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Malaria
Alternative names:
·        Quartan malaria
·        Falciparum malaria
   
·        Blackwater fever
·        Tertian malaria
A vector-borne infectious
disease caused by protozoan
parasites.
It is widespread in tropical and
subtropical regions
A bite from an infective female
Anopheles mosquito.
Anopheles must be infected
through a previous blood meal
taken on an infected person to
transmit malaria
At risk for malaria:
40% of the world’s population
more than 500 million are ill of malaria
yearly
If treated in the early stages, malaria can be
cured.
HIV, malaria and TB are among the most important
infectious agents in the world. and all have the same
property of establishing chronic infection without an
effective immune response.”
Plasmodium falciparum - most common
and deadly type of malaria infection
- can lead to cerebral malaria
P.vivax - most common
- causes relapse if treatment was not
completed.
P.malaria
P.ovale.
Female Anopheles are:
Anthropophilic : from humans
Zoophilic : from animals
Endophagic : prefer to bite indoors
Exophagic : prefer outdoor biting
Liver Stage. Human infection is initiated when sporozoites
are injected with the saliva during mosquito feeding. The sporozoites
enter the circulatory system and within 30-60 minutes will invade a
liver cell. Host cell entry, as in all apicomplexa, is facilitated by the
apical organelles. After invading the hepatocyte, the parasite
undergoes an asexual replication. This replicative stage is often
called exoerythrocytic (or pre-erythrocytic) schizogony.
PATHOPHYSIOLOGY
:
In P. vivax and P. ovale some of the sporozoites
do not immediately undergo asexual replication,
but enter a dormant phase known as the
hypnozoite. This hypnozoite can reactivate and
undergo schizogony at a later time resulting in a
relapse.
Blood Stage. Merozoites released from
the infected liver cells invade erythrocytes.
The merozoites recognize specific proteins
on the surface of the erythrocyte and actively
invade the cell in a manner similar to other
apicomplexan parasites.
After entering the erythrocyte the parasite undergoes a
trophic period followed by an asexual replication. The
young trophozoite is often called a ring form due to its
morphology in Geimsa-stained blood smears. As the
parasite increases in size this 'ring' morphology
disappears and it is called a trophozoite.
parasites.
Nuclear division marks the end of the
trophozoite stage and the beginning of the
schizont stage. Erythrocytic schizogongy
consists of 3-5 rounds (depending on species) of
nuclear replication followed by a budding
process. Late stage schizonts in which the
individual merozoites become discernable are
called segmenters.
The host erythrocyte ruptures and releases the
merozoites. These merozoites invade new
erythrocytes and initiate another round of
schizogony. The blood-stage parasites within a
host usually undergo a synchronous schizogony.
Sexual Stage. As an alternative to schizogony some of
the parasites will undergo a sexual cycle and terminally
differentiate into either micro- or macrogametocytes.
Gametocytes do not cause pathology in the human host
and will disappear from the circulation if not taken up by
a mosquito.
Gametogenesis, or the formation of micro- and
macrogametes, is induced when the gametocytes are
ingested by a mosquito. After ingestion by the mosquito,
the microgametocyte undergoes three rounds of nuclear
replication. The macrogametocytes mature into
macrogametes.
The highly mobile microgametes will seek out and fuse with
a macrogamete. Within 12-24 hours the resulting zygote
develops into an ookinete. The ookinete is a motile
invasive stage which will transverse both the peritrophic
matrix and the midgut epithelium of the mosquito.
Sporogony. After reaching the extracellular space
between the epithelial cells and the basal lamina, the
ookinete develops into an oocyst. The oocysts
undergo an asexual replication, called sporogony,
which culminates in the production of several
thousand sporozoites. This generally takes 10-28
days depending on species and temperature. Upon
maturation the oocyst ruptures and releases the
sporozoites which cross the basal lamina into the
hemocoel (body cavity) of the mosquito.
