Paediatrics chapters
Malaria in children
Malaria in children: the five Plasmodium species, life cycle and relapse, why fever, anaemia and a big spleen occur, how young children present, severe malaria, blood film diagnosis, treatment of vivax and falciparum, and prevention.
- Malaria is caused by Plasmodium (falciparum, vivax, ovale, malariae, knowlesi) spread by the female Anopheles mosquito; vivax is commonest and falciparum is most dangerous; vivax and ovale relapse from liver hypnozoites.
- Children have fever, anaemia and splenomegaly, often without the classic periodic fever; falciparum can cause severe malaria: severe anaemia, cerebral malaria, hypoglycaemia, acidosis, shock and blackwater fever.
- Diagnose with thick (screen) and thin (species) Giemsa films, repeated if negative; treat vivax with chloroquine plus primaquine and falciparum with an artemisinin combination, severe disease with parenteral artemisinin or quinine, following the current national guideline.
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Overview
Malaria is an acute or chronic protozoal infection that causes recurrent high fever, anaemia and splenomegaly. It is a major cause of illness and death in tropical countries, and most deaths are in infants and young children. It is endemic in parts of Pakistan, and Akbar notes that chloroquine-resistant P. falciparum is present in most endemic areas. Cerebral malaria is covered in its own chapter in the neurology section.
Aetiology
Malaria parasites are obligate intracellular protozoa of the genus Plasmodium. Five species infect humans:
| Species | Key points |
|---|---|
| P. falciparum | Most virulent; invades red cells of all ages, so parasite counts can be very high; causes severe and cerebral malaria; no hypnozoites |
| P. vivax | Most common worldwide; prefers young red cells (reticulocytes); relapses from hypnozoites; risk of splenic rupture |
| P. ovale | Like vivax; relapses |
| P. malariae | Older red cells; 72-hour (quartan) fever; can persist for years; nephrotic syndrome |
| P. knowlesi | 24-hour cycle; can be fatal |
Transmission
- Bite of an infected female Anopheles mosquito (main route); standing water and a warm climate favour spread.
- Blood transfusion, contaminated needles and organ transplant.
- Congenital: across the placenta from an infected mother.
In transfusion and congenital malaria merozoites enter the blood directly, so there is no liver stage and no relapse; primaquine is not needed.
Life cycle
- Mosquito bite: sporozoites are injected and reach the liver within minutes.
- Liver (exo-erythrocytic) stage: each parasite grows into a schizont containing thousands of merozoites; after about 1-2 weeks the schizont bursts. In vivax and ovale, some parasites stay dormant as hypnozoites and wake months or years later (relapse).
- Red cell (erythrocytic) stage: merozoites invade red cells → ring form (trophozoite) → schizont → red cell bursts, releasing merozoites to infect new cells. Each burst causes a febrile paroxysm.
- Some merozoites become male and female gametocytes.
- Mosquito (sexual) stage: a feeding mosquito takes up gametocytes, which form a zygote in its gut; new sporozoites move to its salivary glands.
Humans host the asexual cycle; the mosquito hosts the sexual cycle, so the mosquito is the definitive host.
Incubation periods (Akbar)
| Species | Incubation (days) | Red cell cycle |
|---|---|---|
| P. falciparum | 9 to 14 | 48 hours |
| P. vivax | 12 to 17 | 48 hours |
| P. ovale | 16 to 18 | 48 hours |
| P. malariae | 18 to 40 (longest) | 72 hours |
Pathophysiology
- Fever: red cell rupture releases parasite material; tumour necrosis factor and other cytokines cause the fever.
- Anaemia: haemolysis of infected (and uninfected) cells, splenic removal of red cells and bone marrow suppression. Worst in falciparum because of the heavy parasite load.
- Splenomegaly: stiff infected cells are trapped in the spleen; macrophages multiply. The congested spleen can rupture.
- Hypoglycaemia: low glycogen stores, poor gluconeogenesis and parasite glucose use; worsened by quinine.
- Falciparum sequestration: infected cells grow knobs, become sticky and block capillaries in the brain, kidney, lung and gut, causing cerebral malaria, renal failure, pulmonary oedema and malabsorption.
- Massive haemolysis may cause hyperkalaemia, jaundice and haemoglobinuria.
Protective factors
- Sickle cell trait, thalassaemia, G6PD deficiency, pyruvate kinase deficiency and fetal haemoglobin.
