Malaria is caused by Plasmodium parasites and transmitted via the bites of infected Anopheles mosquitoes. The parasite has a complex life cycle alternating between human and mosquito hosts. In humans, it causes flu-like symptoms including fever, chills, and headaches during the blood stage of infection. Diagnosis is usually by microscopic examination of blood smears, and treatment depends on the infecting parasite species. Complications can occur if not treated promptly, with cerebral malaria being the most severe manifestation. Prevention relies on mosquito control and the use of prophylactic drugs for travelers visiting malaria-endemic regions.

1. MALARIA
DR. SUMESH KUMAR DASH
PG RESIDENT,
DEPARTMENT OF MICROBIOLOGY,
IMS & SUM HOSPITAL.

2. INTRODUCTION
• Malaria is one of the oldest documented diseases of mankind.
• The name “Malaria” (“Mal” means bad and “aria” means air) was derived from the
ancient false belief that “disease is spread by air pollution through stagnant water
and marshy lands”
• French army surgeon Alphonse Laveran (1880) was the first to discover the causative
agent Plasmodium, in the red blood cell (RBC) of a patient in Algeria.
• Golgi had described the asexual cycle of the parasite in RBC.
• Sir Ronald Ross, in 1897 had described the sexual cycle of the parasite in female
Anopheles mosquito in Secunderabad, India.

3. CAUSATIVE AGENT
• P
. vivax causes benign tertian malaria. (periodicity of fever is once in 48 hours, i.e. recurs every
third day)
• P
. falciparum causes malignant tertian malaria. (severe malaria, periodicity of fever is once in
48 hours, recurs every third day)
• P
. malariae causes benign quartan malaria. (periodicity of fever is once in 72 hours, i.e. recurs
every fourth day)
• P
. ovale causes ovale tertian malaria. (periodicity of fever is once in 48 hours, i.e. recurs every
third day)
• P
. knowlesi causes quotidian malaria. (fever periodicity is once in 24 hours, i.e. recurs every
day).

4. LIFE CYCLE
Host: Plasmodium completes its life cycle in two hosts:
• Female Anopheles mosquito is the definitive host where the sexual cycle
(sporogony) takes place.
• Man acts as intermediate host where the asexual cycle (schizogony) takes place.
• Male Anopheles doesn’t feed on man and feeds exclusively on fruit juices, i.e.
why male Anopheles doesn’t transmit the disease.
• Whereas female Anopheles needs at least two blood meals before laying eggs.

5. Infective form:
• Sporozoites are the infective form of the parasite.
• They are present in the salivary gland of female Anopheles mosquito.
• When Plasmodium species is transmitted by blood transfusion or through placenta,
act as infective form.
Mode of transmission:
• Man gets infection by the bite of female Anopheles mosquito.
• Sporozoites from the salivary gland of the mosquito are directly introduced into the blood
circulation.
• Rarely, it can also be transmitted by: Blood transfusion
Transplacental transmission.

6. HUMAN CYCLE
In humans, the asexual cycle takes place through the following stages:
• Pre-erythrocytic schizogony
• Erythrocytic schizogony
• Gametogony.

7. Pre-erythrocytic Schizogony
• This stage occurs in liver and it is so named because it occurs before the invasion of RBC.
• The motile sporozoites leave the circulation within 30 minutes and enter liver.
• After entering into hepatocytes, the spindle shaped sporozoites become rounded and lose
their apical complex and transform into trophozoites.
• Trophozoite is the feeding stage of the parasite which later on undergoes several nuclear
divisions (schizogony) and transforms into pre-erythrocytic schizont.
• Pre-erythrocytic schizont contains several merozoites; which are released outside on rupture
and attack RBCs to perform erythrocytic schizogony.
• Some sporozoites of P
. vivax and P
. ovale don’t develop further and may remain in liver as
hypnozoites and cause relapse of malaria after many years.

9. Erythrocytic Schizogony
• The hepatic merozoites after released from pre-erythrocytic schizont, attack RBCs.
• The process of entry into RBC takes about 30 seconds .
• Trophozoite: Soon the pear shaped hepatic merozoites round up, lose their internal
organelle and transform into trophozoites.
• Ring form: Early trophozoite form is known as ring form. It is annular or signet ring
appearance containing a central vacuole and peripheral thin rim of cytoplasm and a
nucleus.
• Late trophozoite: Ring form enlarges and becomes more irregular due to amoeboid
movement and transforms into late trophozoite or amoeboid form.
• Schizogony: Late trophozoite undergoes multiple nuclear divisions (erythrocytic
schizogony or merogony) and produces 6–30 daughter merozoites arranged in the form
of rosette.

