoimmune hemolysis
••Suppression of erythropoesis in
the bone marrow
••Increased clearance of both
parasitied and non parasitized
RBCs by the spleen.
••Failure of the host to recycle the
iron bound in hemozoin pigment.
CAUSES OF ANAEMIA IN MALARIA
A colour atlas of tropical medicine and
Parasitology 2nd E

14. Plasmodium vivax,
P malariae, and P ovale
parasitemias are relatively
low grade, primarily
because the parasites favor
either young or old red
cells but not both.
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Source:Internet

15. PATHOGENESIS OF SEVERE
MALARIA
P. Falciparum infects all ages of RBCs
P. falciparum erythrocyte membrane protein1
(PfEMP1), associate and form knobs on the
surface of infected red cells
PfEMP1 binds to ligands on
endothelial cells, including
CD36,
thrombospondin,VCAM-1,
ICAM-1, and E-selectin
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16. PATHOGENESIS OF SEVERE
MALARIA
Infected RBCs to clump
together(ROSETTE)
Stick to endothelial cell lining
of small blood vessels
(SEQUESTRATION)
Blood flow blocks which
decreases tissue perfusion
and leads to Ischemia
[Manifestation of cerebral malaria] Robbins and Cotran
Pathologic Basis of diseases
SAE
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17. 17
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Atlas of Medical Helminthology and Protozoology
Robbins and Cotran Pathologic Basis of diseases SAE

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Davidson’s Medicine 23rd E

19. SUMMARY
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Markell and Voge’s Medical Parasitology 9E

20. CORRELATION:
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Malaria is vector borne infectious disease
caused by protozoan parasites of genus
Plasmodium.
It can be transmitted to people of all ages,
bitten by the vector female Anopheles
mosquitoes.
It reflect multifactorial pathogenic process
affecting many different organs.
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21. BIBILOGRAPHY:
 Atlas of Medical Helminthology and Protozoology
 Robbins and Cotran Pathologic Basis of
diseases SAE
 Markell and Voge’s Medical Parasitology 9E
 Paniker’s Textbook of Medical Parasitology
 Davidson’s Medicine 23rd E
 Kayser Medical Microbiology © 2005 Thieme
 A colour atlas of tropical medicine and
Parasitology 2nd E
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22. THANK YOU !
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