Malaria is caused by plasmodium parasites transmitted via mosquito bites. The document discusses the life cycle and species of malaria parasites, which includes P. falciparum, P. vivax, P. malariae, and P. ovale. It then covers the pathogenesis of malaria, including the hepatic and erythrocytic phases. Finally, it outlines the clinical features of malaria like febrile paroxysms, splenomegaly, hepatomegaly, anemia, and complications of P. falciparum malaria such as cerebral malaria. Diagnostic methods for malaria are also summarized, including microscopy, fluorescent microscopy, and rapid diagnostic tests.

2. -Trishna Kattel
roll no. 20
INTRODUCTION

3. MALARIA
• Name is derived from Italian
Mal’ aria or bad air
• Malaria is a mosquito-borne infectious
disease of caused by parasitic protozoan of the
genus Plasmodium.
• the disease is transmitted by a bite from an
infected female Anopheles mosquito
• In humans, the parasites multiply in liver and
infect the RBCs.

4. • Malaria is the fifth cause of death of infectious
diseases worldwide.
• It is a disease that can be cured within 48 hours, yet
it can cause fatal complications if the diagnosis and
treatment are delayed.
• Malaria Kills more people than AIDS
• Malaria kills in one year what AIDS kills in 15 years.
For every death due to HIV/AIDS there are about 50
deaths due to malaria.

5. Malaria–Early History
• The symptoms of
malaria were described
in ancient Chinese
medical writings. In
2700 BC, several
characteristic
symptoms of what
would later be named
malaria were described
in the Nei Ching.

6. HippocratesandMalaria
Hippocrates, who is
regarded as the "Father
of Medicine", was the
first to describe the
manifestations of the
disease, and relate them
to the time of year and
to where the patients
lived. He is the first
known malariologist.

7. History–Events onMalaria
• 1880 - Charles Louis Alphose Lavern discovered
malarial parasite in wet mount
• 1883 - Methylene blue stain - Marchafava
• 1891 - Polychrome stain- Romanowsky
• 1898 - Roland Ross - Life cycle of parasite
transmission, wins Nobel Prize in 1902
• 1948 - Site of Exoerythrocytic development in Liver
by Shortt and Garnham

8. EPIDEMIOLOGY

9. KEY AFFECTED AREAS
WHO. World Malaria Report 2010
Estimated 300-500 million clinical
cases each year
Approximately 2.5 million die
each year

11. CAUSATIVE AGENTS OF
MALARIA
PRESENTED BY:
SOFIYA MAKAJOO
ROLL NO:27

12. • Malaria is an infectious disease
caused by plasmodium species.
• Plasmodium is a protozoa
discovered by Alphonse
Laveran.
• Transmission of this parasite to
human is by blood sucking bite
of female anopheles mosquito
of various species.
ANOPHELES MOSQUITO

13. Four species of plasmodium which typically
infect humans are;
1. Plasmodium falciparum
2. Plasmodium vivax
3. Plasmodium malariae
4. Plasmodium ovale
• The genus plasmodium includes about 200
named species of intra-erythrocytic parasites.
• These species infect a wide range of mammals,
birds, reptiles, and amphibians.

14. SPECIES TYPES OF MALARIA
Plasmodium falciparum Malignant tertian malaria
Plasmodium vivax Benign tertian malaria
Plasmodium malariae Benign quartan malaria
Plasmodium ovale Benign tertian malaria
• Out of the four species PLASMODIUM VIVAX and
PLASMODIUM FALCIPARUM are the most common.

