Plasmodium
PRESENTED BY
APOORVA S
S NITHIN
KUMAR
PLASMODIUM
Plasmodium is a genus of parasitic micro-organisms known to cause
malaria in humans.
Parasites, like Plasmodium, are organisms that live in or on other
organisms (the hosts), to the detriment of those organisms.
Plasmodium can infect many different types of animals, including
reptiles, birds and mammals.
These parasites are transmitted to vertebrate hosts by insect
(notably mosquito) vectors and cause malaria in human.
MORPHOLOGY
Type: Protozoan parasite (unicellular, eukaryotic).
Shape & Size:
generally oval to spherical inside host cells.
Size :1–2 µm (merozoite) to 15 µm (sporozoite)
Cytoplasm: Delicate, often pale blue with a central vacuole in ring
forms.
Nucleus: Single, dense chromatin mass.
Motility: Uses gliding motility (no flagella/cilia, except male
gametes).
SPECIES OF PLASMODIUM
PLASMODIUM VIVAX (P.VIVAX)
PLASMODIUM FALCIPARUM
(P.FALCIPARUM)
PLASMODIUM MALARIAE (P.MALARIAE)
PLASMODIUM OVALE (P.OVALE)
PLAMODIUM.VIVAX
Plasmodium vivax is a protozoal parasite and a human pathogen.
This parasite is the most frequent and widely distributed
causes benign tertian malaria (most common in India).
The parasite is transmitted through the bite of a female
Anopheles mosquito
PLASMODIUM.FALCIPARUM
Plasmodium falciparum is a unicellular protozoan
parasite of humans and is the deadliest species of
Plasmodium that causes malaria in humans.
The parasite is transmitted through the bite of a
female Anopheles mosquito and causes the disease's
most dangerous form, falciparum malaria.
CAUSES:malignant tertian malaria, most severe, can
cause cerebral malaria.
PLASMODIUM.MALARIAE
Plasmodium malariae is a parasitic protozoan that causes malaria in
humans
Plasmodium malariae causes quartan malaria. This type of malaria is
characterized by fever cycles that occur approximately every 72 hours
(every three days
PLASMODIUM.OVALE
Plasmodium ovale is a species of parasitic protozoon that causes
tertian malaria in humans.
Plasmodium ovale causes tertian malaria.
HOST:
Definitive host – Female Anopheles mosquito (sexual
cycle / sporogony)
Intermediate host – Humans (asexual cycle / schizogony)
LIFE CYCLE STAGES
IN HUMAN:
Sporozoites:The life cycle begins when a mosquito injects
sporozoites into a human during a blood meal.
Exo-erythrocytic Schizogony:Sporozoites travel to the liver
and infect liver cells. They multiply asexually, forming schizonts that
rupture, releasing merozoites.
Trophozoites: Inside red blood cells, merozoites
develop into trophozoites, feeding on hemoglobin and
growing.
Schizonts (Erythrocytic): Trophozoites mature
into schizonts, which undergo asexual multiplication,
producing more merozoites.
Gametocytes: Some merozoites differentiate into
male (microgametocytes) and female
(macrogametocytes) gametocytes, which can be
ingested by a mosquito.
IN MOSQUITO:
Gametocytes (Mosquito): When a mosquito takes a blood
meal from an infected human, it ingests gametocytes.
Fertilization: Male and female gametocytes fuse in the mosquito's
gut to form a zygote.
Ookinetes: The zygote develops into an ookinete, which penetrates
the mosquito's gut wall.
Oocysts: The ookinete transforms into an oocyst on the gut wall
Oocysts: The ookinete transforms into an oocyst on the gut
wall
Sporozoites (Mosquito): The oocyst releases
sporozoites, which migrate to the mosquito's salivary glands,
completing the cycle.
PATHOGENESIS
Entry & Liver Stage (Silent Phase)
Infection begins when an infected Anopheles mosquito injects sporozoites
into the blood.
Sporozoites invade liver cells (hepatocytes).
Inside hepatocytes → undergo asexual multiplication (schizogony) →
produce merozoites.P.
vivax and P. ovale can form hypnozoites → remain dormant → cause
relapse later.
Blood Stage (Clinical Disease)
Merozoites infect red blood cells (RBCs).
Inside RBCs: progress through stages → ring → trophozoite
→ schizont.
RBCs burst, releasing more merozoites and parasite
toxins.
SYMTOMS LIKE: CHILLS, FEVER,SWEATING
PATHOGENSIS IS MAINLY DUE TO:
RBC DESTRUCTION: Anemia,Jaundice
CYTOKINE STORM: Fever, systemic illness
MICROVASCULAR OBSTRUCTION: CEREBRAL MALARIA
METABOLIC DERANGEMENTS: Hypoglycemic, Acidosis
Mode of transmission
Vector borne tansmission (most common):
Female Anopheles Mosquito
Congenital transmission: Infected mother to fetus via
placenta(leads to congenital malaria)
Blood transfusion: infected blood,needle sharing(IV
grug use)
Organ transplantation from infected donor
CLINICAL MANIFESTATIONS
INCUBATION PERIOD: Varies with species
P.FALCIPARUM: 9-14 DAYS
P.VIVAX And P.OVALE: 12-18 DAYS
P.MALARIAE: 18-40 DAYS
PRODROMAL SYMPTOMS:
Headache,fatigue,nausea,malaise
Resembles viral illness
P. vivax / P. ovale → every 48 hrs (tertian malaria).
P. falciparum → irregular (malignant tertian).
P. malariae → every 72 hrs (quartan malaria).
GENERAL CLINICAL FEATURES:
Anemia (due to hemolysis of RBCs).
