3. Exhibits a complex life cycle
Alternating cycles of asexual development
(schizogony ) in man and sexual development
(sporogony) in mosquito
Alternation of host and alternation of generation
Man –Intermediate host
Mosquito –Definitive host
7. Shortest in P. falciparum (6 days)
Longest in P.malariae (13—16
days)
8 days & 9 days in P.vivax & P.
ovale respectively.
Pre erythrocytic schizont may
contain 2000– 50000
merozoites.
Rupture of liver cells and
invasion of RBCs by merozoites
8. Merozoites multiply inside
RBCs
Trophozoites, schizonts, &
merozoites formed.
Rupture of RBCs,liberation of
merozoites
Heralding of clinical illness
Haemoglobin of RBCs
converted into malaria pigment
P.ovale & P.vivax
P.malariae
P.falciparum
9. In Falciparum malaria alone
the erythrocytic schizonts
aggregate in the capillaries
of internal organs (brain
,kidney)
All forms seen in the
peripheral blood except in P.
falciparum ( ring forms &
gametocytes)
P.ovale & P.vivax
P.malariae
P.falciparum
10. Conversion of merozoites into
micro & macro gametocytes
Asymptomatic phase
Human carriers
Half life in blood –2—3 days.
Gametocytes ingested by the
biting mosquito
P.ovale & P.vivax
P.malariae
P.falciparum
11. Hypnozoites in liver get reactivated after
weeks months or years
responsible for relapse
No hypnozoites in P. falciparum-no relapse,
recrudescence present-reappearence of
symptoms due to existing infection due to
drug resistance or incomplete elimination by
the immune system
12. Minimum of 12 gametocyte/ ml of
blood to infect mosquito
Microgametocytes undergo
exflagellation-8 micro gametes
formed
Fusion of micro and macro gametes
Zygote, ookinete,oocyst (with
sporozoites)
Migration of sporozoites to the
salivary gland
Mosquito infective
13. Bite of female Anophelus mosquito—sporozoite
induced.
Blood transfusion, vertical transmission–
trophozoite induced, inc. pd . short & no relapse
Incubation period–
12 days for falciparum,
13-17 days for vivax & ovale,
28-30 days for malariae
14. Febrile paroxysms with chills - cold stage (15 mts),
hot stage (2 – 6 hrs) &
Stage of sweating.
Periodicity of attack depends on species-
TERTIAN 48 hrs - P. falciparum,
P. vivax, P. ovale
QUARTAN 72 hrs - P. malariae.
QUOTIDIAN every 24 hrs - in mixed
infection or in Falciparum malaria.
15. ANAEMIA
Mechanical destruction of RBCs
Decreased erythropoiesis in bone marrow
Lysis and phagocytosis of uninfected RBCs
Autoimmune destruction of RBCs
(falciparum malaria)
SPLENOMEGALY
Massive proliferation of macrophages which phagocytize
both infected and uninfected RBCs
16. More pathogenic.
High level parasitaemia (2,50,000 – 3,00,000/ml of
blood), 30 – 40 % of RBCs parasitised.
Invades RBCs of all ages.
Blockade of small capillaries and venules due to sticky
parasitised RBCs – tissue hypoxia.
17. Pernicious Malaria – cerebral malaria, algid
malaria, septicaemic malaria.
Blackwater Fever - repeated infections of
falciparum, inadequate treatment with quinine &
resumption of quinine therapy for new attack –
autoimmune haemolysis.
18. 2 types– INNATE & ACQUIRED
Innate immunity
Age of RBCs
Nature of haemoglobin
G6PD deficiency
Absence of Duffy antigen
Acquired immunity
Concomitant, premunition or infection
immunity
19. Humoral or CMI
Antibodies –Species,stage or strain specific
NK cell activity, & activated macrophages for
CMI
Malarial parasite evades the immune system
by periodically changing the expression of
antigens
20. Collection of blood few hrs after at the peak of a paroxysm
Thick smear & thin smear
Thick smear for spotting the parasite & thin smear for identification
of species
All stages of the parasite are seen in all
types except falciparum malaria
Absence of parasite & presence of malaria pigments is diagnostic
of falciparum infection
21. Multiple rings and accole forms in falciparum
malaria
RBCs enlarged in vivax infection
Acridine orange staining & screening is a quicker
method
Microscopy – sensitive, inexpensive, but laborious
and technique dependent
22. DETECTION OF ANTIGENS
Dipstick with monoclonal antibody (15 mts)
HRP II– for P. falciparum only
pLDH– for all four species- can differentiate P.f from other
species.
Pan malarial antigen
RDTs sensitive & specific for P. falciparum (90%)
23. ADVANTAGES
simple
no special equipment
minimal technical skill
can detect sequestered antigens (falciparum malaria)
DISADVANTAGES
Costly
False positive results in asymptomatic patients(pLDH)
Cannot distinguish between infection of the species other than P.
falciparum
24. Identification of M.P in peripheral blood
Staining of centrifuged and compressed red cell layer
with Acridine orange and viewing under an U.V. source
More sensitive than thick smear examination
Negative test within 1 minute and positive test in few
mts
27. First reported in Columbia
Present in India
Poses a huge challenge
Reasons
Inadequate drug doses
Lack of adequate drugs
Poor quality drugs
Inappropriate consumption
All these resulting in mutation
28. WHO DEFINITION
Ability of the parasite to multiply or survive in the presence of
concentrations of the drug that normally destroy the parasite of
the same species or prevent their multiplication
LEVELS OF RESISTANCE
R1– Parasitaemia clears . Recrudescence occurs
R2—Decrease in parasitaemia but no clearance
R3—No reduction in parasitaemia
29. Spraying of insecticides-(DDT, MALATHION)
Spraying of larvicides on breeding sites-Petroleum oils, Paris
Green
Using larvivorous fish—(Gambusia affinis) & Bacillus thuringiensis
Avoid exposure to mosquito bites—nets,repellant creams, mats
Chemoprophylaxis—pyrimethamine and proguanil
Flooding & flushing of breeding places
Elimination of breeding places such as lagoons and swamps
Early diagnosis and treatment
Vaccines –not successful