Bacterial Meningitis in Children

Acute bacterial meningitis is a medical emergency and a perennial favourite of NEET PG paediatrics and microbiology. The exam loves three things here: age-specific organisms, CSF interpretation, and the ceftriaxone + dexamethasone management algorithm. Master those and most questions fall.

Definition & classification

Bacterial meningitis is acute inflammation of the leptomeninges (pia and arachnoid) and the cerebrospinal fluid (CSF) in the subarachnoid space, caused by pyogenic bacteria. It is distinguished from aseptic (viral) meningitis, tuberculous meningitis and fungal meningitis chiefly by CSF analysis and time-course.

Practical classification used in paediatrics:

• Neonatal meningitis — first 28 days of life; early-onset (≤72 h, vertical/maternal flora) vs late-onset (>72 h to 28 days, often nosocomial/community).
• Meningitis beyond the neonatal period — infants, children and adolescents, where the community-acquired triad of S. pneumoniae, N. meningitidis and (historically) H. influenzae type b dominates.

High-yield: The single most important determinant of the likely organism — and therefore empirical therapy — is the age of the child.

Age-based causative organisms

This is the most repeatedly asked sub-topic. Commit the table.

Age group	Common organisms (in order)	Empirical antibiotic
0–28 days (neonate)	Group B Streptococcus (S. agalactiae), E. coli (and other gram-negative bacilli), Listeria monocytogenes	Ampicillin + Cefotaxime (± gentamicin)
1–3 months	Overlap: GBS, E. coli, Listeria plus S. pneumoniae, N. meningitidis, Hib	Ampicillin + Cefotaxime/Ceftriaxone ± vancomycin
3 months–18 years	S. pneumoniae, N. meningitidis, H. influenzae type b (now rare post-vaccine)	Ceftriaxone (or Cefotaxime) + Vancomycin

High-yield: The neonatal "big three" mnemonic — "GEL" = Group B Strep, E. coli, Listeria. These three drive the ampicillin requirement (cephalosporins do NOT cover Listeria).

High-yield: Ceftriaxone is avoided in neonates (especially <28 days, and contraindicated with calcium-containing IV fluids due to ceftriaxone–calcium precipitation, and because it displaces bilirubin → kernicterus risk). Cefotaxime is the preferred third-generation cephalosporin in neonates.

Special situations worth a line:

• Penetrating head trauma / neurosurgery / CSF shunt → S. aureus, coagulase-negative staph, Pseudomonas → add vancomycin + antipseudomonal cephalosporin (cefepime/ceftazidime) or meropenem.
• Asplenia / sickle cell / complement (terminal C5–C9) deficiency → encapsulated organisms, especially S. pneumoniae and N. meningitidis.

Etiology & pathophysiology

The classic sequence: nasopharyngeal colonisation → mucosal invasion → bacteraemia → crossing the blood–brain barrier at the choroid plexus → multiplication in CSF (where opsonic/complement activity is low) → release of bacterial cell-wall components → host inflammatory cytokine cascade (TNF-α, IL-1) → BBB breakdown, vasogenic + cytotoxic + interstitial oedema → raised ICP and decreased cerebral blood flow → neuronal injury.

Pathophysiology flow:

Colonisation → bacteraemia → BBB invasion → CSF inflammation → cytokine surge (TNF-α, IL-1) → cerebral oedema + vasculitis → raised ICP & ↓ cerebral perfusion → ischaemia / infarction / herniation

It is this inflammatory cytokine cascade — not the bacteria directly — that drives much of the neuronal damage, which is the rationale for adjunctive dexamethasone (it blunts the cytokine response, ideally given before or with the first antibiotic dose).

The encapsulated pathogens (S. pneumoniae, N. meningitidis, Hib) resist phagocytosis via their polysaccharide capsule — the basis for both their virulence and the conjugate vaccines.

Clinical features

Age dramatically changes presentation — a key exam trap.

Neonates / young infants (non-specific, "sick baby"):

• Poor feeding, lethargy or irritability, temperature instability (fever OR hypothermia)
• High-pitched cry, bulging anterior fontanelle (late sign), seizures
• Apnoea, jaundice, vomiting
• Nuchal rigidity is often ABSENT in neonates — its absence does NOT exclude meningitis.

Older children / adolescents (classic):

• Fever, headache, photophobia, vomiting
• Neck stiffness, altered sensorium, seizures
• Meningeal signs: Kernig sign (resistance/pain on knee extension with hip flexed) and Brudzinski sign (involuntary hip/knee flexion on passive neck flexion).
• Petechial/purpuric rash → suspect meningococcaemia (N. meningitidis); may progress to purpura fulminans and Waterhouse–Friderichsen syndrome.

High-yield: Waterhouse–Friderichsen syndrome = fulminant meningococcaemia with bilateral adrenal haemorrhage, refractory shock and DIC. Classic eponym question.

High-yield: A bulging anterior fontanelle in an infant suggests raised ICP; look for it but remember it is a relatively late sign.

Diagnosis & investigation of choice

Lumbar puncture for CSF analysis is the investigation of choice and is both diagnostic and confirmatory.

CSF interpretation — the make-or-break table

Parameter	Normal	Bacterial	Viral (aseptic)	Tuberculous
Appearance	Clear	Turbid/purulent	Clear	Clear/cobweb
Opening pressure	10–20 cm H₂O	Raised	Normal/mild ↑	Raised
Cells (predominant)	<5 lymphocytes	↑↑ Neutrophils (PMN)	↑ Lymphocytes	↑ Lymphocytes
Cell count	<5/µL	100s–1000s/µL	10–500/µL	25–500/µL
Protein	20–45 mg/dL	High (>100)	Normal/mild ↑	Very high
Glucose (CSF:blood)	≥0.6 (≈⅔)	Low (<0.4)	Normal	Low
Lactate	<2.1 mmol/L	>3.5 mmol/L	Normal	Raised

High-yield: Bacterial meningitis = neutrophilic pleocytosis + high protein + LOW glucose (hypoglycorrhachia). Always interpret CSF glucose as a ratio to a paired blood glucose (normal ≥ 0.6; bacterial < 0.4).