Exoerythrocytic schizogony and
prepatent and incubation periods
P.
falciparu
m
P. vivax P. ovale P. malariae
Prepatent
period
(days)
6-9 8-12 10-14 15-18
Incubatio
n period
(days)
7-14 12-17 16-18 18-40
Merozoite
maturatio
n (days)
5-7 6-8 9 12-16
Merozoite
s
produced
40,000 10,000 15,000 2000
• P. falciparum P. vivax P. ovale P. malariae
Hypnozoite -- + + --
Size of RBC normal normal normal normal
Parasite size 1/3 1/3 1/3 1/6
Multi parasite -- -- + --
Schuffners dots -- -- + --
*Trophzoite:
Size of RBC normal enlarge enlarge normal
Parasite size 67% 100% 67% 100%
Parasite shape ameboid band ameboid compact
Schuffner dots -- + + --
Maure dots + -- -- --
• P. falciparum P. vivax P. ovale P.
malariae
Schizont :
size of RBC normal enlarge enlarge normal
Parasite size 67% 100% 67% 100%
Suffner duts -- + + --
# of merozoite 16-24 12-24 6-12 6-12(rostte s
not seen inP.B hpe)
Gamitosite:
Size of RBC crecent shape enlarge enlarge normal
Parasite size hall cell 100% 67% 100%
Age of cell any young young old
Disease malegnant benign benign benign
Sign and symptoms
Fever: Fever can be very high from the first day.
Temperatures of 40°C and higher are often
observed. Fever is usually continuous or irregular.
Hepatomegaly: The liver may be slightly tender.
Splenomegaly: Splenomegaly takes many days,
especially in the first attack in nonimmune
children. In children from an endemic area, huge
splenomegaly sometimes occurs.
• Anemia: Prolonged malaria can cause anemia,
and malarial anemia causes significant mortality.
• Jaundice: With heavy parasitemia and large-scale
destruction of erythrocytes, mild jaundice may
occur. This jaundice subsides with the treatment
of malaria.
• Dehydration: High fever, poor oral intake, and
vomiting all contribute to dehydration.
Laboratory Diagonosis of Malaria
• Two kinds of blood smear is prepared from
the peripheral blood, thick and thin smear
Preparation and examination of smear
1. Site of Sampling:-Sample can be taken from
peripheral blood or internal blood.(most common
from the tip of the finger.
2. Microscopic Slide:- Scratch free, dust free, grease
free.
3. Pricking needle:- Sterile, sharp point and preferably
a cutting edge.
Thin blood smear preparation
1. Clean the finger tip with ethyl alcohol or ether.
2. Give a prick and wipe off the first drop of blood.
3. Next drop is placed towards the one end of the
slide (1-1.5
4. A second slide (spreader) is used spread the
blood.
Thick blood smear preparation
1. Can be prepare in the same slide
2. 3 drops of blood are spread over a small area(about
10 mm)
3. Thick smear is more sensitive than thin smear
Fixation and staining
• Thin film is fixed with methanol for 30
seconds
• Thick film is not fixed as it is to be
dehamoglobinised
• Smear are stained by JSB stain, Field’s or
Giemsa stain and examine under the oil
immersion lens of microscope
Plasmodium Falciparum in thin and thick
smear
Complication of malaria
• Anaemia
• Splenomegaly
• Hepatomegaly
• Cerebral malaria
• Acute renal failure
• Hyperpyrexia
• Dehydration
• Hypoglycemia
• Blackwater fever
Black water fever
• Due to P. falciprum
• Massive intravascular hemolysis
• Severe acute hemolytic anemia
• RBC=1-2*106 /ml
• Hemoglobinuruia (black coloured urine)
• Increase bilirubin
Prevention and control
• Avoid or minimise contact with mosquitoes
• Biological control:- Destruction of mosquito
breeding sites by land drainage and using
antilarval parasites such as Bacillus sphericus
or larvivorous fish (Gambusia).
