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Malaria
Mal - air
Causative organism
Malaria caused by plasmodium
species :
P.vivax----benign tertian M.
P.ovale-----benign tertian M.
P.Malariebenign quartan M.
p.FalciparumMalignant subtertian M.
Life cycle
Habitat: RBCs & liver cells of man
Hosts :
D.host: Female anopheles mosquito
I.host : Man.
R.host : chimpanzee in Africa.
Mode of infection
1-Biological transmission by
Female anopheles mosquito.
2-Blood transmission.
3-The use of contaminated syringes.
4-congenital through placenta.
Any other route of transmission
other than mosquito bite …does
not lead to chronic malaria or
relapse and will cause only
clinical attack of malaria as there
is no liver stage
No exo-erythrocytic schizogony
IMMUNITY
After many attacks protection of human
body against re infection with the same
plasmodium occur but patient remain
susceptible to infection with other
species with plasmodium ( no cross
immunity between different species) .
CLINICAL PICTURE
I.P: 6-40 days.
It’s the pre-erythrocyte cycle:
P.F : 6 days
P.M:11 days
P.V & OVAL :in between
General symptoms: flu like .
bone ache.
chills.
Clinical picture
There are no recognized symptoms associated with
liver phase of malaria or rupture of tissue schizont.
Development of blood phase is necessary for
malarial illness as red cell rupture is associated
with release of malaria toxins
CLINICAL PICTURE
Malarial paroxysm due to:
synchronous rupture of large number of blood
schizonts (at least 200/ml) .
The classical paroxysm has sudden onset and show three
stages:
Cold stage ( 1-2 hr ) : sever coldness, rigors,
because ( his temperature rises sharply )
Hot stage ( 3-4 hr ) : sensation of great heat (39 –
41),headache , thirst , hot-dry-flushed skin and rapid full
pulse
Sweat stage (1-4 hr ) : profuse sweating , descend of fever
and relieve of symptom .
CLINICAL PICTURE
After sweating stage the patient is exhausted
and falls sleep .
If patient not treated the paroxysm will
repeated every :
4 days (quartan ) in P.malaria.
3 days (tertian) in P.ovale & P.vivax.
1-2 days (subtertian ) in P.falciparum.
CLINICAL PICTURE
The paroxysm occurs for few weeks with
decreasing intensity then stop due to elimination
of erythrocyte stage.
In P.M & P.F a low grade parasitaemia that can
not cause paroxysm may persist for along period
up to 20 years leading to recurudescence if the
patient become immuno suppresed
(recrudescence).
CLINICAL PICTURE
Repeated paroxysm will lead to :
Anemia
Jaundice
Hepatosplenomegaly
Always consider malaria in the traveler from a
developing country who presents with:
- Influenza-like syndrome. Or
- Attacks of fever. Or
- Jaundice. Or
- Confusion or coma.
CLINICAL PICTURE
complications
They are more common in P.F due to :
1-shot pre-erythrocyt stage 6 days.
2-large number of merozoites in liver
schizont (40,000).
3-these merozoites attack RBC’s of all
ages.
complications
1. severe hemolytic anemia.
2. Huge splenomegaly.
3. Splenic rupture in acute cases which
may occur spontaneous or following
minor truma.
4. Nephrotic syndrome in P.M due to
immune complex deposition. There is
no response to anti malarial drug or
steroids.
complications
5. Complications of P.F (malignant malaria):
it occurs due to adhesion phenomena due to
adhesion of infected RBCs that contain
trophozoites and schizonts together and to
capillary endothelium leading to:
Vascular obstruction.
Ischaemia and anoxia
complications
both of them leading to destruction of the
surrounding tissue giving clinical manifestation
according to affected organs as :
a. cerebral malaria : severe headache,
hyperpyrexia
paralysis
convulsions
death
complications
b. GIT : gastric hemorrhage, vomiting
cholera like diarrhea and dysentery
c. Algig malaria .shock ,collapse and
perepheral circulatory center due to generalized vascular
thrombosis
d. pulmonary edema
e. Retinal heamorrage
f. abortion
j. renal faliure
h. hypoglycaemia due to impaired hepatic
glucuneogenesis
complications
I. Black water fever:
Produce by acute massive intravascular hemolysis
which result from either :
1- high level of parasitaaemia >100000
organism per ml.
2- insufficient treatment with quinine which
renders the infected RBCs antigenic leading to
autoimmune reaction against these RBC.
3- primaquine to patient with G6PD deficency.
DIAGNOSIS
Clinical picture :
malarial paroxysms
history of visiting endemic area
Laboratory :
Direct : examination of thin and thick blood
films stained with Giemsa and Leishman
stains reveal all erythrocyte stages except in
P.F (only ring & Gametcyte) .
Blood film
DIAGNOSIS
Indirect :
1- serological test: ELISA are of value in
chronic and relapsing case but not in acute malaria
2- PCR : useful for diagnosis and
identification of species of plasmodium.
3- rapid immunodiagnostic test as strip or
dipstick tests for detection of circulating parasite
antigen using monoclonal antibodies.
Treatment
Supportive ttt:
 Bed rest
 Fluid replacement with care to avoid pul.
Edema
 Antipyretics or cold foment.
 Blood & platlet transfusion
 Treatment of hypoglycemia
 Corticosteroids may be used for life saving
 Renal dialysis in case of an/oliguia
Specific ttt‫الصحة‬ ‫وزارة‬ ‫بروتوكول‬
Specific ttt ‫الصحة‬ ‫وزارة‬ ‫بروتوكول‬
‫ثم‬
Prevention & control
 Massive ttt of cases to prevent transmission of
infection to mosquitos
 Mosquito control
 Chemoprophylaxis.
