Paediatrics II

Malaria

Table of Contents

Malaria in Newborns (Congenital Malaria)

Definition

Congenital malaria refers to the infection of a newborn with Plasmodium parasites acquired through transplacental transmission from an infected mother during pregnancy or, rarely, at delivery via contaminated blood. The infection becomes clinically apparent within the first 28 days of life, with most cases presenting between day 7 and day 21. Unlike typical malaria, it is not transmitted by mosquito bites in the neonatal period. The term “congenital” emphasizes intrauterine acquisition, distinguishing it from postnatal mosquito-borne infection.


Causative Organisms

Four main species of Plasmodium infect humans; all can cause congenital malaria, though severity and frequency differ:

 
 
SpeciesExplanation
Plasmodium falciparumMost dangerous; causes severe malaria. Responsible for nearly all severe congenital cases. Adheres to placental vessels via VAR2CSA protein, leading to heavy placental sequestration.
Plasmodium vivaxCauses milder disease but can relapse due to liver hypnozoites. Less common in congenital transmission but reported in Asia and Latin America.
Plasmodium malariaeChronic, low-grade parasitemia. Rarely causes congenital malaria; associated with quartana nephrotic syndrome in older children.
Plasmodium ovaleRare in neonates; similar to P. vivax with liver dormancy. Endemic in West Africa.
 

Mixed infections (e.g., P. falciparum + P. vivax) may occur in co-endemic areas.


Pathophysiology
  1. Placental Infection
    • Infected maternal red blood cells (iRBCs) adhere to chondroitin sulfate A (CSA) on syncytiotrophoblast via PfEMP1 (VAR2CSA).
    • Results in placental malaria: inflammation, fibrinoid deposition, reduced nutrient/oxygen transfer → IUGR, prematurity.
  2. Transplacental Passage
    • Parasitized RBCs cross into fetal circulation through micro-hemorrhages or active transport.
    • Fetal monocytes may phagocytose iRBCs but fail to clear due to immature immunity.
  3. Neonatal Immune Response
    • Passive IgG from mother offers partial protection (highest at birth, wanes by 6 months).
    • Neonatal spleen and liver have poor parasite clearance.
    • Low IFN-γ and IL-12 → inadequate Th1 response.
  4. Pathological Effects
    • Hemolysis: Parasites rupture RBCs → anemia, jaundice.
    • Cytokine release (TNF-α, IL-1): Fever, irritability, poor feeding.
    • Hypoglycemia: Parasite glucose consumption + reduced intake.
    • Sequestration (in severe P. falciparum): Microvascular obstruction in brain, lungs, kidneys.

Epidemiology
  • Global: ~125 million pregnancies annually in malaria-endemic areas.
  • Prevalence of Congenital Malaria:
    • 0.3% in low-transmission settings
    • Up to 33% in high-transmission areas with heavy maternal parasitemia
  • Risk Highest In:
    • Sub-Saharan Africa (P. falciparum dominant)
    • Primigravidae (no prior immunity to VAR2CSA)
    • HIV-co-infected mothers (impaired placental immunity)
  • Mortality:
    • 75,000–200,000 neonatal deaths/year linked to malaria in pregnancy
    • Direct congenital malaria mortality: 5–20% in treated severe cases

Risk Factors
Maternal
  • Active malaria in 2nd/3rd trimester
  • No IPTp-SP (sulfadoxine-pyrimethamine)
  • HIV infection (↑ placental parasitemia)
  • Anemia, malnutrition
Fetal/Neonatal
  • Prematurity (<37 weeks)
  • Low birth weight (<2.5 kg)
  • Intrauterine growth restriction
Environmental
  • Rainy season (peak mosquito density)
  • Lack of LLINs (long-lasting insecticidal nets)
  • Residence in hyperendemic area

Clinical Presentation

Symptoms are nonspecific and overlap with neonatal sepsis, making clinical diagnosis challenging.

 
 
SymptomFrequencyPathophysiological Explanation
Fever70–90%Cytokine-mediated (TNF-α, IL-1); irregular, not paroxysmal
Irritability / Lethargy80%Cerebral irritation, hypoglycemia, anemia
Poor feeding / Refusal to suck75%Oral motor fatigue, metabolic stress
Pallor60–80%Hemolysis of parasitized and non-parasitized RBCs
Jaundice50–70%Hemolysis + hepatic immaturity → unconjugated hyperbilirubinemia
Hepatosplenomegaly60%Extramedullary hematopoiesis + parasite sequestration
Vomiting / Diarrhea40%Gut inflammation or co-infection
Respiratory distress30%Anemia, acidosis, pulmonary sequestration
Seizures10–20%Cerebral malaria: cytoadherence in brain microvessels
Hypoglycemia20–40%Parasite glucose use + reduced intake + liver dysfunction
 

Diagnosis
1. Blood Smear Microscopy
  • Thick smear: Screens for parasites (ring forms, gametocytes)
  • Thin smear: Species ID, parasitemia %
  • Timing: Repeat every 12–24 hours × 3 if initial negative but high suspicion
  • Parasitemia Calculation:
    • Parasites per 200 WBCs × (WBC count / 200) = parasites/μL
2. Rapid Diagnostic Test (RDT)
  • Detects HRP-2 (P. falciparum) or pLDH (pan-malaria)
  • Sensitivity: >95% at >100 parasites/μL
  • False positives: HRP-2 persists 2–4 weeks post-treatment
3. Polymerase Chain Reaction (PCR)
  • Detects <5 parasites/μL
  • Used in research or reference labs
4. Maternal Blood Smear
  • Positive in 70–80% of congenital cases
  • Supports diagnosis even if neonatal smear initially negative
5. Supporting Laboratory Tests
 