Thank you

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Malaria 19

  • 2. Alternative names: ·        Quartan malaria ·        Falciparum malaria     ·        Blackwater fever ·        Tertian malaria
  • 3. A vector-borne infectious disease caused by protozoan parasites. It is widespread in tropical and subtropical regions
  • 4. A bite from an infective female Anopheles mosquito. Anopheles must be infected through a previous blood meal taken on an infected person to transmit malaria
  • 5. At risk for malaria: 40% of the world’s population more than 500 million are ill of malaria yearly If treated in the early stages, malaria can be cured.
  • 6. HIV, malaria and TB are among the most important infectious agents in the world. and all have the same property of establishing chronic infection without an effective immune response.”
  • 7. Plasmodium falciparum - most common and deadly type of malaria infection - can lead to cerebral malaria P.vivax - most common - causes relapse if treatment was not completed. P.malaria P.ovale.
  • 8. Female Anopheles are: Anthropophilic : from humans Zoophilic : from animals Endophagic : prefer to bite indoors Exophagic : prefer outdoor biting
  • 9. Liver Stage. Human infection is initiated when sporozoites are injected with the saliva during mosquito feeding. The sporozoites enter the circulatory system and within 30-60 minutes will invade a liver cell. Host cell entry, as in all apicomplexa, is facilitated by the apical organelles. After invading the hepatocyte, the parasite undergoes an asexual replication. This replicative stage is often called exoerythrocytic (or pre-erythrocytic) schizogony. PATHOPHYSIOLOGY : In P. vivax and P. ovale some of the sporozoites do not immediately undergo asexual replication, but enter a dormant phase known as the hypnozoite. This hypnozoite can reactivate and undergo schizogony at a later time resulting in a relapse.
  • 10. Blood Stage. Merozoites released from the infected liver cells invade erythrocytes. The merozoites recognize specific proteins on the surface of the erythrocyte and actively invade the cell in a manner similar to other apicomplexan parasites. After entering the erythrocyte the parasite undergoes a trophic period followed by an asexual replication. The young trophozoite is often called a ring form due to its morphology in Geimsa-stained blood smears. As the parasite increases in size this 'ring' morphology disappears and it is called a trophozoite. parasites.
  • 11. Nuclear division marks the end of the trophozoite stage and the beginning of the schizont stage. Erythrocytic schizogongy consists of 3-5 rounds (depending on species) of nuclear replication followed by a budding process. Late stage schizonts in which the individual merozoites become discernable are called segmenters. The host erythrocyte ruptures and releases the merozoites. These merozoites invade new erythrocytes and initiate another round of schizogony. The blood-stage parasites within a host usually undergo a synchronous schizogony.
  • 12. Sexual Stage. As an alternative to schizogony some of the parasites will undergo a sexual cycle and terminally differentiate into either micro- or macrogametocytes. Gametocytes do not cause pathology in the human host and will disappear from the circulation if not taken up by a mosquito. Gametogenesis, or the formation of micro- and macrogametes, is induced when the gametocytes are ingested by a mosquito. After ingestion by the mosquito, the microgametocyte undergoes three rounds of nuclear replication. The macrogametocytes mature into macrogametes. The highly mobile microgametes will seek out and fuse with a macrogamete. Within 12-24 hours the resulting zygote develops into an ookinete. The ookinete is a motile invasive stage which will transverse both the peritrophic matrix and the midgut epithelium of the mosquito.
  • 13. Sporogony. After reaching the extracellular space between the epithelial cells and the basal lamina, the ookinete develops into an oocyst. The oocysts undergo an asexual replication, called sporogony, which culminates in the production of several thousand sporozoites. This generally takes 10-28 days depending on species and temperature. Upon maturation the oocyst ruptures and releases the sporozoites which cross the basal lamina into the hemocoel (body cavity) of the mosquito.
  • 14.
  • 15.
  • 16.
  • 17.
  • 18.
