Over 200 million malaria cases and 655,000 deaths occurred globally in 2010 according to WHO estimates. Plasmodium falciparum causes the most severe form of malaria, characterized by high parasitemia levels and life-threatening complications such as cerebral malaria and acute renal failure. The malaria parasite has a complex life cycle involving sexual reproduction in mosquitoes and asexual reproduction in human hosts, causing cyclic fever symptoms. Definitive diagnosis of malaria requires microscopic examination of blood films to identify the plasmodium species. Treatment depends on the identified species, with chloroquine used for chloroquine-sensitive P. falciparum and P. ovale infections.

3. Epidemiology
 According to estimates from the World Health
Organization, over 200 million cases and about
655.000 deaths have occurred in 2010 due to Malaria.
 According to the World Health Organization (WHO)
Malaria Report 2011, a total of 106 countries in the
world are at risk of transmission of malaria infection.

4. Pathogenesis
 Malaria caused by Plasmodium falciparum is more
severe than that caused by other plasmodia. It is
characterized by far more red cells than the other
malarial species and by occlusions of capillaries with
aggregates of parasitized red cells.
 P. falciparum causes a high level of parasitemia
because it can infect red cells of all ages.

5.  This leads to life threatening hemorrhages and
necrosis particularly in the brain further more
extensive hemolysis kidney damage occur which result
in heamoglobinuria. The dark color of the patient’s
urine given rise to the term black water fever. The
hemoglobinuria can lead to acute renal failure.

6.  The timing of fever cycle is 48 hours for P. falciparum
as well as P. ovale.

7.  The vector and definitive host for plasmodia is the
female Anopheles mosquito (only the female takes a
blood meal). There are two phases in the life cycle: the
sexual cycle, which occurs primarily in mosquitoes,
and the asexual cycle, which occurs in humans, the
intermediate hosts.

8.  The sexual cycle is called sporogony because
sporozoites are produced, and the asexual cycle is
called schizogony because schizonts are made.

9. Life Cycle
 The life cycle in humans begins with the introduction
of sporozoites into the blood from the saliva of the
biting mosquito. The sporozoites are taken up by
hepatocytes within 30 minutes. This "exoerythrocytic"
phase consists of cell multiplication and
differentiation into merozoites.P. vivax and P. ovale
produce a latent form (hypnozoite) in the liver; this
form is the cause of relapses seen with vivax and ovale
malaria.

10.  Merozoites are released from the liver cells and infect
red blood cells. During the erythrocytic phase, the
organism differentiates into a ring-shaped
trophozoite. The ring form grows into an ameboid
form and then differentiates into a schizont filled with
merozoites. After release, the merozoites infect other
erythrocytes. This cycle in the red blood cell repeats at
regular intervals typical for each species. The periodic
release of merozoites causes the typical recurrent
symptoms of chills, fever, and sweats seen in malaria
patients

11.  The sexual cycle begins in the human red blood cells
when some merozoites develop into male and others
into female gametocytes.

12.  The gametocyte-containing red blood cells are
ingested by the female Anopheles mosquito and,
within her gut, produce a female macrogamete and
eight spermlike male microgametes. After fertilization,
the diploid zygote differentiates into a motile ookinete
that burrows into the gut wall, where it grows into an
oocyst within which many haploid sporozoites are
produced. The sporozoites are released and migrate to
the salivary glands, ready to complete the cycle when
the mosquito takes her next blood meal.

14. Incubation period
 10-15 days for P. falciparum and vary weeks to month.

15. Clinical Features
 Fever
 Anemia
 Splenomegaly

16. Complications
 Severe anaemia
Cerebral Malaria
Renal failure
pulmonary edema
Intestine—diarrhoea
Liver—jaundice

17.  Intravascular haemolysis
Black water fever
 Metabolic acidosis
 Spleenic rupture
 In pregnancy
Maternal death, abortion, still birth,low-birth weight.

18. Laboratory Diagnosis
 Collection of Blood:-
Blood should be collected s soon as malaria is
suspected(it may be necessary to collect blood on
several occasions to detect the parasites)
Before the patient receives antimalarial drug.

19. Microscopic examination of Blood
Films
 Two types of blood films(Thick and thin) are taken. It
is a good practice to take both, the thick and thin
films, at the same time either or same side or on two
different slides so that the parasite may be quickly
detected in thick film and then thin film examined for
identifying the species.

20. Following steps are taken:
I. Thick and thin films are made and allowed to dry.
II. Thick, films are stained with field’s stain and
giemsa’s stain.
III. Films are washed and dried.
IV. Then examined under oil immersion objective lens.

21.  If more than 5% of red blood cells are parasitized, the
diagnosis is usually P. falciparum malaria.

22. Red cells:
Crescent shaped.
Banana shaped, Gametocyte with attached Red cell
ghost.
Seen in peripheral blood smear 10 days after infection.

23.  Complete blood count
o Haemoglogin Level:-
Low
o Eosinophilia
o ESR
Raised

24. • Total Bilirubin:-
Raised
 CSF Examination:-
In Cerebral Malaria
Protein-Raised
Glucose-Decreased

25.  Urine Analysis
Oliguria, protein casts and RBC’s in urine suggest
Black water fever.

26.  Bone Marrow Examination:-
Chronic cases
 Other
Rapid Diagnostic Test (RDT).

27.  Chest X-ray helpful if respiratory symptoms are
present.
 CT scan to evaluate Cerebral edema or hemorrhage.
 PCR to determine the specie.

28. Treatment
 Chloroquine-sensitive plasmodium falciparum =>
Chloroquine
 P. ovale => Chloroquine plus primaquine