 No vaccines untill now
`
 Apomefloquine 250mg
8 tablet 65 LE.

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Malaria

  • 1.
  • 3. Causative organism Malaria caused by plasmodium species : P.vivax----benign tertian M. P.ovale-----benign tertian M. P.Malariebenign quartan M. p.FalciparumMalignant subtertian M.
  • 5. Habitat: RBCs & liver cells of man Hosts : D.host: Female anopheles mosquito I.host : Man. R.host : chimpanzee in Africa.
  • 6. Mode of infection 1-Biological transmission by Female anopheles mosquito. 2-Blood transmission. 3-The use of contaminated syringes. 4-congenital through placenta.
  • 7. Any other route of transmission other than mosquito bite …does not lead to chronic malaria or relapse and will cause only clinical attack of malaria as there is no liver stage No exo-erythrocytic schizogony
  • 8.
  • 9. IMMUNITY After many attacks protection of human body against re infection with the same plasmodium occur but patient remain susceptible to infection with other species with plasmodium ( no cross immunity between different species) .
  • 10.
  • 11. CLINICAL PICTURE I.P: 6-40 days. It’s the pre-erythrocyte cycle: P.F : 6 days P.M:11 days P.V & OVAL :in between General symptoms: flu like . bone ache. chills.
  • 12. Clinical picture There are no recognized symptoms associated with liver phase of malaria or rupture of tissue schizont. Development of blood phase is necessary for malarial illness as red cell rupture is associated with release of malaria toxins
  • 13. CLINICAL PICTURE Malarial paroxysm due to: synchronous rupture of large number of blood schizonts (at least 200/ml) . The classical paroxysm has sudden onset and show three stages: Cold stage ( 1-2 hr ) : sever coldness, rigors, because ( his temperature rises sharply ) Hot stage ( 3-4 hr ) : sensation of great heat (39 – 41),headache , thirst , hot-dry-flushed skin and rapid full pulse Sweat stage (1-4 hr ) : profuse sweating , descend of fever and relieve of symptom .
  • 14. CLINICAL PICTURE After sweating stage the patient is exhausted and falls sleep . If patient not treated the paroxysm will repeated every : 4 days (quartan ) in P.malaria. 3 days (tertian) in P.ovale & P.vivax. 1-2 days (subtertian ) in P.falciparum.
  • 15. CLINICAL PICTURE The paroxysm occurs for few weeks with decreasing intensity then stop due to elimination of erythrocyte stage. In P.M & P.F a low grade parasitaemia that can not cause paroxysm may persist for along period up to 20 years leading to recurudescence if the patient become immuno suppresed (recrudescence).
  • 16. CLINICAL PICTURE Repeated paroxysm will lead to : Anemia Jaundice Hepatosplenomegaly
  • 17. Always consider malaria in the traveler from a developing country who presents with: - Influenza-like syndrome. Or - Attacks of fever. Or - Jaundice. Or - Confusion or coma. CLINICAL PICTURE
  • 18.
  • 19. complications They are more common in P.F due to : 1-shot pre-erythrocyt stage 6 days. 2-large number of merozoites in liver schizont (40,000). 3-these merozoites attack RBC’s of all ages.
  • 20. complications 1. severe hemolytic anemia. 2. Huge splenomegaly. 3. Splenic rupture in acute cases which may occur spontaneous or following minor truma. 4. Nephrotic syndrome in P.M due to immune complex deposition. There is no response to anti malarial drug or steroids.
  • 21. complications 5. Complications of P.F (malignant malaria): it occurs due to adhesion phenomena due to adhesion of infected RBCs that contain trophozoites and schizonts together and to capillary endothelium leading to: Vascular obstruction. Ischaemia and anoxia
  • 22. complications both of them leading to destruction of the surrounding tissue giving clinical manifestation according to affected organs as : a. cerebral malaria : severe headache, hyperpyrexia paralysis convulsions death
  • 23. complications b. GIT : gastric hemorrhage, vomiting cholera like diarrhea and dysentery c. Algig malaria .shock ,collapse and perepheral circulatory center due to generalized vascular thrombosis d. pulmonary edema e. Retinal heamorrage f. abortion j. renal faliure h. hypoglycaemia due to impaired hepatic glucuneogenesis
  • 24. complications I. Black water fever: Produce by acute massive intravascular hemolysis which result from either : 1- high level of parasitaaemia >100000 organism per ml. 2- insufficient treatment with quinine which renders the infected RBCs antigenic leading to autoimmune reaction against these RBC. 3- primaquine to patient with G6PD deficency.
  • 25.
  • 26. DIAGNOSIS Clinical picture : malarial paroxysms history of visiting endemic area Laboratory : Direct : examination of thin and thick blood films stained with Giemsa and Leishman stains reveal all erythrocyte stages except in P.F (only ring & Gametcyte) .
  • 28. DIAGNOSIS Indirect : 1- serological test: ELISA are of value in chronic and relapsing case but not in acute malaria 2- PCR : useful for diagnosis and identification of species of plasmodium. 3- rapid immunodiagnostic test as strip or dipstick tests for detection of circulating parasite antigen using monoclonal antibodies.
  • 29. Treatment Supportive ttt:  Bed rest  Fluid replacement with care to avoid pul. Edema  Antipyretics or cold foment.  Blood & platlet transfusion  Treatment of hypoglycemia  Corticosteroids may be used for life saving  Renal dialysis in case of an/oliguia
  • 31.
  • 32. Specific ttt ‫الصحة‬ ‫وزارة‬ ‫بروتوكول‬ ‫ثم‬
  • 33.
  • 34.
  • 35. Prevention & control  Massive ttt of cases to prevent transmission of infection to mosquitos  Mosquito control  Chemoprophylaxis.  No vaccines untill now