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Internal Medicine›Condition·Updated Apr 17, 2026·v1

Malaria

Malaria is a protozoan infection characterized by paroxysmal fevers and potential multi-organ failure. *P. falciparum* is the most dangerous species, while *P. vivax* and *P. ovale* require radical cure to prevent relapse. Diagnosis is via microscopy or RDT. Treatment is ACT-based for uncomplicated cases and IV artesunate for severe cases. G6PD screening is mandatory before using primaquine.

High Evidence200 references·5,972 words·24 min read·v1
Infectious DiseaseTropical MedicineParasitologyCritical Care

Quick Reference

RxDrug of choiceArtemether-lumefantrine (uncomplicated); IV Artesunate (severe)
AltAlternativesDihydroartemisinin-piperaquine; Quinine plus Doxycycline
⊘AvoidPrimaquine in G6PD deficiency; Artemether-lumefantrine in the first trimester of pregnancy (relative, ACTs now generally preferred if benefits outweigh risks)
DxTest of choiceThick and thin blood smears (Microscopy)
ScKey scoreBlantyre Coma Scale (pediatric); Glasgow Coma Scale (adult)
→When to referAny sign of severe malaria (altered mental status, respiratory distress, AKI, or parasitemia > 5%)
Fever in a traveler from an endemic area is malaria until proven otherwise; treat severe cases immediately with IV artesunate to reduce mortality.
Malaria is a life-threatening febrile illness caused by obligate intracellular protozoan parasites of the genus [[Plasmodium]], transmitted to humans via the bite of infected female [[Anopheles]] mosquitoes. While five species regularly infect humans—*P. falciparum*, *P. vivax*, *P. ovale*, *P. malariae*, and the zoonotic *P. knowlesi*—*P. falciparum* remains the primary driver of global mortality, particularly in sub-Saharan Africa. The clinical spectrum ranges from asymptomatic parasitemia to multi-organ failure, with severe disease characterized by cerebral malaria, severe anemia, and acute kidney injury. Diagnosis relies on rapid parasitological confirmation via microscopy or rapid diagnostic tests (RDTs). Management is strictly stratified by severity: uncomplicated cases require artemisinin-based combination therapies (ACTs), while severe malaria is a medical emergency requiring immediate intravenous [[Artesunate]]. Prevention integrates vector control, seasonal chemoprevention, and the recent implementation of the RTS,S and R21 vaccines.

Overview and Recommendations

Background

  • •Recognize malaria as a major global health threat, with approximately 250 million cases and over 600,000 deaths annually, disproportionately affecting children under five and pregnant women in sub-Saharan Africa.
  • •Identify the five primary human pathogens: (most virulent), P. vivax (common in Asia/Americas, forms dormant liver stages), P. ovale (also forms liver stages), P. malariae (72-hour cycle), and P. knowlesi (zoonotic, 24-hour cycle).
  • •Understand the life cycle involving the female mosquito vector, which injects sporozoites that first infect the liver (exo-erythrocytic cycle) before entering the bloodstream to infect red blood cells (erythrocytic cycle).
  • •Note the emergence of artemisinin partial resistance (ART-R), particularly in Southeast Asia and parts of Africa, characterized by delayed parasite clearance and mutations in the pfk13 gene.
  • •Consider host genetic factors that influence disease course, such as (risk of hemolysis with certain drugs), the Duffy-negative phenotype (historically protective against P. vivax), and sickle cell trait (protective against severe P. falciparum).

Evaluation

  • •Suspect malaria in any patient with an unexplained fever who has lived in or traveled to an endemic region within the last year, even if they took chemoprophylaxis.
  • •Ask about the pattern of fever paroxysms (chills, high fever, and sweating), though classic 48- or 72-hour cycles are often absent in the early stages or in non-immune individuals.
  • •Examine for signs of severe disease, including altered mental status (cerebral malaria), respiratory distress (acidotic breathing), jaundice, and spontaneous bleeding or petechiae.
  • •Order immediate parasitological testing with thick and thin blood smears; the thick smear is used for screening (sensitivity 50–100 parasites/µL), while the thin smear is used for species identification and quantification.
  • •Utilize Rapid Diagnostic Tests (RDTs) for Histidine-Rich Protein 2 (HRP2) or parasite Lactate Dehydrogenase (pLDH) when microscopy is unavailable, but be aware of false negatives in HRP2-deleted strains.
  • •Repeat blood smears every 6–12 hours for 48 hours if the initial test is negative but clinical suspicion remains high, as parasitemia can fluctuate significantly.
  • •Screen for red flags of severe malaria: Glasgow Coma Scale (GCS) < 11, hemoglobin < 7 g/dL, serum creatinine > 3 mg/dL, or blood glucose < 40 mg/dL.
  • •Perform pulse oximetry on all patients; an SpO2 < 90% is a high-risk marker for mortality and indicates the need for urgent respiratory support.
  • •Evaluate for (CM) by assessing consciousness using the Blantyre Coma Scale in children or GCS in adults; CM is defined by a GCS < 11 persisting for >1 hour after a seizure.
  • •Obtain a complete blood count (CBC) to assess for thrombocytopenia and anemia, and a metabolic panel to monitor for acute kidney injury (MAKI) and hypoglycemia.
  • •Rule out other tropical febrile illnesses such as , , and , which often present with overlapping symptoms.
  • •Test for using a point-of-care biosensor before initiating radical cure therapy for P. vivax or P. ovale to prevent life-threatening hemolysis.

