4. Malarial Parasites of Medical Importance
Plasmodium falciparum
Plasmodium vivax
Plasmodium ovale
Plasmodium malariae
Plasmodium knowlesi
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5. Plasmodium falciparum-LIFE CYCLE
Malarial parasites shows alteration of
generation with alteration of hosts in Human
(INTERMEDIATE HOST) and in Mosquitos
(DEFINITE HOST ).
HUMAN CYCLE
Human is the intermediate host.
Parasite reproduce by ASEXUAL METHOD
(SCHIZOGONY)
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7. Plasmodium falciparum-LIFE CYCLE
Human cycle begins with a bite of
• Infected Female Anopheles mosquito or
• Transfusion of Infected blood (Transfusion malaria
and Congenital malaria)
There are 2 stages in the Human cycle-
1. Exo-erythrocytic (EE) schizogony in the Liver
2. Erythrocytic schizogony in the RBCs.
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8. Exo-erythrocytic Schizogony
Mosquito during biting inject SPOROZOITES along with
saliva into the small blood vessels.
Motile sporozoites are carried to the LIVER by the blood
stream (30 mins)
The surface of the sporozoites is covered by a protein k/a
Circumsporozoite protein (CSP) which has a ligand for
receptor in the hepatocyte cell membrane.
Within the hepatocytes, the sporozoites undergo a stage of
ASEXUAL REPRODUCTION k/a- Primary EE schizogony (PE)
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9. Exo-erythrocytic Schizogony
During this cycle, the sporozoites are transformed into
TROPHOZOITES. (Organelles of the Apical complex
disappear and growing trophozoites feed on host cell
cytoplasm.)
Mature trophozoites begin schizogony- numerous
daughter nuclei are first produced subsequently
leading to the development of Multinucleate Liver
Stage Schizonts (EE Schizont)
Mature EE Schizonts are Spherical, 60µm in diameter,
contain 2,000- 50,000 uninuclate MEROZOITES.
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10. Exo-erythrocytic Schizogony
Finally mature EE schizonts and enlarged liver
cells ruptures releasing thousands of merozoites
into the blood straem.
In P. falciparum only a single cycle of Primary EE
schizogony takes place. It is completed in 6 days.
• The secondary schizogony which occur in P. vivax and
P. ovale, is absent in P. falciparum and there is no
HYPNOZOITES (the stage responsible for Relapse ).
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11. Exo-erythrocytic Schizogony
Once the merozoites enter the erythrocytes ,
they never reinvade the liver.
So EE forms are absent in Transfusion malaria.
There may be recrudescence of fever even
after remission, due to persistence of small
number of infected RBCs.
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13. erythrocytic Schizogony
This begins with the attachment and invasion of
erythrocytes with blood stream merozoites.
The merozoites became attach to the
GLYCOPHORINS (the major surface glycoproteins
of RBCs) and other Sialoproteins on the RBC
member.
The Erythrocytes of any age & reticulocytes are
infected.
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14. erythrocytic Schizogony
During invasion the apical end of the merozoites
first come in contact with the erythrocytes.
Then the merozoite lies within an
Intraerythrocytic Parasitophorus vacuole formed
by erythrocyte plasma membrane.
The nature of Haemoglobin and RBC enzymes
influence the development of merozoites inside
the RBC. (as Fetal Hb & HbS inhibit the
development.)
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15. erythrocytic Schizogony
Inside the RBCs, the Merozoite develop into Young
TROPHOZOITES or, RING FORMS.
These feed on Hb by ingesting the RBC cytoplasm.
HAEMAZOIN- Malarial pigment
• A compound of Haematin and Ferric acid, is produced as an end
product of haemoglobin break down.
The trophozoites multiply by division of nucleus by mitosis
followed by division of cytoplasm , to become MATURE
SCHIZONTS.
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16. erythrocytic Schizogony
A mature ERYTHROCYTIC SCHIZONT is
asymmetrical and contains 8-32 MEROZOITES &
Haemazoin.
Rupture of schizont releases merozoites into
circulation. These merozoites within seconds
attach and penetrate new RBCs.
The process of intracellular maturation leading to
the development of Schizont and subsequent
rupture is k/a- SCHIZOGONY.
