Malaria is caused by protozoan parasites of the genus Plasmodium which belong to the phylum Apicomplexa. It remains a major global health problem affecting over 40% of the world's population, with estimates of 350-500 million cases annually. The malaria parasite has a complex life cycle involving sexual reproduction in mosquitos and asexual replication in human hosts. Symptoms in humans include fever, chills, sweats and headaches. Complications can be severe especially with P. falciparum infection, potentially causing cerebral malaria, respiratory distress or kidney failure. Diagnosis involves identification of the parasite in blood smears and treatment depends on the infecting species, such as chloroquine for P. viv

2. Malaria parasite belongs to
Phylum: Apicomplexa
Class: Sporozoa
Order: Haemosporida
Genus: Plasmodium.
Calassification of Malaria

3. Malaria remains the world's most
devastating human parasitic infection.
Malaria affects over 40% of the world's
population. WHO, estimates that there
are 350 - 500 million cases of malaria
worldwide. In India 2 million cases and
1000 deaths annually
Distribution of Malaria

4. Protozoan parasites characterized by the production
of spore-like oocysts containing sporozoites were
known as sporozoa.
They live intracellularly, at least during part of their
life cycle.
At some stage in their life cycle, they possess a
structure called the apical complex, by means of which
they attach to and penetrate host cells.
These protozoa are therefore grouped under the
Phylum Apicomplexa.
The medically important parasites in this group are
the malaria parasites, Coccidia, and Babesia.
The Phylum Apicomplexa includes 2 classes viz.
haematozoa and coccidia and 3 orders—eimeriida,
haemosporida, and piroplasmida.
Characteristics of Malaria

5. Plamodium vivax: Benign Tertian
Malaria.
Plasmodium falciparum: Malignant
Tertian Malaria.
Plasmodium malariae: Benign Quartan
Malaria.
Plasmodium ovale: Benign Tertian Malaria.
Causative Agents of Human Malaria

6. Malaria parasites—Erythrocytic stages of the
four species (Giemsa stain. Magn × 2000)

7. The malaria life cycle is a complex system
with both sexual and asexual aspects . cycle
of all species that infect humans is basically
the same. There is an exogenous sexual
phase in the female Anopheles mosquito (the
definitive host) called sporogony during which
the parasite multiplies. There is also an
endogenous asexual phase that takes place
in the vertebrate or human(the intermediate
host) host that is called schizogeny
The malaria life cycle

8. life cycle of malaria

9. occurs due to enhanced phagocytosis of
remnants of ruptured red cells and debris of
schizont.
Remnants
Pathogenesis and Clinical Picture
 Enlargement of liver and spleen.

10. The common first symptoms – fever, headache,
chills and vomiting – usually appear 10 to 15 days
after a person is infected. If not treated promptly
with effective medicines, malaria can cause severe
illness and is often fatal.
Stage1 (cold stage): Chills for 15 mt to 1 hour
Caused due to rupture from the host red cells escape
into Blood Preset with nausea, vomitting,headache.
Stage 2 (hotstage): Fever may reach upto 400c
may last for several hours starts invading newer red
cells.
Early symptoms

11. Stage3: (sweating stage) Patent starts sweating,
concludes the episode Cycles are frequently
Asynchronous Paroxysms occur every 48 – 72 hours
In P.malariae pyrexia may last for 8 hours or more
and temperature my exceed 410c
More commonly, the patient presents with a combination
of the following symptoms
Fever
 Chills
 Sweats
 Headaches
 Nausea and vomiting
 Body aches
 General malaise.

12. Complications
• Vivax, ovale & malariae malaria Relatively benign.
• Chronic malariae malaria Nephrotic syndrome.
Parasite produces increased amount
of antigens
Immune system produces increased
amount of antibodies.
Antigens attach to antibodies producing
immune-complex in blood.
Immune-complexes are deposited on
the glomerular walls activating the
complement
Child has
nephrotic syndrome
C1, 4, 2,3, 5, 7, 96, 8, MAC
Kidney tissue damage.