10. • RBCs then rupture to release the daughter merozoites, malarial pigments and toxins
into the circulation which result in malarial paroxysm of fever at the end of each
erythrocytic cycle.
• Each merozoite is potentially capable of invading a new RBC and repeating the cycle.
• The time interval between entry of the parasite to the body and appearance of the
first clinical feature is known as incubation period.
• It varies between the species:
• P. vivax - 14 days (ranges 8–17 days)
• P. falciparum - 12 days (ranges 9–14 days)
• P. malariae - 28 days (ranges 18–40 days)
• P. ovale - 17 days (ranges 16–18 days)

11. Gametogony
• After a series of erythrocytic cycles, some merozoites after entering into RBCs, instead of developing into
trophozoites, they transform into sexual forms called as gametocytes.
• The gametocytic development takes place in the blood vessels of internal organs such as spleen and bone
marrow and only the mature gametocytes appear in the peripheral blood.
• The gametocytes of all the species are round in shape except in P
. falciparum in which they are crescent or
banana shaped .
• They are of two types—(1) Male gametocyte (or microgametocyte) and (2) Female gametocyte (or
macrogametocyte)
• Neither gametocytes don’t cause any clinical illness nor they divide.
• Individuals harboring gametocytes are considered as carriers or reservoirs of infection and play an
important role in the transmission of the disease.

12. MOSQUITO CYCLE
• A female Anopheles mosquito during
the blood meal, takes both the
asexual forms and the sexual forms.
• The asexual forms get digested
whereas the sexual forms, i.e. the
gametocytes undergo further
development.
• Hence considered as infective form of
the parasite to mosquito

13. CLINICAL MANIFESTATION
• Fever
• Chills
• Sweats
• Headaches
• Nausea and vomiting
• Body aches
• General malaise.

14. How Malaria Present Clinically
• FEBRILE PAROXYS
1. Cold stage: Lasts for 15 minutes to 1 hour. The patient feels lassitude, headache, nausea,
intense cold, chill and rigor.
2. Hot stage: Patient develops high grade fever of 39–41°C and dry burning skin.
Headache persists but nausea diminishes.
3. Sweating stage: Fever comes down with profuse sweating. Skin becomes cold and
moist. Patient feels relieved and often asleep. This stage lasts for 2–4 hours.
• ANEMIA: After a few paroxysms of fever, patient deve lops a normocytic normochromic
anemia
• SPLENOMEGALY: After a few weeks of febrile paroxysms, spleen gets enlarged and
becomes palpable. Splenomegaly is due to massive proliferation of macrophages that
engulf parasitized and nonparasitized coated RBCs.

15. LABORATORY DIAGNOSIS
Microscopic tests
• Peripheral blood smear - Gold standard
• Fluorescence microscopy (Kawamoto’s technique)
• Quantitative buffy coat examination (QBC)
Non-microscopic tests
• Antigen detection tests (RDTs) or ICTs
• Antibody detection – ELISA
• Culture - RPMI 640 medium
• Molecular diagnosis - PCR

16. Peripheral Blood Smear
Collection of blood
• Best prepared directly from capillary blood
• In EDTA bulb (used within 30 mins)
Time of collection
• As soon as possible if malaria is suspected
• Before administering antimalarials
• During pyrexial phase
Type of blood film
• Thick film
• Thin film

17. THICK FILM
• 30 to 40 times more sensitive than thin films
• More suitable for detection of malarial parasite when they are few in number
• Blood is not fixed, RBCs are lysed during staining (only parasitic forms will be seen)
THIN FILM
• To confirm the plasmodium species
• Assists in the identification of mixed infections
• Blood is fixed, parasites are seen within the RBCs
• Also helps in assessing the response to treatment especially in areas where drug
resistance is suspected (by counting the number of parasitised RBCs before & after
the treatment)

18. Making Of Film

19. Fixation & Staining
• Fixation – thin films are fixed with absolute alcohol for 1 to 2 mins.
• Staining – films are stained with Romanowsky stain: Giemsa, Field’s, Wright’s
• Giemsa - 10% solution for 10 mins

20. Reporting Of Blood Film
Look for the different morphological
forms of parasite in blood smear:
1. Trophozoites / ring forms
2. Schizont
3. Gametocytes
Identify species – differences in the
characteristics of morphological
forms in different species

21. QUANTITATIVE BUFFY COAT
• Capillary tube is coated with an anticoagulant & Acridine orange
fluorescent dye.
• After centrifugation, the tube can be used for two purpose:
1. Complete blood count
2. Identification of malarial parasite using a fluorescence microscope

22. RAPID DIAGNOSTIC TESTS DETECT MALARIA
ANTIGENS

23. TREATMENT
• Chloroquine can be used for P.vivax.
• P.Falciparum is resistant to chloroquine, mefloquine used.
• Artemisinin is being used increasingly and has been found to be useful the
parasite is resistant, and hence is the drug of choice.

24. COMPLICATIONS
• Cerebral malaria: Occurs due to plugging of brain capillaries by the rosettes of sequestered
parasitized RBCs leading to vascular occlusion and cerebral anoxia.
• Pernicious malaria: It is characterized by blackwater fever, algid malaria and septicemic malaria
• Black water fever: This syndrome is characterized by sudden intravascular hemolysis followed by
fever, hemoglobinuria and dark urine.
• Algid malaria: Characterized by cold clammy skin, hypotension, peripheral circulatory failure and
profound shock.
• Pulmonary edema
• Hypoglycaemia
• Renal failure
• Bleeding/disseminated intravascular coagulation
• Severe jaundice

25. THANK YOU