 
TestExpected FindingExplanation
CBCHb <10 g/dL, thrombocytopeniaHemolysis, bone marrow suppression
Bilirubin↑ IndirectRBC breakdown
Glucose<40 mg/dLParasite metabolism
CRPMildly elevatedNon-specific inflammation
Blood cultureOften negativeRule out bacterial co-infection
 
6. Placental Histology (if available)
  • Hemozoin pigment, parasitized RBCs in intervillous spaces
  • Confirms intrauterine exposure

Management Workflow
1. Stabilization (First 30 Minutes)
  • Airway, Breathing, Circulation
  • Oxygen via nasal prongs if SpO₂ <92%
  • IV cannula (avoid umbilical vein if possible)
  • Capillary glucose:
    • If <40 mg/dL → 10% dextrose 2–4 ml/kg IV bolus → D10 maintenance
  • Empirical antibiotics (cover sepsis overlap):
    • Ampicillin 50 mg/kg IV 12-hourly +
    • Gentamicin 5 mg/kg IV once daily
2. Antimalarial Therapy (WHO 2021 Guidelines)
 
 
Clinical StatusDrugDoseDurationNotes
UncomplicatedArtemether-Lumefantrine (AL)Only if weight ≥5 kg Day 1: 1.5/9 mg/kg ×2 (6 hrs apart) Day 2–3: same3 daysGive with milk/fat
 OR Artesunate-Amodiaquine (AS-AQ)≥4.5 kg: 4/10 mg/kg daily3 daysLess cardiotoxicity
Severe MalariaIV Artesunate2.4 mg/kg at 0, 12, 24 hrs Then daily until oral possibleMin 24 hrs → complete with full AL courseDrug of choice
 If unavailable: IV QuinineLoading: 20 mg salt/kg over 4 hrs Maintenance: 10 mg/kg every 8 hrs7 daysMonitor QTc
 

Neonates <5 kg: Use IV artesunate only; no oral ACT until weight threshold met.

3. Supportive Care
  • Blood transfusion:
    • Hb <7 g/dL or
    • Hb <10 g/dL with tachycardia/respiratory distress
    • 10–15 ml/kg packed RBCs over 3–4 hrs
  • Phototherapy: For jaundice (per NICU protocol)
  • Seizures:
    • Phenobarbitone 20 mg/kg IV loading → 5 mg/kg/day maintenance
  • Fluid management:
    • 4 ml/kg/hr (D5½NS or D10½NS)
    • Avoid overload (risk of pulmonary edema)
4. Monitoring
  • Parasitemia: Thick/thin smear daily until negative
  • Glucose: 4-hourly × 48 hrs
  • Hb, platelets: Daily
  • Vital signs: Continuous cardiorespiratory monitor
  • Input/output: Strict fluid balance
5. Exchange Transfusion (Rare Indications)
  • Parasitemia >10%
  • Severe anemia + cardiac failure
  • Cerebral malaria with coma
  • Removes parasites, toxins, and inflammatory mediators

Complications
  • Severe anemia → high-output cardiac failure
  • Cerebral malaria → coma, seizures, death
  • Hypoglycemia → brain injury
  • Acute kidney injury (rare)
  • Pulmonary edema (from overhydration)
  • Secondary bacterial sepsis
  • Mortality: 5–20% in severe treated cases

Prognosis
  • Uncomplicated: Full recovery with prompt treatment
  • Severe:
    • Mortality 10–20% even in ICU
    • Survivors usually neurologically intact if treated early
  • Long-term: Rare sequelae (hearing loss, developmental delay) if cerebral involvement

Prevention
1. Maternal Interventions (Cornerstone)
  • IPTp-SP
    • Start at 13–16 weeks, monthly until delivery
    • ≥3 doses reduce placental malaria by 50–70%
  • LLINs
    • Free distribution + education on nightly use
  • Case management
    • Test and treat maternal fever with ACT
2. Neonatal
  • No routine chemoprophylaxis
  • Avoid blood transfusion unless lifesaving
3. Community
  • IRS (Indoor Residual Spraying) with actellic/pirimiphos-methyl
  • SMC (Seasonal Malaria Chemoprevention) in Sahel (not for neonates)

Key Nursing Responsibilities
  • Fever control:
    • Tepid sponging
    • Paracetamol 15 mg/kg 6-hourly
  • Feeding support:
    • NGT with expressed breast milk if poor suck
    • 10–20 ml/kg/feed every 2–3 hrs
  • Infection prevention:
    • Hand hygiene before/after handling
    • Isolate if co-infection suspected
  • Parental counseling:
    • Complete full antimalarial course
    • Sleep under LLIN
    • Return if fever recurs
  • Documentation:
    • Parasitemia % daily
    • Glucose, Hb, weight
    • Drug timing and side effects

WHO Case Definition (Suspected Congenital Malaria)
  • Infant <28 days old
  • Fever or history of fever
  • Mother resides in or traveled to malaria-endemic area
  • No other obvious cause identified → Perform blood smear and/or RDT immediately

Critical Note: In malaria-endemic areas, every febrile neonate must have a malaria smear/RDT plus full sepsis workup. Co-infection with bacteria is common — never withhold antibiotics. Treat the mother if smear-positive to prevent reinfection and protect future pregnancies.

Join Our WhatsApp Groups!

Are you a nursing or midwifery student looking for a space to connect, ask questions, share notes, and learn from peers?

Join our WhatsApp discussion groups today!

Join Now