13. Complications of falciparum malaria
1- Knobs develop on surface of infected RBCs
Knobs are parasite antigens expressed on the
surface of infected red cells containing
trophozoites and schizont stages.
They adhere to receptors found on endothelium of
blood capillaries of blood supply internal organs
anoxia and necrosis.
Normal RBC
Infected RBC
Parasite antigens
Blood capillary

14. In brain : cerebral malaria. Headache, drowsiness,
convulsions & coma
In GIT : ischaemia in capillary bed of intestinal wall.
Diarrhoea, dysentery, gastrointestinal bleeding
In liver : impaired glycogenolysis, Hypoglycaemia.
In the kidney: acute renal failure.
In the lung : Pulmonary oedema, difficulty in breathing.
Hypotension, circulatory collapse & chock
,

15. Complications of falciparum malaria
2- Hyper-reactive malarial splenomegaly
The spleen is markedly enlarged with increased IgM
production. This is due to reduction of T-suppressor
cells that control B-cell activation.
3- Black water fever
Occurs: when?
- Repeated attacks of P.falciparum infection.
- Incomplete quinine therapy.
Pathogenesis
Massive intravascular haemolysis occurs producing
Anaemia, haemoglobinuria, jaundice.
Cause This is autoimmune with development of
antibodies to infected red blood cells.

16. Pathogenesis of Black Water Fever
Normal urine
Haemoglobinuria
Jaundiced patient
Blood Vessel of the infected patient
Normal RBCs Infected RBCs
Auto-antibodies

18. 1- Thin and thick blood films to demonstrate the parasite.
Thin blood film
Thick blood film
5-Giemsa stained
blood films
Microscopic Diagnosis
3-One drop of
blood spread on a
slide
4- drops of blood
spread in a small
circle on a slide
1-Finger prick
2-put drop of
blood on slide

19. Buffy Coat Method
RBCs
Plasma
WBCs, platelets, parasite
Patient’s
blood
Buffy coat
Centrifugation of
blood sample
A technique used for collection of parasite from blood sample

20. P. vivax P. ovale P. malariae P. falciparum
♂♀ ♀ ♀♀ ♂ ♂♂
Schuffner’s dots Ziemann’s dots Maurer’s clefts
Malaria pigments (Haemozoin)
X
X
Enlarged,
rounded
Enlarged,
oval Normal size & shape
Ring 1/6
RBC size
Ring 1/3
RBC size
Ring 1/3
RBC size
Ring 1/3
RBC size
Multiple rings
Not seen in
peripheral blood
Band-
shaped

21. Diagnosis
2- Detection of circulating parasite
antigen using monoclonal antibodies.
3- Detection of parasite DNA and RNA in patient’s
blood using DNA and RNA probes.
Malaria pigments = Haemozoin
It is the remnants of haemoglobin that
was digested by Plasmodium parasite
Schuffner’s dots
Ziemann’s dots
Maurer’s clefts It is degeneration process
occurring in Plasmodium
infected RBCs
Called: Stippling
T
C

22. Control
• Treatment of cases.
• Mosquito control.
• Chemoprophylaxis.
• Vaccination trials:
The problem is antigenic variation. A synthetic
vaccine with separation of the gene responsible for
antigenic variation.

23. Chrooquine sulfadoxine, and pyrimethamine
along with primaquine. In chlroquine
resistance, quinine or artemesinin are used.
Treatment

25. Babesia species causes Babesiosis
Hard tick
‫القراد‬
Geographical Distribution: North and South
America and Europe.
Babesia is an animal parasite that causes Texas
cattle fever.
It affects humans in contact with animals.

26. Mode of Infection
• Through the bite of hard ticks.
• Through blood transfusion.
budding
merozoites
Sporozoites
infective stage
Hard tick
Rings
diagnostic
stage
Rupture

27. Pathogenesis and Clinical Picture
Asymptomatic.
Malaria-like picture with haemolytic anaemia
but NO periodicity.
Fulminant disease that may end fatally in:
Splenectomized OR Immunodefficient
patients.
Babesia is an opportunistic protozoan

28. Diagnosis
1- Blood film
2- Serology
3- PCR
Prevention and Control
Measures to control ticks
Treatment
Clindamycin + Quinine

29. Compare between
Blood picture of falciparum malaria and babesia
infected patient.
Ring stage
Gametocyte stage
Ring stage
P.falciparum Babesia
Malaria pigments: present
No malaria pigments