The document summarizes the life cycle and transmission of malaria parasites. It discusses: 1) Malaria is caused by protozoan parasites of the genus Plasmodium, which are transmitted through the bites of infected Anopheles mosquitoes. The parasites have a complex life cycle involving both human and mosquito hosts. 2) In humans, the parasites initially infect and multiply in the liver before infecting and destroying red blood cells. Parasites developing in red blood cells cause the cyclical symptoms of malaria. 3) Mosquitoes can acquire the parasite by biting infected humans and ingesting sexual forms of the parasite. In the mosquito's gut the parasite undergoes further development before migrating

1. MALARIA
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2. 2

3. 1. Mal-aria (Bad air) till 1880
2. Tropical disease due to presence of sporozoa of
plasmodium
3. Transmitted to humans by the infected female
mosquito Anopheles
4. Malarial parasite is a single cell protozoa called
Plasmodium.
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
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4. •
Malaria is caused by four species of
protozoa
Plasmodium malariae.
P. falciparum. (more lethal)
P. vivax.
P. ovale (rare).
•
The plasmodium transmitted to human by
the bite of an infected female anopheles
mosquito.
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5. • NMEP (National Malaria Eradication Program) in India
1958.
• Nearly complete eradication in due to
powerful insecticides.
• In 1970’s due to emergent of drug and
insecticides resistant all attempts failed.
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6. 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
asexual cycle
• NO AVAILABLE DRUGS ARE LETHAL TO
SPOROZOITES
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7. Pre-erythrocyitc
state
Zygote
Oocysts
Sporozoites
Sporozoites
Schizonts
Exo-erythrocyitc
state
Asexual
Erythrocytic
stage
Schizogony
Merozoites
Merozoites
Tropozoites
Blood
Schizonts
Merozoites
Tropozoites
Pyrogen + TNF-α+
Haem
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8. Sporozoites hardly survived in blood hence get
sheltered in Liver parenchymal cell
In Liver it divide and developed into multinucleated
SCHIZONTS. Hosts are asymptomatic
(PRE-ERHTHROCYTIC STATE)
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
TROPHOZOITES
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
ERYTHROCYTIC
STATE
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10. 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,
producing zygotes.
The zygotes become motile and elongated, developing into ookinetes.
The ookinetes invade the midgut wall of the mosquito where they develop
into oocysts.
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.
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11. • 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
polymerase
• RBCs infected with merozoite, ruptures and
releases thousands of merozoites along with
pyrogens, TNF- α and polymerised haem to
show symptoms of Malaria
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12. • 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
liver
• 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)
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14. Clinical presentation
• Early symptoms
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Headache
Malaise
Fatigue
Nausea
Muscular pains
Slight diarrhea
Slight fever, usually not intermittent
• Could mistake for influenza or gastrointestinal
infection

15. Clinical presentation
• 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
• Anemia,
thrombocytopenia,
jaundice,
hepatosplenomegaly, respiratory distress
syndrome, renal dysfunction, hypoglycemia,
mental status changes, tropical splenomegaly
syndrome

16. Drugs used to treat Malaria-First group
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4-aminoquinolones: Eg. Chloroquine, Amodiaquine
Chincona alkaloids: Quinine
Quinoline methanol: Mefloquine
Acridine: Mepacrine, Quinacrine
8-aminoquinolines: Primaquine, Bulaquine
Biguanides: Porguanil
Diaminopyrimidines: Pyrimethamine
Artemisinin derivative: Artesunate,Artemether, Arteether
Phenanthrene methanol: Halofantrine, Lumefantrine
Naphthoquinone: Atovaquone
Antibiotics: TTC, Doxycycline, Clindamycin
Sulfonamides and Sulfones: Sulfadoxine and Dapsone
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17. CLOROQUINE
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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
MOA
• 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
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synthesis