Management

  • •Administer intravenous (IV) 2.4 mg/kg at 0, 12, and 24 hours for all cases of severe malaria, regardless of the infecting species.
  • •Transition to a full 3-day course of oral Artemisinin-based Combination Therapy (ACT) once the patient with severe malaria can tolerate oral intake.
  • •Treat uncomplicated P. falciparum with oral Artemether-lumefantrine (20/120 mg tablets, weight-based dosing twice daily for 3 days) as the first-line regimen.
  • •Use Dihydroartemisinin-piperaquine as an alternative ACT in regions with documented resistance to artemether-lumefantrine.
  • •Provide radical cure for P. vivax and P. ovale by administering Primaquine 0.25–0.5 mg/kg daily for 14 days to eliminate latent liver hypnozoites.
  • •Ensure G6PD activity is >30% before giving primaquine; in patients with intermediate deficiency (30-70% activity), consider weekly primaquine (0.75 mg/kg) for 8 weeks under close supervision.
  • •Manage hypoglycemia aggressively with IV Dextrose (e.g., 10% dextrose 5 mL/kg in children) and monitor blood glucose every 4 hours, as quinine and the infection itself can cause profound drops.
  • •Control seizures with IV Diazepam 0.3 mg/kg or Midazolam 0.1 mg/kg; if seizures recur, escalate to Phenobarbital 20 mg/kg IV.
  • •Maintain fluid homeostasis using balanced crystalloids (Lactated Ringer's) at 3-4 mL/kg/hr, but avoid aggressive fluid boluses in cerebral malaria unless the patient is in shock to prevent cerebral edema.
  • •Monitor for delayed post-artesunate hemolysis (PADH), which can occur 1–3 weeks after treatment with IV artesunate, particularly in patients with high initial parasitemia.
  • •Avoid using artemisinin monotherapy, as this rapidly drives the development of drug resistance.
  • •Refer all pregnant women with malaria for specialist obstetric and infectious disease consultation, as they are at high risk for severe anemia and placental sequestration.
  • •Implement Seasonal Malaria Chemoprevention (SMC) with sulfadoxine-pyrimethamine plus amodiaquine (SPAQ) in children aged 3–59 months in high-transmission seasonal areas.
  • •Recommend the R21/Matrix-M or RTS,S/AS01 vaccine for children in endemic regions as part of a multi-tiered prevention strategy.
  • •Discharge patients only after they have completed at least 24 hours of oral therapy, are afebrile, have a declining parasite count, and can tolerate oral medications and fluids.

Board Review — High Yield

  • •Cerebral malaria — Defined by GCS < 11 or Blantyre ≤ 2 in the presence of P. falciparum parasitemia.
  • •Blackwater fever — Severe intravascular hemolysis leading to hemoglobinuria (dark urine), often associated with P. falciparum.
  • •Schüffner dots — Fine stippling seen in red blood cells infected with P. vivax or P. ovale.
  • •Banana-shaped gametocytes — Pathognomonic microscopic finding for P. falciparum.
  • •Hypnozoites — Dormant liver stages of P. vivax and P. ovale responsible for clinical relapses months later.
  • •Maurer clefts — Membranous sacs seen in P. falciparum-infected erythrocytes used for protein transport.
  • •Duffy Antigen — The receptor required for P. vivax entry; Duffy-negative individuals (common in West Africa) are largely resistant.
  • •Sequestration — P. falciparum cytoadherence to vascular endothelium via PfEMP1, causing microvascular obstruction.
  • •Recrudescence — Reappearance of parasitemia from the blood cycle (due to treatment failure), distinct from relapse (from liver).

Deep Dive — Evidence Details

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