- Duffy-negative red cells resist P. vivax.
- Maternal antibody protects young infants for a few months; repeated infection in endemic areas gives partial immunity, so older children may have few symptoms despite parasites.
Clinical features
The classic paroxysm
Cold stage with chills and rigors → hot stage with high fever, headache, vomiting, aches and sometimes delirium → sweating stage as the fever breaks. Between attacks the child may feel fairly well.
| Periodicity | Species |
|---|---|
| Every 48 hours (tertian) | P. vivax, P. ovale |
| Every 72 hours (quartan) | P. malariae |
| Irregular or daily | P. falciparum (no regular pattern); P. knowlesi every 24 hours |
In children
- Children often lack the classic periodic pattern: fever is continuous or irregular.
- Anorexia, vomiting, diarrhoea, abdominal pain, headache, irritability, febrile convulsions.
- Pallor (anaemia) and splenomegaly, sometimes massive; hepatomegaly; jaundice; herpes labialis; dehydration.
The clinical triad of malaria is fever, anaemia and splenomegaly. Consider malaria in any febrile child from an endemic area.
Congenital malaria
- Usually in babies of non-immune mothers; presents mostly at 10-30 days of age (range from the first day to months).
- Looks like neonatal sepsis: fever, irritability, poor feeding, vomiting, jaundice, anaemia and hepatosplenomegaly.
- Malaria in pregnancy also causes abortion, stillbirth, prematurity and growth restriction.
Severe malaria
Almost always due to P. falciparum. Diagnosis of falciparum malaria is a medical emergency.
| Feature | Note |
|---|---|
| Severe anaemia | Hb under 5 g/dl; the commonest severe complication in children |
| Impaired consciousness / cerebral malaria | Coma with falciparum parasites and no other cause; CSF usually normal |
| Respiratory distress | Due to metabolic acidosis; a bad sign |
| Multiple seizures | Treat with benzodiazepines, then phenobarbital or phenytoin |
| Prostration | Cannot sit, stand or eat without help while conscious |
| Hypoglycaemia | Commoner in children and with quinine |
| Algid malaria | Circulatory collapse: hypotension, cold skin, weak pulse |
| Blackwater fever | Massive haemolysis, dark urine, acute renal failure; quinine may play a part |
| Others | Jaundice, DIC, pulmonary oedema, high-output heart failure, renal failure |
Severe anaemia is the commonest severe complication of malaria in children; hypoglycaemia must be looked for in every sick child, especially on quinine.
High parasitaemia (Akbar: over 10% of red cells or over 500,000/microlitre) predicts high mortality.
Tropical splenomegaly syndrome: a chronic abnormal immune response to repeated malaria with massive spleen, hepatomegaly, anaemia and high IgM; needs long-term antimalarial treatment.
Diagnosis
Blood films (Giemsa stain)
| Film | Use |
|---|---|
| Thick film | Screening: many red cells examined at once, so it detects low parasite counts |
| Thin film | Species identification from parasite shape, and the percentage of infected red cells (to follow treatment) |
- Films are repeated every 4-6 hours (several times a day) for up to 3 days if the first is negative; one negative film does not exclude malaria.
- Falciparum: ring forms and crescent (banana)-shaped gametocytes.
- Films may be negative early (symptoms can precede detectable parasites by 1-2 days) or after antimalarials have been taken.
- Rapid diagnostic tests detect parasite antigen.
Other tests
- Blood count: normocytic normochromic anaemia, raised reticulocytes, normal white count with more monocytes, low platelets.
- Blood glucose (hypoglycaemia), urea and creatinine, bilirubin, urine for haemoglobin.
- Response to treatment: the parasite count should fall daily; a steady or rising count after 48 hours means treatment failure.
Differential diagnosis
Typhoid, tuberculosis, septicaemia, urinary infection, pneumonia, meningitis and encephalitis, hepatitis, amoebic liver abscess, brucellosis, leptospirosis, endocarditis, leukaemia and lymphoma, and kala-azar.
Treatment
Start treatment as soon as malaria is diagnosed; delay worsens outcome, especially with falciparum.
Supportive care
- Correct dehydration; paracetamol for fever.
- Blood transfusion for severe anaemia.
- Check and treat hypoglycaemia.
- Treat seizures, renal failure and pulmonary oedema.
- Exchange transfusion may save life in non-immune children with parasitaemia over 15% (Akbar).