15. PLASMODIUM FALCIPARUM
• Malaria caused by P. falciparum
is known as malignant tertian
or pernicious malaria.
• The specific name ‘falciparum’
is derived from the
characteristic sickle-shape of
the gametocytes.
DISTRIBUTION : Found mainly
in tropical, sub- tropical, Africa,
South America and Asia.
PLASMODIUM
FALCIPARUM

16. INCUBATION PERIOD : 12 days
RBC CYCLE : 48 hrs or continuous
MALARIAL PIGMENT : Dark,brown or blackish,one
or two solid blocks
DRUG RESISTANCE : Yes
Average plasmodia per cubic mm : 50,000–500,000
Length of sexual cycle : 9 – 10 days
Length of asexual cycle : 36 - 48 hrs

17. Microscopical
appearance :
• Double “signet ring”
forms (two chromatin
dots per ring )
• Presence of Maurer’s
cleft.
• Crescent shaped
gametes.
PLASMODIUM
FALCIPARUM

18. Why P. falciparum is most highly pathogenic ??
• This species infects all RBCs, resulting in prominent
anemia.
• Its changes the RBC surface which causes endothelial
adherence with decreased microcirculation and
cerebral malaria.

19. PLASMODIUM VIVAX
• Malaria caused by P. vivax is
vivax malaria or Benign tertian
malaria.
DISTRIBUTION : Prevalent in
tropical and sub tropical countries
like Asia and America.
• The species of P. vivax contains
several sub species. Some are :
• Plasmodium vivax multinucleatum
• Plasmodium vivax hybernans
PLASMODIUM VIVAX

20. INCUBATION PERIOD : 14 days
RBC CYCLE : 44 – 48 hrs
MALARIAL PIGMENT : Yellowish, brown, fine granules.
DRUG RESISTANCE : No
Average plasmodium per cubic mm : 20,000
Length of sexual cycle : 8 – 9 days
Length of asexual cycle : 48 hrs

21. Microscopical
Appearance:
• Schuffner’s granules are
seen.
• May have ring forms.
• Enlarged RBC. PLASMODIUM VIVAX

22. PLASMODIUM MALARIAE
• Malaria caused by P. malariae is
known as Benign quartan malaria or
malariae malaria.
• It infects only senescent red cells.
DISTRIBUTION : It is prevalent in
tropical Africa and accounts for upto 25%
of Plasmodium infection.
PLASMODIUM MALARIAE

23. Microscopic
Appearance :
• Rosette schizont is seen.
• Presence of Ziemann’s
dots.
INCUBATION PERIOD : 30 days
RBC CYCLE : 72 hrs
MALARIAL PIGMENT : Dark, brown, coarse granules.
DRUG RESISTANCE : No
PLASMODIUM MALARIAE

24. PLASMODIUM OVALE
• Malaria caused by Plasmodium
ovale is Benign tertian malaria.
• It may infect only reticulocytes.
(<2 % of the RBC )
DISTRIBUTION : It is mainly
found in West Africa where
it is responsible for upto 10%
of malarial infection.
PLASMODIUM OVALE

25. INCUBATION PERIOD : 14 days
RBC CYCLE : 48 hrs
MALARIAL PIGMENT : Dark, yellowish, brown, coarse granules.
DRUG RESISTANCE : No
Microscopic Appearance :
• Enlarged oval red cells.
• Schuffner’s granules are
seen.
PLASMODIUM OVALE

26. Life Cycle of
Malarial Parasite
Presented by,
Rajitha Kodithuwakku Arachchi
Roll No 22

27. • Four species of genus plasmodium infect human with malaria
1. Pasmodium vivax
2. Plasmodium falciparum
3. Plasmodium malariae
4. Plasmodium ovale
• P.vivax and P.falciparum are more common.
• Requires 2 hosts to complete it’s life cycle.
• Human acts as the intermediate host.
• Female anopheles mosquito acts as the vector and the definitive host.

