skip to main content
ukmla 2026

Malaria

Protozoal infection transmitted by Anopheles mosquitoes — Plasmodium falciparum causes the most severe form; diagnose with thick and thin blood films, treat urgently

Infectious Diseasesless-commonacute
On this page
Condition details
Infectious Diseases
less-common
6 min read
reviewed 2026-04-05
practice ukmla questions →

About This Page

This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.

Key points

  • Five Plasmodium species infect humans: P. falciparum (most dangerous — >90% of UK malaria deaths), P. vivax, P. ovale, P. malariae, P. knowlesi
  • ALWAYS consider malaria in any febrile patient with travel to an endemic area (even remote travel history) — fever + travel = malaria until proven otherwise
  • Diagnosis: thick and thin blood films (×3 over 48 hours). Thick film detects parasites; thin film identifies species and quantifies parasitaemia. Also: rapid diagnostic test (RDT)
  • Severe falciparum malaria: IV artesunate is first-line (NICE). Oral treatment for uncomplicated falciparum: artemether-lumefantrine (Riamet) or atovaquone-proguanil
  • Chemoprophylaxis: atovaquone-proguanil (Malarone), doxycycline, or mefloquine depending on destination. No prophylaxis is 100% effective

Overview

Malaria is a protozoal infection caused by Plasmodium species, transmitted through the bite of infected female Anopheles mosquitoes. P. falciparum is the most dangerous species — it causes the highest parasitaemia (can infect RBCs of all ages), sequesters in cerebral microvasculature (cerebral malaria), and is responsible for virtually all malaria deaths. P. vivax and P. ovale produce hypnozoites (dormant liver stages) causing relapse months to years later. The UK sees approximately 1,500-2,000 imported malaria cases annually, with 5-10 deaths — almost all from P. falciparum.

Epidemiology

Malaria is endemic in tropical and subtropical regions of Africa (90% of global burden), South-East Asia, and South America. In the UK, malaria is an imported disease, primarily in travellers returning from sub-Saharan Africa (especially Nigeria, Ghana, Sierra Leone) and South Asia. VFR (visiting friends and relatives) travellers are at highest risk — they may not take chemoprophylaxis. The incubation period is typically 7-30 days for P. falciparum but can be up to 1 year for P. vivax/ovale.

Clinical Features

Symptoms
Fever — the cardinal symptom. May be cyclical (tertian: every 48h for P. vivax/ovale/falciparum; quartan: every 72h for P. malariae) but often irregular, especially with falciparum
Rigors and chills
Headache (severe)
Myalgia and arthralgia
Nausea, vomiting, diarrhoea (may mimic gastroenteritis)
Confusion, drowsiness (cerebral malaria — P. falciparum)
Jaundice
Dark urine (haemoglobinuria — blackwater fever)
Signs
Fever (>38°C) with rigors
Pallor and jaundice (haemolytic anaemia)
Hepatosplenomegaly (especially with repeated infections)
Altered consciousness, seizures (cerebral malaria)
Tachypnoea, respiratory distress (ARDS, metabolic acidosis)
Hypotension (severe malaria/co-infection)