Uncomplicated vivax (and ovale, malariae) malaria
- Chloroquine acts on the red cell stage. Akbar's regimen: 10 mg base/kg at once, then 5 mg base/kg at 6, 24 and 48 hours.
- Add primaquine for vivax and ovale to kill liver hypnozoites and prevent relapse (radical cure). Check for G6PD deficiency first, because primaquine causes haemolysis.
Start: 10 mg base/kg × 12 kg = 120 mg base
At 6, 24 and 48 hours: 5 mg base/kg × 12 = 60 mg base each
Total = 120 + 60 + 60 + 60 = 300 mg base (= 25 mg base/kg)
Uncomplicated falciparum malaria
- Chloroquine is no longer reliable because resistance is widespread.
- Use an artemisinin-based combination, such as artemether-lumefantrine (Nelson and Akbar), or atovaquone-proguanil; oral quinine plus doxycycline (over 8 years) or clindamycin is an older alternative. Doses are given by weight bands.
- Akbar: if the parasite count does not fall within 24-48 hours, or clear by day 4, suspect resistance and change the drug.
Severe malaria
- Parenteral treatment until the child can swallow, then a full oral course.
- Akbar lists IM artemether (3.2 mg/kg, then 1.6 mg/kg daily) or IV quinine (20 mg salt/kg loading over 4 hours, then 10 mg/kg every 8 hours), and names artesunate in the IMCI section.
- Monitor glucose closely, especially on quinine.
Malaria treatment policy changes with resistance patterns; current WHO and national guidance prefer injectable artesunate for severe malaria and an ACT for falciparum. Check the current national guideline and WHO malaria guidance (checked 8 Nov 2026).
Chloroquine does not kill hypnozoites. Without primaquine, vivax can relapse even after a perfect chloroquine course.
Primaquine is the drug against liver hypnozoites (vivax, ovale) and must be avoided in G6PD deficiency.
Prevention
Personal protection
- Bed nets, screened rooms, long clothes, insect repellents.
- Remove standing water around homes.
Chemoprophylaxis (for non-immune travellers)
- Start before travel, continue during the stay and for 4 weeks after leaving.
- Chloroquine weekly in chloroquine-sensitive areas; mefloquine weekly where falciparum is chloroquine-resistant; doxycycline daily for children over 8 years.
- No drug gives complete protection.
Prognosis
- Non-falciparum malaria is usually benign with treatment.
- Falciparum malaria can kill within hours; delay in diagnosis and treatment, severe anaemia, hypoglycaemia, acidosis and coma worsen the outlook.
Expect: the five species and which is commonest and most virulent; female Anopheles; life cycle stages and where each occurs; hypnozoites in vivax and ovale causing relapse and the role of primaquine; no relapse in transfusion or congenital malaria; tertian and quartan fever; fever, anaemia and splenomegaly; severe anaemia as the commonest severe complication in children; features of severe malaria including blackwater fever and algid malaria; thick versus thin film; chloroquine regimen; ACT for falciparum; G6PD testing before primaquine; protective red cell traits; P. malariae and nephrotic syndrome.
Quick revision
- Female Anopheles; vivax commonest, falciparum deadliest.
- Liver schizont → red cell ring → schizont → burst = fever.
- Vivax and ovale: hypnozoites, relapse, primaquine (check G6PD).
- Tertian: vivax, ovale. Quartan: malariae (nephrotic syndrome).
- Child: irregular fever, pallor, splenomegaly; congenital malaria mimics sepsis.
- Severe anaemia (Hb under 5) is the commonest severe complication in children.
- Thick film to find, thin film to name; repeat over 3 days.
- Chloroquine 10, then 5 mg base/kg at 6, 24, 48 hours; ACT for falciparum; parenteral artemisinin or quinine for severe malaria.
Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics).
FAQ
Why does vivax malaria come back after treatment?
Some vivax parasites sleep in the liver as hypnozoites, which chloroquine does not reach. Primaquine is added to clear them.
Why do children often not show the classic alternate-day fever?
In young children the fever is usually continuous or irregular, so the pattern cannot be relied on. A blood film is needed.
Why is primaquine not given to every child?
It can cause severe haemolysis in G6PD deficiency, and it is only needed for the relapsing species, vivax and ovale.
Which severe complication of malaria is seen most often in children?
Severe anaemia, with haemoglobin below 5 g/dl, followed by cerebral malaria, respiratory distress from acidosis, and repeated seizures.