Meningococcal disease and paediatric sepsis

Invasive Meningococcal Disease (IMD) & Sepsis

Invasive meningococcal disease caused by Neisseria meningitidis is an acute, fulminant medical emergency. The organism is an encapsulated Gram-negative diplococcus carried asymptomatically in the human nasopharynx. Invasive disease occurs when virulent strains breach the mucosal barrier, enter the bloodstream, and rapidly proliferate.

Pathophysiology

Meningococcal endotoxin—specifically lipooligosaccharide (LOS)—is shed in massive quantities during intravascular bacterial replication. Circulating LOS triggers an explosive systemic inflammatory cascade via Toll-like receptor 4 (TLR4), causing:

1. Severe endothelial disruption: Generalized microvascular damage with loss of endothelial barrier function.
2. Capillary leak syndrome: Massive plasma extravasation into interstitial tissues, resulting in profound intravascular hypovolaemic shock and pulmonary oedema.
3. Disseminated Intravascular Coagulation (DIC): Extensive microvascular thrombosis with secondary consumption of coagulation factors and platelets, leading to skin necrosis (purpura fulminans) and peripheral gangrene.
4. Waterhouse-Friderichsen Syndrome: Bilateral massive adrenal haemorrhagic infarction, causing acute adrenal insufficiency and refractory catecholamine-resistant vasodilatory shock.

Clinical Manifestations and Red Flags

• Early Phase (First 4 to 12 Hours): Often indistinguishable from ordinary viral illness. Early discriminating red-flag features include:
  • Cold hands and feet (peripheral vasoconstriction) despite a high core temperature.
  • Severe leg pain or muscular myalgias preventing weight-bearing.
  • Abnormal skin colour (pallor, mottling, or ashen grey appearance).
  • Excessive irritability or lethargy disproportionate to fever.
• Late Phase (12 to 24 Hours):
  • The Petechial and Purpuric Rash: Begins as sparse, tiny pink maculopapular or petechial lesions ($< 2\text{ mm}$) that rapidly evolve within hours into dark purple, jagged purpuric plaques ($> 2\text{ mm}$) and ecchymoses.
  • The Glass Tumbler Test: Petechiae and purpura represent true intradermal microvascular haemorrhage and do not blanch when compressed under a transparent glass tumbler.
  • Progression to septic shock: Tachycardia, delayed capillary refill ($> 3\text{ to }5\text{ seconds}$), weak thready pulses, and ultimately hypotension (an ominous, late indicator of uncompensated circulatory collapse).

Pre-Hospital & Emergency Life-Saving Management

• The Golden Rule: When invasive meningococcal disease is suspected in any clinical setting (GP surgery, rural clinic, or tertiary triage), administer parenteral antibiotics immediately:
  • Intravenous or Intramuscular Ceftriaxone: $100\text{ mg/kg}$ (maximum single dose $4\text{ g}$); or
  • Intravenous or Intramuscular Benzylpenicillin: $60\text{ mg/kg}$ (maximum $2.4\text{ g}$).
  • If peripheral intravenous access cannot be secured within two minutes, inject ceftriaxone intramuscularly into the anterolateral thigh without delay. Do not withhold or postpone antibiotics to transfer the patient or perform diagnostic tests.
• Fluid resuscitation: Give measured 10–20 mL/kg isotonic boluses under the local paediatric shock pathway, checking perfusion and signs of overload after each. Obtain early senior/critical-care help and start vasoactive support when indicated by response; do not automatically wait for 60 mL/kg. Resource setting, cardiac function and the cause of shock change the balance.
• Laboratory Confirmation: Blood cultures; collect EDTA whole blood for meningococcal PCR (nucleic acid amplification testing remains positive for several days following antibiotic administration, ensuring diagnostic confirmation).
• Statutory Public Health Notification & Contact Chemoprophylaxis:
  • IMD is a notifiable medical condition across all Australian States and Territories, mandating immediate telephone notification to the local Public Health Unit.
  • Chemoprophylaxis eradicates nasopharyngeal carriage of N. meningitidis, preventing secondary spread. Indicated for close household contacts, day care contacts who spent $> 4\text{ hours}$ together in the 7 days prior, or healthcare workers directly exposed to the patient's respiratory secretions during intubation:
    • Oral Ciprofloxacin: Preferred in Australia as a single oral dose ($30\text{ mg/kg}$, maximum $500\text{ mg}$) for all ages including children;
    • Oral Rifampicin: Given twice daily for 2 days ($10\text{ mg/kg}$ BD, maximum $600\text{ mg}$);
    • Intramuscular Ceftriaxone: Single IM dose ($125\text{ mg}$ for children $< 12\text{ years}$, $250\text{ mg}$ for $\ge 12\text{ years}$); safe in pregnant contacts.

Escalation and contacts

A febrile child with poor perfusion and a rapidly spreading purpuric rash needs immediate sepsis treatment and senior support. Do not wait for a lumbar puncture or full rash evolution. Reassess perfusion, breathing and fluid tolerance after each intervention; early critical-care input may be needed. Public-health notification and prophylaxis assessment protect defined close contacts, but do not replace treating the child. Explain to families that contact eligibility depends on the exposure and health-authority guidance, not merely attendance at the same school. Document treatment times and send an urgent structured handover if transfer is needed.

Sampling during suspected meningococcal disease

Obtain cultures and relevant molecular samples promptly when this will not delay antibiotics. A negative early culture, especially after treatment, does not remove clinical concern. LP is often deferred in a shocked child; blood testing and treatment proceed while stability and safety are reassessed. Communicate the suspected diagnosis to the receiving team and public health, including antibiotics already given, and document the time of deterioration and interventions.

Primary references (checked 7 October 2026): RCH Kawasaki disease; RCH meningitis/encephalitis.