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MALARIA
By : mohammed almaleesi &
sinan
KNOW MALARIA AND WHY
 Malaria is an acute and chronic illness characterized by
paroxysms of fever, chills, sweats, fatigue, anemia, and
splenomegaly.
 Malaria is of overwhelming importance in the developing
world today, with an estimated 300 to 500 million cases and
more than 1 million deaths each year.
 Most malarial deaths occur among infants and young
children.
MODES OF MALARIA TRANSMISSION
 Bite of female anopheline mosquitoes: Infective form:
sporozoites
 Infection of blood of a malaria patient containing asexual
forms- ‘trophozoite’ induced malaria
1. Trasfusion malaria
2. Congenital malraia
3. Malaria in drug addicts
HOSTS INVOLVED IN TRANSMISSION OF MALARIA
Man Female anopheles mosquito
Secondary host Primary host
Intermediate host Definitive host
Asexual cycle Sexual cycle
Schizogony Sporogony
HUMAN CYCLE OF PLASMODIUM
1. Pre erythrocytic schizogony
 Development of sporozoites in liver parenchyma
 Liberated merozoites are called as cryptozoites
 Blood is sterile
2. Erythorcytic schizogony
 Parasite resides inside RBCs; passes through stages of
Trophozoite, Shcizont, Merozoite
 Parasitic multiplication brings clinical attack of malaria
3. Gametogony
 Some merozoites develop in RBCs of spleen and bone
marrow to form ‘Gametocytes’
4. Exo erythorocytic schizogony
 Persistence of late tissue phase in liver
 Seen in P vivax and P ovale
 Cause relapses in Vivax and Ovale malaria
 Liberated merozoites are known as ‘Phanerozoites’
MOSQUITO CYCLE OF PLASMODIUM
1. Completion of gametogomy
 Exflagellation of microgamete and maturation of gametes
 Fusion of gametes form Zygote; Zygote matures to Ookinite
2. Sporogony
 Ookinite develops into oocyst
 On 10th day of infection, oocyst ruptures, relasing
sporozoites; sporozoites reach salivary glands
 Mosquito at this stage is capable of transmitting infection.
Once inside the erythrocyte, the parasite transforms
into the ring form, which then enlarges to become a
trophozoite.
These latter 2 forms can be identified with Giemsa
stain on blood smear, the primary means of
confirming the diagnosis of malaria
 Paroxysms coincide with the rupture of schizonts that occurs
 every 48 hr with P. vivax and P. ovale, resulting in fever spikes
every other day- tertian malaria
 every 72 hr with P. malariae, resulting in fever spikes every 3rd
or 4th day- quartan marlaria
 Periodicity is less apparent with
 P. falciparum and mixed infections
 travelers from nonendemic regions
Symptoms Signs lab
Fever Splenomegaly Anemia
Headache hepatomegaly Thrombocytopenia
Drowsiness Pallor Normal/ low TLC
Anorexia Elevated ESR
Nausea
Vomiting
Diarrhea
DIAGNOSIS
 The diagnosis of malaria
Giemsa-stained smears of peripheral blood or
rapid immunochromatographic assay.
 Stains used for diagnosis
Giemsa stain >Wright stain or Leishman stain.
Thick and Thin blood smears
 The concentration of erythrocytes on a thick smear is 20-40 times
that on a thin smear and is used to quickly scan large numbers of
erythrocytes.
 The thin smear allows for positive identification of the malaria
species and determination of the percentage of infected
erythrocytes and is useful in following the response to therapy
DIAGNOSIS
 A single negative blood smear does not exclude
malaria.
 Most symptomatic patients with malaria will have
detectable parasites on thick blood smears within
48 hr.
DIFFERENTIAL DIAGNOSIS
 viral infections such as influenza and hepatitis,
 sepsis,
 pneumonia,
 meningitis, encephalitis,
 endocarditis,
 gastroenteritis,
 pyelonephritis,
 babesiosis, Brucellosis, leptospirosis,
 tuberculosis,
 relapsing fever,
 typhoid fever,
 yellow fever,
PREVENTION
 Malaria prevention consists of
 Reducing exposure to infected mosquitoes and
 Chemoprophylaxis
 Chemoprophylaxis is necessary for
 all visitors to and
 residents of the tropics who have not lived there since
infancy, including children of all ages.
 Health care providers should consult the latest information
on resistance patterns before prescribing prophylaxis for their
patients.