28. Life cycle in Human
• Life cycle starts when an infected mosquito bites a human.
• Sporozoite – infective form of the parasite, elongated and spindle shaped.
• Present in salivary glands of the infected mosquito.
• Sporozoites are introduced to the blood stream during the blood meal.
•Consists with several stages
1. Pre – erythrocytic Schizogony
2. Erythrocytic Schizogony
3. Gametogony
4. Exo – erythrocytic Schizogony

29. Pre – erythrocytic Schizogony
• Sporozoites leave the blood stream and enter in to liver parenchymal cells.
• Elongated and spindle shaped sporozoites become round in shape.
• Undergo multiple nuclear division and develop in to merozoites.
• 20,000 – 50,000 merozoites.
• After compleion of the cycle liver cells rupture and release merozoites in to the blood
stream

30. Erythrocytic Schizogony
• Merozoites released from ruptured liver cells penetrates RBC.
• Pass through stages of trophozoite, schizont and merozoite.
• 6- 24 merozoites in a RBC (depends on the species of the parasite)
• RBCs rupture and release merozoites.
• Merozoites attacks healthy RBCs and continue their multiplication.

31. Gametogony
• Some merozoites develop in to male and female gametocytes.
• Known as microgametocytes and macrogametocytes respectively.
• Develop in the RBCs of the capillaries of the internal organs such as spleen and bone
marrow.
• Microgametocytes – Smaller in size, large nucleus, light blue stained cytoplasm
• Macrogametocytes – Larger in size, small and compact nucleus, deep blue stained
cytoplasm

32. Exoerythrocytic schizogony
• Resembles the preerythrocytic cycle.
• Some sporozoites do not undergo asexual multiplication but enter into a dormant stage
known as hypnozoites.
• After some time these dormant forms reactivates to become sporozoites to form
merozoites and responsible for the relapse of malaria. Cannot be seen in malaria caused
by P. Falciparum.

33. Life cycle in mosquito
• Male and female gametocytes enter in to the female anopheles mosquito during a blood
meal from an infected human.
• In the mid gut of the mosquito each microgametocytes develops into 4 to 8 micro
gametes by the process of exflagellation.
• one macrogametocyte forms only one macrogamete and does not show any
exflagellation.
• Macrogamete and microgamete fuse together to form a zygote which develops in to
ookinete.
• Ookinete develops into oocyst. Oosyct matures and develops into thousanda of
sporozoites.

36. MALARIAL
PATHOGENESIS
By: Prithul Koirala

37. PATHOGENESIS
Malaria infection develops via two phases:
• Liver (exoerythrocytic phase),
• Erythrocytes (erythrocytic phase).

38. HEPATIC PHASE
• Sporozoites from mosquito's saliva enter the
bloodstream
• Migrate to the liver where they infect
hepatocytes, multiplying asexually for a period of
8–30 days.
• After a dormant period organisms differentiate to
yield merozoites
• Rupture host cells, escape into the blood and
infect red blood cells

39. • P.vivax and P.ovale form hypnozoites in
hepatocytes remains dormant, then
reactivates and form merozoites causing
late relapse in P.vivax malaria.

40. ERYTHROCYTIC PHASE
• Binds to RBCS
• Hydrolyze Hb by enzymes
• Trophozoites formed(single chromatin)
• Formation of schizonts
• Lysis of RBCs

41. • Gametocytes are formed by parasites in
RBCs which infect mosquito when it bites
infected person

42. • Parasite is protected from body's immune
system because it resides within the liver and
blood cells invisible to immune surveillance.

43. CEREBRAL MALARIA
• P.Falciparum infect RBCs leading to parasitic burden and
anemia
• RBCs clump together(rosette)and stick to endothelial
cells of blood vessel(sequestration)

44. • Sequestered red blood cells can
breach the blood–brain barrier
• Proteins like PfEMP1 forms
knob
• Stimulates production of
cytokines TNF,IL-1
• Induce fever,suppreses RBCs
production, stimulate Nitric
oxide production(tissue
damage)

45. Showing adhesion and sequestration

46. IMPACT OF SICKLE CELL TRAIT
Sickle cell trait causes cell to distort into curved shape
The molecule is ineffective in releasing oxygen.
Reduces the frequency with which malaria parasites
complete their life cycle in the cell.