Splenomegaly & hepatomegaly.
Jaundice (from hemolysis).
Mild thrombocytopenia
SEVERE/COMPLICATED MALARIA
Cerebral malaria → seizures, coma, altered sensorium.
Severe anemia → profound pallor, weakness.
Acute renal failure
dark urine (“blackwater fever”): A rare and severe complication
of malaria that involves the bursting of RBC’S in bloodstream
Pulmonary edema / ARDS.Hypoglycemia (especially in children &
pregnancy).
Metabolic acidosis.
COMPLICATIONS BY EACH
PLASMODIUM SPECIES
1. Plasmodium falciparum (Most Dangerous –
Malignant malaria):
Cerebral malaria (coma, seizures, neurological deficits).
Severe anemia (massive RBC destruction).
Hypoglycemia (common in children & pregnancy).
Acute renal failure
(blackwater fever → hemoglobinuria).
2. Plasmodium vivax:
(Benign tertian malaria, but can be severe in
some cases): ANEMIA,SPLENOMEGALY,JAUNDICE
3.Plasmodium ovale: Similar to P.Vivax
4.Plasmodium malariae:
(Quartan malaria) : Causes chronic, low-grade
infection
Nephrotic Syndrome,Chronic Anemia
LAB DIAGNOSIS
Sample Collection: BLOOD/BLOOD SMEAR
1. Microscopy (Gold Standard)
Peripheral blood smear examination:
Thick smear → more sensitive, used to detect presence of
parasites.
Thin smear → helps to identify species (morphology of ring
forms, schizonts, gametocytes).
Best done during or just before fever spike.
Staining: Giemsa, Leishman, Wright’s stain.
PROCEDURE
A) Thick Smear Preparation
1. Place a large drop of blood in the center of a clean glass
slide.
2. Spread it into a small circular area (1–2 cm), about the
size of a dime.
3. Allow to air dry without fixing (RBCs must be lysed so
parasites remain).
4. Stain with Giemsa stain (pH 7.2) for 10–15 minutes.
5. Wash gently with buffered water and air dry.
6. Examine under oil immersion (100× objective).
B) Thin Smear Preparation
1. Place a small drop of blood near one end of a slide.
2. Use another slide at a 45° angle to spread the drop into a thin film
(like a tongue shape).
3. Air dry the film.
4. Fix with methanol for 1–2 minutes (prevents RBC lysis).
5. Stain with Giemsa stain (10–15 minutes).
6. Wash, air dry, and examine under oil immersion.
2. Rapid Diagnostic Tests (RDTs)
Detect parasite antigens in blood (immunochromatographic tests).
Examples:HRP-2 (Histidine-rich protein 2): specific for P. falciparum.
pLDH (Plasmodium lactate dehydrogenase): detects all species.
Useful in field settings, quick (15–20 min).
Limitation: less sensitive at low parasitemia, cannot always differentiate
species.
Quantitative Buffy Coat
Examination
The quantitative buffy coat (QBC) malaria test is an advanced
microscopic technique for malaria diagnosis. It consists of three basic
steps;
(1) concentration of blood by centrifugation
(2) staining with acridine orange stain
(3) examination under ultravoilet (UV) light source
PROCEDURE
The commercially available quantitative buff y coat (QBC) capillary tube
is precoated internally with acridine orange stain
• 60 µL of peripheral blood is collected from one end of the tube,
which is then closed by a plastic closure.
• A cylindrical float is inserted to the other end of the QBC tube.
The tube is centrifuged at 12,000 rpm for 5 minutes
• The components of the blood are separated according to their
densities, forming discrete bands
• Because the cylindrical float occupies 90% of the interior
lumen of the tube, it forces all the surrounding blood cells into 40 µ
space between its outside circumference and inside of the tube
• Following centrifugation, the buff y coat region of the QBC
tube, i.e. at the RBC/WBC interface is examined under UV light
source
• The whole 60 μL blood sample can be visualized by rotating
the QBC tube under the fluorescent microscope.
Fluorescence microscopy
Kawamoto technique is a fluorescent staining method
for demonstrating malaria Parasites. Blood smears are
prepared on a slide and are stained with acridine
orange and examined under a fluorescence
microscope. Nuclear DNA is stained green.
3. Molecular Methods
PCR (Polymerase Chain Reaction):
Highly sensitive and specific. Detects low parasitemia &
mixed infections.
4. Serology:
Detects antibodies against Plasmodium.
Used in epidemiological surveys.
TREATMENT
Severe / Complicated Malaria
Artemisinin Combination Therapy
Artemether–lumefantrine,Artesunate–amodiaquine,Artesunate–
mefloquine
First-line (IV therapy):IV Artesunate (preferred, less toxic)
ALTERNATIVE: IV Quinine/ IV Quinidine
Supportive / Adjunct Therapy
IV fluids (avoid overload).
Antipyretics for fever. Blood transfusion for severe anemia.Manage
hypoglycemia, acidosis, renal failure, seizures
PREVENTION
1. Use insecticide-treated bed nets
2.apply insect repellents: (DEET,Citronella,Picaridin)
3.Wear protective cloathing
Eliminate mosquito breeding site: remove standing water
around homes and public areas
Vaccination: RTS, S/AS01:Provides partial protection
Chemoprophylaxis:Chloroquine,Mefloquine,Doxycycline
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