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malaria

  • 1. MALARIA By : mohammed almaleesi & sinan
  • 2. KNOW MALARIA AND WHY  Malaria is an acute and chronic illness characterized by paroxysms of fever, chills, sweats, fatigue, anemia, and splenomegaly.  Malaria is of overwhelming importance in the developing world today, with an estimated 300 to 500 million cases and more than 1 million deaths each year.  Most malarial deaths occur among infants and young children.
  • 3. MODES OF MALARIA TRANSMISSION  Bite of female anopheline mosquitoes: Infective form: sporozoites  Infection of blood of a malaria patient containing asexual forms- ‘trophozoite’ induced malaria 1. Trasfusion malaria 2. Congenital malraia 3. Malaria in drug addicts
  • 4. HOSTS INVOLVED IN TRANSMISSION OF MALARIA Man Female anopheles mosquito Secondary host Primary host Intermediate host Definitive host Asexual cycle Sexual cycle Schizogony Sporogony
  • 5.
  • 6. HUMAN CYCLE OF PLASMODIUM 1. Pre erythrocytic schizogony  Development of sporozoites in liver parenchyma  Liberated merozoites are called as cryptozoites  Blood is sterile 2. Erythorcytic schizogony  Parasite resides inside RBCs; passes through stages of Trophozoite, Shcizont, Merozoite  Parasitic multiplication brings clinical attack of malaria
  • 7. 3. Gametogony  Some merozoites develop in RBCs of spleen and bone marrow to form ‘Gametocytes’ 4. Exo erythorocytic schizogony  Persistence of late tissue phase in liver  Seen in P vivax and P ovale  Cause relapses in Vivax and Ovale malaria  Liberated merozoites are known as ‘Phanerozoites’
  • 8. MOSQUITO CYCLE OF PLASMODIUM 1. Completion of gametogomy  Exflagellation of microgamete and maturation of gametes  Fusion of gametes form Zygote; Zygote matures to Ookinite 2. Sporogony  Ookinite develops into oocyst  On 10th day of infection, oocyst ruptures, relasing sporozoites; sporozoites reach salivary glands  Mosquito at this stage is capable of transmitting infection.
  • 9. Once inside the erythrocyte, the parasite transforms into the ring form, which then enlarges to become a trophozoite. These latter 2 forms can be identified with Giemsa stain on blood smear, the primary means of confirming the diagnosis of malaria
  • 10.
  • 11.  Paroxysms coincide with the rupture of schizonts that occurs  every 48 hr with P. vivax and P. ovale, resulting in fever spikes every other day- tertian malaria  every 72 hr with P. malariae, resulting in fever spikes every 3rd or 4th day- quartan marlaria  Periodicity is less apparent with  P. falciparum and mixed infections  travelers from nonendemic regions
  • 12. Symptoms Signs lab Fever Splenomegaly Anemia Headache hepatomegaly Thrombocytopenia Drowsiness Pallor Normal/ low TLC Anorexia Elevated ESR Nausea Vomiting Diarrhea
  • 13. DIAGNOSIS  The diagnosis of malaria Giemsa-stained smears of peripheral blood or rapid immunochromatographic assay.  Stains used for diagnosis Giemsa stain >Wright stain or Leishman stain. Thick and Thin blood smears  The concentration of erythrocytes on a thick smear is 20-40 times that on a thin smear and is used to quickly scan large numbers of erythrocytes.  The thin smear allows for positive identification of the malaria species and determination of the percentage of infected erythrocytes and is useful in following the response to therapy
  • 14. DIAGNOSIS  A single negative blood smear does not exclude malaria.  Most symptomatic patients with malaria will have detectable parasites on thick blood smears within 48 hr.
  • 15. DIFFERENTIAL DIAGNOSIS  viral infections such as influenza and hepatitis,  sepsis,  pneumonia,  meningitis, encephalitis,  endocarditis,  gastroenteritis,  pyelonephritis,  babesiosis, Brucellosis, leptospirosis,  tuberculosis,  relapsing fever,  typhoid fever,  yellow fever,
  • 16. PREVENTION  Malaria prevention consists of  Reducing exposure to infected mosquitoes and  Chemoprophylaxis  Chemoprophylaxis is necessary for  all visitors to and  residents of the tropics who have not lived there since infancy, including children of all ages.  Health care providers should consult the latest information on resistance patterns before prescribing prophylaxis for their patients.