47. CLINICAL FEATURES
OF MALARIA
By: Aishath Maeesha
Roll no. 26

48. • The signs and symptoms of
malaria typically begin 8–25
days following infection.
• Symptoms may occur later in
those who have taken
antimalarial medications as
prevention.
• Initial manifestations of the
disease—common to all
malaria species—are similar
to flu-like symptoms and can
resemble other conditions
such as septicemia,
gastroenteritis and viral
diseases

49. Febrile paroxysm
• Compromises of 3 stages:-
1. Cold stage : Patient feels
intense cold and shivering
2. Hot stage : Patient develops
high fever – 40.0°-40.6°C ,
severe headache and
vomitting
3. Sweating stage : Patient
sweats profusely

50. Splenomegaly
• Enlarged spleen is observed after paroxysms
which is often palpable

51. Hepatomegaly

52. Anaemia
• Anaemia of a microcytic or normocytic hypochromic
type develops due to hemolysis of infected and as well
as uninfected RBC’s
• Therefore patient may complain of extreme
fatigue,myalgia and weakness

53. Complications of P.Falciparum
Malaria
• Pernicious Malaria:
 Arises due to heavy parasitization
 Manifestations are grouped as:
 Cerebral malaria : Hyperpyrexia,
confusion, palsy, abnormal posturing
coma and paralysis
 Algid Malaria: severe abdominal pain,
vomitting, diarhhea, low blood pressure,
hypodermia and cold clammy skin
 Septicaemic Malaria: continuous fever,
shock, liver or kidney failure

54. • Black water fever:
 A complication of malaria in which RBC’s burst
in the bloodstream releasing hemoglobin
directly into the blood vessels and into the
urine, frequently leading to kidney failure.
 Occurs in persons who have been previously
infected.
 Clinical manifestations include:
 Bilious vommiting
 Intense Jaundice
 Anuria
 Passage of dark red or blackish urine

56. SRUTHI KRISHNAN
ROLL NO. 24
SEM- II
Presented by

57. • Light Microscopy
• Fluorescent Microscopy
• Quantitative buffy coat test
• Serological tests
• Molecular methods
• Rapid diagnostic tests

58.  Most reliable, economic and preferred
diagnostic procedure in malaria.
 Specimen : Peripheral Blood
Two types of peripheral blood smears are
prepared:

60.  All asexual erythrocytic stages (ring forms,
trophozoites, schizonts) as well as gametocytes
detected in P. vivax, P. malariae, P. ovale.
Only ring forms and gametocytes detected in P.
falciparum.

61. 2. Plasmodium vivax
Presence of Schuffner’s dots
Enlarged RBCs.
1. Plasmodium ovale
Presence of Schuffner’s dots
Schizonts do not have more
than 12 nuclei.

62. 3. Plasmodium malariae
Presence of Ziemann’s dots.
4. Plasmodium falciparum
Presence of Maurer’s dots.
Multiple rings in individual RBCs
with accole forms.

63. Kawamoto technique:
Blood smear stained with
acridine orange.
Stained slide examined
under fluorescent microscope.
Nuclear DNA – stained
green
Cytoplasmic RNA – stained
red

64. QBC tube coated with
acridine orange
(fluorescent dye)
Blood sample collected in
QBC tube centrifuged.
Buffy coat examined
directly under fluorescent
microscope.
Acridine-orange
stained malarial
parasites
appear brilliant
green.

65. Indirect immunofluorescence
Indirect Hemagglutinin assay(IHA)
Enzyme linked immmunosorbent assay (ELISA)
ELISA Indirect immunofluorescence

66. Polymerase Chain Reaction
More sensitive than microscopy.
Amplification of 18S rRNA genes.
Expensive
Requires specialized laboratory
set-up.

68. Kits available detect:
Histidine-rich
protein (HRP-II) of
P. falciparum.
Parasite lactate
dehydrogenase(pLDH)
of all four Plasmodium
species can also be
detected.

