Malaria.pdf

DEFINITION, TRANSMISSION, PATHOGENESIS, CLINICAL FEATURES, COMPLICATIONS, MANAGEMENT

1. MALARIA
P/B :-DR NIYATI PATEL (PT)
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3. DEFINITION
Acute febrile illness characterised by paroxysms
of fever as a result of asexual reproduction of
plasmodia within the red cells.
Causes of malaria
Plasmodium vivax,
Plasmodium ovaleand
Plasmodium malariae
Plasmodium falciparumpotentially fatal malaria.
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4. TRANSMISSION
(a) Presence of suitable anophelinemosquito,
(B) Reservoir of malaria infection in the area,
(C) Suitable non-immune or partly immune hosts
(D) An environmental temperature with suitable
humidity.
Infection is normally transmitted to
Man by the bite of a mosquito,
Rarely occur across the placenta
A result of blood transfusion
Syringe-transmitted malaria among drug addicts
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6. Infection is initiated by sporozoitesfrom the bite of
a female Anopheles mosquito.
The sporozoitesmultiply within hepatocytes, giving
rise to thousands of merozoiteinvade RBCs.
The sporozoitesConverted merozoite
In the RBCs the small ring forms grow through the
trophozoitestage to the schizontform, which
ruptures and releases further merozoites
Tropozoitestage schizontmerozoite
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8. This asexual cycle in the blood
lasts 48 hours in P. falciparum, P. vivaxand P.
ovaleinfections,
lasts 72 hours in P.malariya.
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9. PATHOGENESIS
Clinical symptoms and signs are caused by the
asexual forms of the parasite
Invade and destroy RBCs,
Localise in tissues and organs by binding to
endothelial cells (cytoadherence)
Induce release of many pro-inflammatory cytokines
[e.G.Tumour necrosis factor-α (tnf-α)].
Initiating step when merozoitesinvade RBCs 
trophozoiteschizontstagebind to epithelial
cells in post capillary venulesmicrovascular
obstruction (cytoadherent)toxins produced 
cytokine release
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10. CLINICAL FEATURES
ONSET–Lassitude, anorexia, headache, chillness for several
days before actual attack
PAROXYSM –3 CLINICAL STAGES
1. COLD STAGE –Shivers from head to foot , teeth chatter ,
temperature rise body covers with blanket stage for
half n hour
2. HOT STAGE –Shivers absent, feeling of intense heat 
throwing of blanket
Flushed face, headache, vomiting, dry and burning Skin 
Temperature rises to 40°C or more stage lasts for 3-4
hours.
3. SWEATING STAGE -Patient breaks into profuse
perspiration, and the temperature rapidly declines with
feeling of relief.
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12. COMPLICATIONS
Tropical splenomegaly syndrome (TSS) –is seen in
endemic falciparum malaria Clinical features: marked
splenomegaly, lesser degree of hepatomegaly, anaemia
and pancytopenia.
Quartanmalarial nephropathy –is associated with P.
malariaeinfection. Predominantly affects children
between 5-8 years of age Clinical features : nephrotic
syndrome several weeks after onset of quartanfever 
Disease progresses slowly to end-stage kidney failure in 3-
5 years.
Anaemia in malaria, most common complication 
due to accelerated RBC removal by the spleen, RBC
destruction at parasite schizogonyand ineffective
haemopoiesis.
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13. DIAGNOSIS
1. Clinical –Periodic fever with rigour, sweating,
anaemia and perhaps enlarged spleen.
2. Blood film –Identification of the parasites in thick
and thin blood filmfound during a spike of fever.
Common microscopic characters of falciparum
malaria are –high concentration of parasites
predominance of thin ring-shaped trophozoites.
3. Malarial antigen spot test using parasite LDH –P.
falciparum antigens,
4. Immunofluorescentmicroscopy and PCR.
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14. MANAGEMENT
General Management
Admission to ICU
Measurement of glucose and if possible lactate and arterial
blood gases
Fluid balance –because both dehydration and
overhydration
Treatment of convulsions with diazepam
Attention to hypoglycemiaand hyponatremia
Parameters for monitoring treatment include twice daily
parasite counts, regular pH and blood gas measurements
and when appropriate, measurement of glucose (during iv
quinine therapy), lactate, CRP & kidney function
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15. PHARMACOLOGICAL MANAGEMENTS
Non-severe falciparum (initial treatment): choice of three
regimens Quinine sulphate , Atovaquone, Artemether&
Arterolane
2nd agent follow-on treatment: choice of 3 agents 
Doxycycline , Clindamycin, sulfadoxine–pyrimethamine
Non Falciparum Chloroquine
For ovale, vivaxovale& mixed infection Primaquine
For severe falciparum & vivaxquinine sulphate /
dihydrochloride
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16. MANAGEMENT OF
SPECIFIC COMPLICATIONS
Cerebral malaria –Antimalarial drugs+ Mannitol in patients
with raised intracranial pressure.
Hypoglycemia–Dextrose iv
Acute renalfailure–Dialysis+ Nonoliguricrenal failure
Acidosis–Adequate fluid replacement+ bloodTransfusion,
Early haemodiafiltration+ ventilation may be used.
Anaemia–is mainly caused by rupture of infected cells and
haemolysis. Transfusion if Hbfalls below 7.5 g/dl.
Bacterial superinfection–Strep. pneumoniaeor Salmonella
spp. is common antimicrobial
Jaundice –Mild jaundice is mainly caused by haemolysis
liver involvementviral hepatitis
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17. MANAGEMENT FOR CHILDREN
(<5YRS) & PREGNANT WOMEN
Arearwhere p.falciparumabsent 
chloroquinephosphate
Area where p.falciparumpresent 
chloroquinephosphate + proguanil
Area where p.falciparum& p.vivaxhigh
risk of transmission Mefloquine/
chloroquine+ proguanil/doxycycline
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18. THANK YOU
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