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17. erythrocytic Schizogony
In P. falciparum, the erythrocytic schizogony is
completed within 48 hrs.
It always takes place in capillaries and vascular
beds of internal organs.
Therefore, in P. falciparum infection, SCHIZONTS
& MEROZOITES are usually not demonstrated in
the peripheral blood circulation.
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18. Gemetocytogenesis
After 2-3 erythrocytic cycles, some of the merozoites
invade the new erythrocytes and instead of developing
into schizonts, they develop into
• MALE MICROGAMETOCYTES and
• FEMALE MACROGAMETOCYTES.
These gametocytes develop in the RBC of the BONE
MARROW and SPLEEN.
The early gametocytes are of irregular shape but finally
they become CRSCENT- Shaped, a distinctive feature
of P. falciparum.
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19. Gemetocytogenesis
The haemazoin granules of gametocytes of P.
falciparum is found in central part of
cytoplasm surrounding the nucleus of micro-
& macrogamets.
• In P. vivax, heamazoin pigments are distributed
throughout the cytoplasm.
In PBS , only mature gametocytes are found.
Gametocytogenesis completes in 96 hrs.
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26. Diagnostic forms in Human
RING Form – this is the Young Trophozoite
and found inside an RBC.
it’s morphology resembles a Ring like
structure
The ring shaped parasite cytoplasm
surrounding a central vacuole stain blue
The nucleus (Chromatin dot) stain red.
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28. Diagnostic forms in Human
TROPHOZOITES- they are vacuolated, more or less
amoeboid, uninucleate.
thin ring of cytoplasm and darkish stained nucleus.
In heavy infection, the growing forms assume a compact
form
A single large mass of Pigment (Heamazoin) is present.
In falciparum malaria both early and late trophozoites are
rarely seen in peripheral blood.
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30. Diagnostic forms in Human
ERYTHROCYTIC SCHIZONTS – they are asexual and
dividing forms of the parasite.
they occupy 2/3 of the infected RBCs.
They contain 2-3 merozoites and dark stained pigments.
Mature Schizonts contain 10-36 merozoites which are
arranged in grape like clusters.
Schizonts are very rarely seen and indicates severe
infection.
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32. Diagnostic forms in Human
GAMETOCYTES – They are sexual and
erythrocytic stages of the parasite and
Infectious for mosquitoes.
they are crescent/ banana shaped with round or
pointed ends.
Mature gamatocytes are 1 and ½ times larger than
the RBC
Gamatocytes are 2 types- Microgamatocyte
(Male) and Macrogamatocyte (female)
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37. Complications of Severe Falciparum malaria
Appropriately and promptly treated, uncomplicated
falciparum malaria (i.e., the patient can swallow
medicines and food) carries a mortality rate of ~0.1%.
However, once vital-organ dysfunction occurs or the
total proportion of erythrocytes infected increases to
>2% (a level corresponding to >1012 parasites in an
adult), mortality risk rises steeply.
The condition occurs more frequently in –
• Non-immune persons
• Immuno-suppressed persons
• Pregnant women
• Splenectomy patients. 37
39. Mosquito borne Vs. Transfusion
Malaria
Feature Mosquito borne Transfusion
Infective stage Sporozoite Trophozoite
Incubation period Long Short
PE Schizogony Present Absent
EE Schizogony May be present Absent
Relapse May occur Don’t
T/t Radical cure not possible Radical cure possible
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40. Recurrence of Clinical malaria
Recurrence of clinical malaria after treatment may occur due to 3
reasons-
1. True relapse: It is caused by Hypnozoites in P. vivax & P. ovale.
It is due to re-emrgence of blood stage parasites from latent
parasites(Hypnozoites) in liver. Since no Hypnozoites in P.
falciparum-> No true relapse.
2. Recrudescence- It is seen falciparum malaria d/t inadequate t/t
and seen in – Drug resistance, Immuno-suppression & pregnancy.
3. Latent malaria- This condition refers to a state of asymptomatic
malaria harbouring plasmodia gametocytes in the peripheral
blood. These persons are infectious to mosquitoes and act as
Reservoirs
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