71. Chloroquine
 Rapidly acting erythrocytic schizontocide
 Controls most clinical attacks within 1-2 days
 Acts mainly on trophozoite blood stage; kills gametocytes of P. vivax, P. ovale,
and P. malariae (but not P. falciparum);
 no action on liver stages
 Dose: 600 mg stat, followed by 300 mg after 6 hours and 300 mg for the next
2 days.
 Adverse effect:
 Nausea, dysphoria, pruritus in dark-skinned patients, postural hypotension
 Hypotensive shock (parenteral), cardiac arrhythmias, neuropsychiatric
reactions,Retinopathy (cumulative dose, >g), skeletal and cardiac myopathy

73. Quinine
• Obtained from cinchona bark
• Acts mainly on trophozoite blood stage
• Kills gametocytes of P. vivax, P. ovale, and P. malariae (but not P. falciparum)
• No action on pre-erythrocytic stages
Adverse Effect
• Cinchonism: A large single dose or higher therapeutic dose taken is k/a
CINCHONISM. It includes:
- Ringing of ear
-Nausea & vomiting
-headache & mental confusion
-Vertigo
-difficulty in hearing
-visual defect

75. Primaquine
• It is highly active against gametocytes and
hypnozoites.
• Active against the pre-erythrocytic stage
• Poor erythrocytic schizontocide
Adverse effects
 Abdominal pain
 GI upset
 Leucopenia
 Hemolysis in G6PD deficient patients.

76. Artemisinins
• The most important of these analogs are
artesunate, artemether, and arteether.
• act very rapidly against all erythrocytic-stage
human malaria parasites
• increasing role in the treatment of malaria,
including multidrug-resistant P falciparum
malaria

79. • Artesunate
• Artemether
• Quinidine

80. Treatment During Pregnancy
1. IV quinine
2. Chloroquine
3. SP
4. Artesunate combinations
5. Quinine and clindamycin
6. Amodiaquine

81. What Is Drug Resistance?
• The ability of a parasite strain to survive and/or multiply
despite administration & absorption of a drug given in
doses equal to or higher than those usually
recommended but within the limit of tolerance of the
subject .

82. • Drug resistance is complicated by cross-resistance, which
can occur among drugs that belong to the same chemical
family or which have similar modes of action.
• Drug resistance results in a delay in or failure to clear
asexual parasites from the blood, which allows
production of the gametocytes that are responsible for
transmission of the resistant genotype.
MALARIAL DRUG RESISTANCE

83. Malaria Endemic Areas and Drug Resistance
Chloroquine resistance
SP resistance
Multi-drug resistance

84. Dristi Lamichhane
Roll No. 19

85. • Be Aware: risk factor, incubation period, symptom
• Avoid being Bitten by mosquitoes
• Chemoprophylaxis
• Immediately seek Diagnosis & treatment: if fever
occur 1 week – 3 months after arrival in endemic
areas
Key tools of prevention

86. What determines the spread of malaria?
Female Anopheles mosquito
Malaria spread depends on:
•Rainfall pattern
•Types of mosquitoes in the area
•How close are people to the breeding sites?
Some areas constantly have a high rate of malaria.
Other areas have “malaria seasons” or occasional
epidemics of malaria.

87. How often does malaria occur
in your area?
• Is it common and frequent throughout the
year?
– Young children and pregnant women are at
highest risk in these areas
– With frequent exposure, adults develop some
immunity to malaria
• Or is it seasonal, occurring in bursts during
rainy season or times of flooding

88. Where do mosquitoes breed?
Tire tracks Irrigation water
Rice paddiesRice paddies
Any place
there is water!

90. The main strategy for malaria control:
Attack the adult mosquitoes, or prevent
them from biting people.
Some risks:
1. Toxicity of DDT
2. Resistance of
mosquitoes

91. What are ways to prevent mosquito bites?
• Use mosquito repellants.
• Wear long pants and long sleeves.
• Wear light-colored clothes.
• Use window screens
• Use bed nets.

