Plasmodium species

BY GROUP 2 SUBMITTED TO : PRABIN SHAKYA

IN THIS PRESENTATION
▪ INTRODUCTION TO
MALARIA AND
PLASMODIUM SPECIES
▪ MORPHOLOGY OF EACH
PLASMODIUM SPECIES
▪ LIFECYCLE
▪ PATHOGENESIS
▪ LAB DIAGNOSIS
▪ TREATMENT
▪ PREVENTION AND CURE
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INTRODUCTION
MALARIA IS COMMON YET A
FATAL DISEASE FOUND
TROPICAL AND SUBTROPICAL
AREAS AND THE ONES TO
CAUSE IT ARE PLASMODIUM.
Female Anopheles mosquitoes are
their vectors.
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CLASSIFICATION
KINGDOM ANIMALIA
PHYLUM PROTOZOA
CLASS TELOSPORA
SUBCLASS COCCIDIA
ORDER EICOCCIDA
GENUS Plasmodium

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Plasmodium species
Plasmodium ARE DIGENETIC PROTOZOAN PARASITES
AND THERE ARE FIVE SPECIES OF PLASMODIUM
THAT CAUSE MALARIA IN HUMAN BEINGS.
Plasmodium species:
1. Plasmodium vivax
2. Plasmodium falciparum
3. Plasmodium malariae
4. Plasmodium ovale
5. Plasmodium knowlesi (usually found in Monkeys)

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 Causative Agents of Human Malaria
● Plasmodium vivax: Benign Tertian Malaria
● Plasmodium falciparum: Malignant Tertian
Malaria
● Plasmodium malariae: Benign Quartan Malaria
● Plasmodium ovale: Benign Tertian Malaria.

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DISTRIBUTION OF MALARIA

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MORPHOLOGY OF Plasmodium

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LIFE CYCLE OF PLASMODIUM

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LIFECYCLE OF Plasmodium

Malaria parasite passes its life cycle in 2 hosts.

Definitive host: Female Anopheles mosquito.
Intermediate host: Man.
● The life cycle of malarial parasite comprises of
2 stages—an asexual phase occurring in
humans, which act as the intermediate host
and a sexual phase occurring in mosquito,
which serves as a definitive host for the
parasite.

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LIFECYCLE OF Plasmodium
Asexual phase:€
In this stage, the malaria parasite multiplies by division
or splitting a process designated to as Schizogony
(from schizo: to split, and gone: generation).
€
Because this asexual phase occurs in man, it is also
called the vertebrate, intrinsic, or endogenous phase.
€
In humans, schizogony occurs in 2 locations—in the
red blood cell (erythrocytic schizogony) and in
the liver cells (exoerythrocytic schizogony or the
Tissue phase)
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LIFE CYCLE OF PLASMODIUM

● € Because schizogony in the liver is an essential step

before the parasites can invade erythrocytes, it is
called pre-erythrocytic schizogony.
● € The products of schizogony, whether erythrocytic
or exoerythrocytic, are called merozoites (meros: a
part, zoon: animal)

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LIFECYCLE OF PLASMODIUM

Sexual phase:
● € The sexual phase takes place in the female Anopheles
mosquito, even though the sexual forms of the
parasite (gametocytes) originate in human red
blood cells.
● € Maturation and fertilization take place in the
mosquito, giving rise to a large number of sporozoites
(from sporos: seed). Hence this phase of sexual
multiplication is called sporogony. It is also called
the invertebrate, extrinsic, or exogenous phase. 17
 There is, thus an alternation of
generations in the
life cycle of malaria
parasites—asexual and sexual
generations, alternatively.

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INCUBATION PERIOD
It is the interval between the infective mosquito bite and
the first appearance of clinical symptoms. The duration of
incubation period varies with the species of the parasite.
The average incubation periods of different species of
Plasmodium are as follows –
• P. vivax—14 (8–31) days
• P. falciparum—12 (8–14) days
• P. ovale—14 (8–31) days
• P. malariae—28 (18–40) days
The incubation period is to be distinguished from the
pre-patent period, which is the interval between the entry
of the parasites into the host and the time when they first
become detectable in blood.
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CLINICAL FEATURES
Typical picture of malaria consist of periodic bouts of fever with rigor followed by
anemia and splenomegaly. Febrile pasoxysms comprise of cold stage, hot stage,
and the sweating stage.
• TSS is a chronic benign condition resulting from abnormal immunological
response to malaria.
• Relapse of malaria occurs in P. vivax and P. ovale infection due to persistence
of dormant stage hypnozoites in liver.
Recrudescence occurs commonly in P. falciparum and P. malariae due to
persistence of parasite in circulation at a subclinical level.

