1. Mal-aria (Bad air) till 1880
2. Tropical disease due to presence of sporozoa of
3. Transmitted to humans by the infected female
4. Malarial parasite is a single cell protozoa called
5. 300-500 millions cases of malaria detected out of
which 1.5-2.7 million death every year
6. Nine major species of anopheline mosquitoes
transmit malaria in India. In urban areas, malaria is
mainly transmitted by Anopheles stephensi
Malaria is caused by four species of
P. falciparum. (more lethal)
P. ovale (rare).
The plasmodium transmitted to human by
the bite of an infected female anopheles
• NMEP (National Malaria Eradication Program) in India
• Nearly complete eradication in due to
• In 1970’s due to emergent of drug and
insecticides resistant all attempts failed.
Life Cycle of Malarial Parasite
• Complex Sexual (in female mosquito) and asexual
Life cycle (in humans).
• Sexual Life Cycle: Fertilization takes place in
mosquito gut and Oocysts liberates matured
sporozoites which migrates and stay in
insects salivary glands.
• Asexual Life Cycle: These sporozoites then
passed to blood of another human to begin
• NO AVAILABLE DRUGS ARE LETHAL TO
Sporozoites hardly survived in blood hence get
sheltered in Liver parenchymal cell
In Liver it divide and developed into multinucleated
SCHIZONTS. Hosts are asymptomatic
In Liver, Schizonts gets matured in 8-21 days to form
mononucleated MEROZOITES liberated from liver and
released in blood stream
If the species is P.
falciparum, merozoites bind
to erythrocytes and forms
If the species is P.vivax / P.ovale,
some merozoites re-enters liver
cell and form dormant
HYPNOZOITES (Sleeping form,
which may lasts for several month and
may get relapse)
EXO OR PARA
The malaria parasite life cycle involves 2 hosts. During a blood meal, a malaria-•
infected female Anopheles mosquito inoculates sporozoites into the human host.
Sporozoites infect liver cells.
There, the sporozoites mature into schizonts.
The schizonts rupture and release merozoites. This initial replication in the liver is
called the exoerythrocytic cycle.
Merozoites infect RBCs. There, the parasite multiplies asexually (called the
erythrocytic cycle). The merozoites develop into ring-stage trophozoites.
Some then mature into schizonts.
The schizonts rupture, releasing merozoites.
Some trophozoites differentiate into gametocytes.
During a blood meal, an Anopheles mosquito ingests the male (microgametocytes)
and female (macrogametocytes), gametocytes beginning the sporogonic cycle.
In the mosquito's stomach, the microgametes penetrate the macrogametes,
The zygotes become motile and elongated, developing into ookinetes.
The ookinetes invade the midgut wall of the mosquito where they develop
The oocysts grow, rupture, and release sporozoites, which travel to the mosquito's
salivary glands. Inoculation of the sporozoites into a new human host perpetuates
the malaria life cycle.
• During merozoite maturation in RBC, host’s
Hb is digested and transported to parasites
food vacuole and provides amino acids
• Free haem which may be toxic to parasite is
polymerised to haemozoin by parasitic haem
• RBCs infected with merozoite, ruptures and
releases thousands of merozoites along with
pyrogens, TNF- α and polymerised haem to
show symptoms of Malaria
• P. vivax causes BENIGN TERTIAN MALARIA
– Benign as it is rarely fatal
– Tertian as fever is on every 3rd day (48 h)
– Relapse may occur because dormant hypnozoites reside in
• P. ovale infection has periodicity and relapse similar
to P. vivax but is milder and can be cured
• P. malariae causes QUARTAN MALARIA
– It has 72 h cycles
– No exo-erythrocytic stage but relapse may occur
• P. falciparum causes MALIGNANT TERTIAN MALARIA
– Malignant as it is severe form of malaria
– Tertian as fever occurs every after 3rd day
– Infected RBCs forms clusters called ROSETTES. Such
rosettes may block capillaries of vital organs causing renal
failure and encephalopathy (Cerebral Malaria)
• Early symptoms
Slight fever, usually not intermittent
• Could mistake for influenza or gastrointestinal
• Acute febrile illness, may have periodic febrile
paroxysms every 48 – 72 hours with
• Afebrile asymptomatic intervals
• Tendency to recrudesce or relapse over
months to years
hepatosplenomegaly, respiratory distress
syndrome, renal dysfunction, hypoglycemia,
mental status changes, tropical splenomegaly
Available as Chloroquine Phosphate
p.o./i.m./slow i.v. infusion
very high volume of distribution
Metabolised in liver
Excreted in urine (70% unionized and 30% metabolized)
T1/2 is 3-4 days
Terminal T1/2 is 1-2 months
• Chloroquine accumulates in parasitized erythrocytes
• Diffuse into parasite lysosomes
• Inhibit peptide formation and reduces supply of amino acid
which is necessary for parasite viability
• Also inhibit parasite haem polymerase and thus protects
host’s haem to get converted into haemozoin.
• At high concentration it also inhibit RNA and DNA