92. Other Ways to Prevent Malaria
Who is at the highest risk of malaria?
– Travelers to an area high in malaria
• Travelers often take prophylactic (preventive)
medicines to prevent malaria.
– Pregnant women (especially those with HIV)
• Pregnant women are given intermittent preventive
treatment. They are given at least 2 doses of a malaria
drug during their pregnancy.

93. • Travellers are at most risk of getting malaria
• Who recommend drugs for travellers
drug uses Adult dose
Chloroquine Areas without resistant Plasmodium
falciparum
500 mg weekly
Malarone Areas with multidrug-resistant P
falciparum
1 tablet (250 mg
atovaquone/100 mg
proguanil) daily
Mefloquine Areas with chloroquine-resistant P
falciparum
5oo mg weekly
Doxycycline Areas with multidrug-resistant P
falciparum
100 mg daily

94. 1. Find out about malaria in your
community
• Visit families to ask them about their
experiences with malaria.
• Ask about bed nets.
• Check for standing water.

95. 2.Teach about malaria
• Teach about malaria
and malaria
prevention.
• Use health stories for
malaria teaching.
• You will enjoy the
malaria comic book.
• Do skits; make
posters; tell stories; be
creative!
Where can you teach
about malaria?
1. During home visits
2. In community
meetings
3. At the health center
and local school

96. 3. Do community cleanup
• Encourage the community for cleaning
programs so that they work together with you
on this.
• Get rid of any sources of standing water (old
tires, cans, jars, pools of water).
• Cover any water containers.

97. 4. Encourage the use of long-lasting nets and
insecticides

98. RECENT ADVANCES
PRASUN KHANAL
ROLL NO. - 21

99. • An effective vaccine is not yet available for malaria
although several are under development
• The highly polymorphic nature of many P. falciparum
proteins results in significant challenges to vaccine
design
• Malaria vaccines in development include:
– Pre-erythrocytic or liver-stage vaccines
That aims to protect against the early stage of malaria
infection
– Blood-stage vaccines
That aims to reduce the severity of disease
– Transmission blocking vaccines
That are intended to prevent mosquitoes that fed on an
infected person from spreading malaria to new hosts

100. • Vaccine candidates that target antigens on
gametes, zygotes, or ookinetes in the
mosquito aims to block the transmission of
malaria.
• These transmission-blocking vaccines induce
antibodies in the human blood; when a
mosquito takes a blood meal from a protected
individual, these antibodies prevent the
parasite from completing its development in
the mosquito.

101. Vaccines
• SPf66
• RTS,S or Mosquirix
• PfSPZ

102. SPf66
• This vaccine was tested extensively in endemic
areas in the 90s, but clinical trials showed it to
be ineffective.

103. RTS,S
• RTS,S or Mosquirix is an
experimental recombinant
protein-based vaccine for
malaria expected to be licensed
in 2015.
• It targets the pre-erythrocytic
stage of the parasite’s life cycle.
• Infection is prevented by
inducing high antibody titers that
block the parasite from infecting
the liver.

104. PfSPZ
• It is a pre-erythrocytic
attenuated vaccine that
uses whole sporozoites
to induce an immune
response
• Sanaria, a US biotech
company, is involved in
it.

105. Different Approach To Immunization
• Genomics is now central to malaria research.
With the sequencing of P. falciparum, one of its
vectors Anopheles gambiae, and the human
genome, the genetics of all three organisms in the
malaria lifecycle can be studied.
• The ability to produce genetically modified
mosquitoes that do not transmit malaria,
potentially allowing biological control of malaria
transmission.

106. World Malaria Day, April 25
• The theme for 2014
and 2015 is:
“Invest in the
future. Defeat
malaria”

107. Thank You