Investigations

First-line
Thick and thin blood filmsGOLD STANDARD. Thick film: detects parasites (higher sensitivity). Thin film: identifies SPECIES and quantifies parasitaemia (percentage of RBCs infected). Send 3 sets over 48 hours if initial negative
Rapid diagnostic test (RDT)Detects malaria antigens (PfHRP2 for P. falciparum). Quick result (<20 min) but does not quantify parasitaemia or reliably detect non-falciparum species. Used alongside films, not instead of
Second-line
FBCThrombocytopenia (very common — >90% of falciparum cases), anaemia (haemolysis), normal or low WCC
U&Es, creatinineAKI is a feature of severe malaria (blackwater fever, renal tubular necrosis)
LFTs, bilirubinRaised unconjugated bilirubin (haemolysis), raised ALT (hepatic involvement)
GlucoseHypoglycaemia — a feature of severe malaria (parasites consume glucose; quinine stimulates insulin secretion)
Blood gasMetabolic acidosis (lactic acidosis from tissue hypoxia) — marker of severity
LDH, haptoglobinHaemolysis markers
Specialist
Parasitaemia quantificationCritical for management decisions. >2% = severe falciparum malaria. >10% = very severe, consider exchange transfusion
1
Uncomplicated falciparum malaria
  • Artemether-lumefantrine (Riamet): 4 tablets at 0, 8, 24, 36, 48, 60 hours (24 tablets total over 3 days) — first-line in UK
  • Alternative: atovaquone-proguanil (Malarone) for 3 days or quinine + doxycycline/clindamycin for 7 days
  • Admit ALL patients with P. falciparum for at least 24 hours for observation and repeat parasitaemia
2
Severe falciparum malaria (any of: parasitaemia >2%, cerebral malaria, renal failure, acidosis, hypoglycaemia, ARDS, DIC, severe anaemia)
  • IV ARTESUNATE — first-line for severe malaria (superior to IV quinine, WHO/NICE recommended)
  • 2.4 mg/kg IV at 0, 12, 24 hours then daily until able to take oral therapy
  • If artesunate unavailable: IV quinine loading dose 20 mg/kg then 10 mg/kg TDS (with cardiac monitoring — QT prolongation risk)
  • Manage in HDU/ITU, monitor glucose (hypoglycaemia), fluids, renal function
3
Non-falciparum malaria (P. vivax, P. ovale, P. malariae)
  • Chloroquine: 600 mg base, then 300 mg at 6, 24, 48 hours (total 25 mg/kg over 3 days)
  • P. vivax and P. ovale: ADD primaquine 14 days to eliminate hypnozoites (liver dormant stage) and prevent relapse
  • Check G6PD BEFORE prescribing primaquine — causes haemolysis in G6PD-deficient patients
4
Chemoprophylaxis for travellers
  • Atovaquone-proguanil (Malarone): start 1-2 days before, daily during, 7 days after travel — well-tolerated
  • Doxycycline: start 1-2 days before, daily during, 28 days after — cheap, also protects against other infections. Photosensitivity warning
  • Mefloquine: start 2-3 weeks before, weekly during, 4 weeks after — CI in psychiatric disease, epilepsy, cardiac conduction disorders
  • No prophylaxis is 100% — also advise DEET insect repellent, long sleeves/trousers at dusk, impregnated bed nets

Complications

  • Cerebral malaria: P. falciparum sequesters in cerebral microvasculature — coma, seizures, ~20% mortality even with treatment
  • Severe anaemia: From RBC destruction (haemolysis) and dyserythropoiesis
  • AKI: Blackwater fever (massive intravascular haemolysis) and acute tubular necrosis
  • ARDS: Non-cardiogenic pulmonary oedema — can develop even as parasitaemia clears
  • Hypoglycaemia: Parasite glucose consumption + quinine-induced insulin release
  • Splenic rupture: Risk in acute malaria (especially P. vivax)
UKMLA Exam Tips
  • 1Fever + travel to endemic area = malaria until proven otherwise. ALWAYS ask about travel history in any febrile patient
  • 2Thick and thin blood films (×3 over 48 hours) = gold standard diagnosis. RDT supports but does not replace films
  • 3IV artesunate is first-line for SEVERE falciparum malaria (not IV quinine, which is second-line)
  • 4P. vivax and P. ovale have HYPNOZOITES — need primaquine to prevent relapse. Check G6PD first (primaquine → haemolysis in G6PD deficiency)
  • 5Thrombocytopenia is almost universal in falciparum malaria — useful diagnostic clue
  • 6No prophylaxis is 100% effective — a negative prophylaxis history does NOT exclude malaria
  • 7Blackwater fever = massive haemolysis → haemoglobinuria → dark urine → AKI

Put your reading into practice

Topic-specific question practice is not linked for this article yet.

Choose UKMLA questions from the existing bank. General exam practice covers your selected topics; it is not filtered to this article. Your usual question-bank access applies.

Choose UKMLA practice

After your session, return to this section to revisit the reading and choose your next review.

Verified Sources & References

UKHSA — Guidelines for Malaria Prevention and Treatment in Travellers from the UK
Your learning path

Save your place and choose what comes next

Infectious Diseases · Article 4 of 16