  • 19. Exoerythrocytic schizogony and prepatent and incubation periods P. falciparu m P. vivax P. ovale P. malariae Prepatent period (days) 6-9 8-12 10-14 15-18 Incubatio n period (days) 7-14 12-17 16-18 18-40 Merozoite maturatio n (days) 5-7 6-8 9 12-16 Merozoite s produced 40,000 10,000 15,000 2000
  • 20. • P. falciparum P. vivax P. ovale P. malariae Hypnozoite -- + + -- Size of RBC normal normal normal normal Parasite size 1/3 1/3 1/3 1/6 Multi parasite -- -- + -- Schuffners dots -- -- + -- *Trophzoite: Size of RBC normal enlarge enlarge normal Parasite size 67% 100% 67% 100% Parasite shape ameboid band ameboid compact Schuffner dots -- + + -- Maure dots + -- -- --
  • 21. • P. falciparum P. vivax P. ovale P. malariae Schizont : size of RBC normal enlarge enlarge normal Parasite size 67% 100% 67% 100% Suffner duts -- + + -- # of merozoite 16-24 12-24 6-12 6-12(rostte s not seen inP.B hpe) Gamitosite: Size of RBC crecent shape enlarge enlarge normal Parasite size hall cell 100% 67% 100% Age of cell any young young old Disease malegnant benign benign benign
  • 22. Sign and symptoms Fever: Fever can be very high from the first day. Temperatures of 40°C and higher are often observed. Fever is usually continuous or irregular. Hepatomegaly: The liver may be slightly tender. Splenomegaly: Splenomegaly takes many days, especially in the first attack in nonimmune children. In children from an endemic area, huge splenomegaly sometimes occurs.
  • 23. • Anemia: Prolonged malaria can cause anemia, and malarial anemia causes significant mortality. • Jaundice: With heavy parasitemia and large-scale destruction of erythrocytes, mild jaundice may occur. This jaundice subsides with the treatment of malaria. • Dehydration: High fever, poor oral intake, and vomiting all contribute to dehydration.
  • 24. Laboratory Diagonosis of Malaria • Two kinds of blood smear is prepared from the peripheral blood, thick and thin smear
  • 25. Preparation and examination of smear 1. Site of Sampling:-Sample can be taken from peripheral blood or internal blood.(most common from the tip of the finger. 2. Microscopic Slide:- Scratch free, dust free, grease free. 3. Pricking needle:- Sterile, sharp point and preferably a cutting edge.
  • 26.
  • 27. Thin blood smear preparation 1. Clean the finger tip with ethyl alcohol or ether. 2. Give a prick and wipe off the first drop of blood. 3. Next drop is placed towards the one end of the slide (1-1.5 4. A second slide (spreader) is used spread the blood.
  • 28. Thick blood smear preparation 1. Can be prepare in the same slide 2. 3 drops of blood are spread over a small area(about 10 mm) 3. Thick smear is more sensitive than thin smear
  • 29.
  • 30. Fixation and staining • Thin film is fixed with methanol for 30 seconds • Thick film is not fixed as it is to be dehamoglobinised • Smear are stained by JSB stain, Field’s or Giemsa stain and examine under the oil immersion lens of microscope
  • 31. Plasmodium Falciparum in thin and thick smear
  • 32. Complication of malaria • Anaemia • Splenomegaly • Hepatomegaly • Cerebral malaria • Acute renal failure • Hyperpyrexia • Dehydration • Hypoglycemia • Blackwater fever
  • 33. Black water fever • Due to P. falciprum • Massive intravascular hemolysis • Severe acute hemolytic anemia • RBC=1-2*106 /ml • Hemoglobinuruia (black coloured urine) • Increase bilirubin
  • 34. Prevention and control • Avoid or minimise contact with mosquitoes • Biological control:- Destruction of mosquito breeding sites by land drainage and using antilarval parasites such as Bacillus sphericus or larvivorous fish (Gambusia).