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PATHOGENESIS
All clinical manifestation in malaria are due to products of erythrocytic schizogony and the host’s reaction to
them.
▪ The disease process in malaria occurs due to the local or systemic response of the host to parasite
antigens and tissue hypoxia caused by reduced oxygen delivery because of obstruction of blood flow
by the parasitized erythrocytes.

▪ Liver is enlarged and congested. Kupffer cells are increased and filled with parasites. Hemozoin
pigments are also found in the parenchymal cells .Parenchymal cells show fatty degeneration, atrophy,
and centrilobular necrosis.
▪ Spleen is soft, moderately enlarged, and congested in acute infection. In chronic cases, spleen is hard
with a thick capsule and slate grey or dark brown or even black in color due to dilated sinusoids,
pigment accumulation, and fibrosis.
▪ Kidneys are enlarged and congested. Glomeruli frequently contain malarial pigments and tubules may
contain hemoglobin casts. 25
PATHOGENESIS
▪ The brain in P. falciparum infection is congested. Capillaries of the brain are plugged
with parasitized RBCs. The cut surface of the brain shows slate grey cortex with
multiple punctiform hemorrhage in subcortical white matter.
▪ Anemia is caused by destruction of large number of red cells by
complement-mediated and autoimmune hemolysis. Spleen also plays an active role by
destroying a large number of unparasitized erythrocytes. There is also decreased
erythropoiesis in bone marrow due to tumor necrosis factor (TNF) toxicity and failure of
the host to recycle the iron bound in hemozoin pigments.
▪ Cytokines such as TNF, interleukin (IL)-1, and interferon (IFN)-gamma play a pivotal
role in the pathogenesis of end organ disease of malaria.

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DIAGNOSIS
By demonstration of parasite in thick and thin smear of peripheral blood
and also by detection of malaria antigen by rapid ICT.

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DIAGNOSIS
▪ CLINICAL DIAGNOSIS
▪ MALARIA BLOOD SMEAR
▪ FLUORESCENT MICROSCOPY
▪ ANTIGEN DETECTION
▪ SEROLOGY
▪ PCR

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BLOOD SMEARING

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FLUORESCENT MICROSCOPY

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TREATMENT
Chloroquine sulfadoxine, and pyrimethamine along
with primaquine. In chloroquine resistance, quinine or
artemesinin are used.

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PREVENTION
A. Be Aware of the risk, the symptoms and understand that malaria is a
serious infection.
B. Avoid mosquito Bites.
C. Take Chemoprophylaxis when appropriate.
D. Seek immediate Diagnosis and treatment if they develop fever during
or after travel.

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PREVENTION
▪ Residual spraying: The spraying of the indoor surfaces of house
with residual insecticides eg. dichloro-diphenyl trichloroethane
(DDT), malathion, and fenitrothin.
▪ Space application: Space Sprays are those where insecticidal
formulation is sprayed into the atmosphere in the form of mist or
fog to kill insects (pyrethrum extracts).
▪ Individual protection: Man-vector contact can be reduced by
other preventive measures such as the use of repellants, protective
clothing, bed net, preferably impregnated with long acting repellant,
mosquito coils, and screening of house
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PREVENTION
Anti-larval Measures
▪ Old antilarval measures such as oiling the collection of standing
water or dusting them with paris green have now become
promising with the increase of insecticide resistance.
▪ Source reduction: Techniques to reduce mosquito breeding sites,
which include drainage or filling, deepening or flushing,
management of water level, intermittent irrigation are among the
classical methods of malaria control, environmental and personal
protection measures.
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PREVENTION
Integrated Control
In order to reduce too much dependence on residual
insecticides, increasing emphasis is being put on integrated
vector control methodology, which includes bio
environmental and personal protection measures.

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