The document summarizes the life cycle of Plasmodium parasites that cause malaria. It describes their complex life cycle between human and mosquito hosts, including the asexual replication stages in humans (schizogony) and the sexual stages in mosquitos (sporogony). It provides details on the different species of Plasmodium, their stages of development, symptoms caused, and methods of diagnosis and treatment of malaria.

2. Plasmodia
 Plasmodium falciparum
 P.vivax
 P.ovale


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

6.  Pre erythrocytic (primary) schizogony
 Erythrocytic schizogony
 Exo erythrocytic schizogony
 Gametogony

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

25.  PCR
 Antibody detection

26.  Quinine
 Chloroquine
 Primaquine
 Quinolones

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

30. TROPHOZOITE-RING STAGE GAMETOCYTE

31. TROPHOZOITES -RING STAGE EXFLAGELATION