Malaria

Parasitic infectious disease caused by protozoa of the genus Plasmodium, transmitted to humans through the bite of an infected female Anopheles mosquito

Aetiology

Plasmodium falciparum → most severe, high mortality

Plasmodium vivax → relapse due to hypnozoites

Plasmodium ovale → relapse (rare)

Plasmodium malariae → chronic infection

Plasmodium knowlesi → zoonotic, common in Southeast Asia

Mode of Transmission

Bite of infected female Anopheles mosquito

Less common:

Blood transfusion
Organ transplantation
Congenital transmission

Pathophysiology

Sporozoites enter bloodstream

Invade liver cells → hepatic schizogony

Release merozoites into bloodstream

Infect red blood cells → erythrocytic cycle

RBC rupture → fever paroxysms

(P. vivax and P. ovale form dormant hypnozoites)

Clinical presentation

Uncomplicated Malaria

Symptoms:

Fever with chills and rigors

Sweating

Headache

Myalgia

Malaise

Nausea, vomiting

Fever Pattern:

P. vivax / ovale: every 48 hours (tertian) → Malaria Tertiana

P. malariae: every 72 hours (quartan) → Malaria Quartana

P. falciparum: irregular → Malaria Tropicana

Severe Malaria (Medical Emergency)

Mostly caused by P. falciparum and P. knowlesi:

Cerebral malaria (coma, seizures)

Severe anemia

Acute kidney injury

Jaundice

Metabolic acidosis

Hypoglycemia

Pulmonary edema / ARDS

Shock

Investigations

Parasitological Diagnosis (Gold Standard)

Peripheral Blood Smear

Thick smear: Species identification

Thin smear: Quantifies parasitemia

Rapid Diagnostic Tests (RDT)

Detect parasite antigens (e.g., HRP2, pLDH)

Useful in endemic or remote areas

Cannot quantify parasitemia

Laboratory Findings (Supportive)

Anemia

Thrombocytopenia

Elevated bilirubin

Elevated LDH

Hypoglycemia (severe cases)

Morphological Features of Plasmodium Species

Plasmodium falciparum

Multiple delicate ring forms in a single RBC

Appliqué (accolé) forms at RBC periphery

Maurer’s dots

Banana-shaped (crescent) gametocytes

Schizonts rarely seen in peripheral blood

Normal-sized RBCs

Plasmodium vivax

Enlarged RBCs

Thick ring forms

Schüffner’s dots

Amoeboid trophozoites

Schizonts with 12–24 merozoites

Plasmodium ovale

Enlarged, oval RBCs with fimbriated edges

James’ dots

Fewer merozoites than P. vivax

Plasmodium malariae

Normal or small RBCs

Band-shaped trophozoites

Ziemann’s dots

Schizonts with rosette (daisy-head) pattern (6–12 merozoites)

Plasmodium knowlesi

Early ring forms resemble P. falciparum

Later stages resemble P. malariae

High parasitemia possible

Requires molecular methods for confirmation

Management

Treatment depends on species and resistance pattern.

Artemisinin-based Combination Therapy (ACT)

First-line worldwide
Example: dihydroartemisinin–piperaquine, artesunate-amoduiaquine (Indonesia)

Primaquine

Added for P. vivax/ovale to eradicate hypnozoites
Also for P. falciparum gametocyte clearance
Check G6PD status if possible

Species-based management

P. falciparum → ACT (3 days) + primaquine (SD)

P. vivax & P. ovale → ACT (3 days) + primaquine (14 days)

P. malariae → ACT 3 days

Prophylaxis

Chloroquine 500mg (2 tab)/week

If resistent:

Doxycyclin 100mg/day
Mefloquine 250mg/week → 1st line for pregnancy and children

Severe Malaria (Cerebral Malaria)

IV/IM artesunate 60mg/vial

1st day → 2.4mg/kg given at hours 0, 12, and 24
then, 2.4mg/kg/day until patient awake

IM artemeter 80mg/ampul

1st day → 3.2mg/kg/day
then, 1.6mg/kg or 1 ampul until patient awake

Followed by full oral ACT (3 days) + primaquine SD

Supportive ICU care