Supporting investigations:

• CSF Gram stain + culture (culture is the gold standard for organism + sensitivity). Gram stain clues: gram-positive diplococci → pneumococcus; gram-negative diplococci → meningococcus; gram-negative coccobacilli → Hib; gram-positive bacilli → Listeria.
• Latex agglutination / bacterial antigen testing, and increasingly multiplex PCR (BioFire meningitis/encephalitis panel) — useful when patient has had prior antibiotics (partially treated meningitis with sterile culture).
• Blood culture (positive in a significant proportion; draw before antibiotics).
• CBC, CRP/procalcitonin, electrolytes (watch for SIADH-induced hyponatraemia), coagulation profile if purpura.

When to do CT head BEFORE lumbar puncture

Do NOT delay antibiotics for imaging if meningitis is suspected. Get CT first only if signs of raised ICP / mass effect to avoid herniation:

• Focal neurological deficit, new-onset seizures
• Papilloedema, GCS deterioration / altered consciousness
• Immunocompromise

Approach if LP delayed: Draw blood culture → start empirical antibiotics immediately → do CT → then LP if safe. (Antibiotics started ~within an hour barely affect CSF cytochemistry but may sterilise culture — PCR/antigen helps.)

High-yield: Never delay antibiotics waiting for the LP or CT. Empirical therapy first if there is any delay; the priority is survival.

Absolute contraindications to LP: signs of raised ICP with impending herniation, cardiorespiratory instability, local skin infection at puncture site, coagulopathy/thrombocytopenia.

Management / drug of choice

Empirical antibiotics (start within the hour)

• Neonate (≤28 d): Ampicillin + Cefotaxime (covers GBS, E. coli, Listeria); gentamicin often added.
• Child >3 months: Ceftriaxone (or cefotaxime) + Vancomycin. Vancomycin is added to cover penicillin/cephalosporin-resistant pneumococci.
• De-escalate once culture and sensitivity return (e.g., fully sensitive meningococcus → penicillin G).

Adjunctive dexamethasone

• Dexamethasone 0.15 mg/kg IV every 6 h for 2–4 days, ideally given 10–20 minutes BEFORE or WITH the first antibiotic dose.
• Strongest, proven benefit: reduces sensorineural hearing loss (the most important neurological sequela) in Hib meningitis. Benefit in pneumococcal meningitis is suggested; routine use in meningococcal is less clearly beneficial.
• NOT recommended routinely in neonates.

High-yield: Dexamethasone must be timed before/with the first antibiotic — given late (after antibiotics) it has little value. Its biggest documented benefit is preventing deafness in Hib meningitis.

Supportive care

• Airway/breathing/circulation; treat shock with fluids and inotropes (especially meningococcaemia).
• Fluid management is nuanced: avoid both dehydration and over-hydration. Monitor for SIADH (hyponatraemia with concentrated urine) → may need fluid restriction; but in hypovolaemia/shock, resuscitate first.
• Anticonvulsants for seizures; manage raised ICP (head-up positioning, osmotherapy if herniation risk).
• Isolation (droplet precautions) for suspected meningococcal/Hib for the first 24 h of effective therapy.

Duration (typical)

• N. meningitidis: 5–7 days
• H. influenzae type b: 7–10 days
• S. pneumoniae: 10–14 days
• GBS: 14–21 days; gram-negative bacilli/Listeria: 21 days

Chemoprophylaxis of close contacts

Organism	Prophylaxis for close contacts
N. meningitidis	Rifampicin (2 days) OR single-dose Ciprofloxacin OR Ceftriaxone (IM, preferred in pregnancy)
H. influenzae type b	Rifampicin (4 days) for household with vulnerable contacts
S. pneumoniae	No chemoprophylaxis

High-yield: Rifampicin is the classic chemoprophylactic agent for both meningococcal and Hib close contacts. Ceftriaxone is the safe choice in pregnancy.

Prevention — vaccines

• Hib conjugate vaccine — dramatic global decline in Hib meningitis; part of pentavalent vaccine in India's UIP.
• Pneumococcal conjugate vaccine (PCV) — now in the Indian Universal Immunisation Programme.
• Meningococcal vaccines: polysaccharide vs conjugate (MenACWY) and protein-based MenB. Indicated for outbreaks, asplenia, complement deficiency, Hajj pilgrims (Saudi Arabia mandates MenACWY), and travellers to the meningitis belt.

High-yield: Conjugate vaccines (Hib, PCV, MenACWY) generate T-cell-dependent responses with memory and work in infants <2 years, unlike plain polysaccharide vaccines which are T-independent and poorly immunogenic in infants.

Complications

Acute and long-term sequelae are heavily examined.

Acute:

• SIADH → hyponatraemia (very commonly tested).
• Subdural effusion — classically with H. influenzae and pneumococcal meningitis in infants; suspect with persistent/recurrent fever or focal signs; transillumination positive; mostly resolves spontaneously.
• Subdural empyema, ventriculitis, brain abscess.
• Seizures, raised ICP, cerebral herniation, infarction (vasculitis), cranial nerve palsies.
• DIC, septic shock, Waterhouse–Friderichsen (meningococcal).

Long-term sequelae:

• Sensorineural hearing loss (SNHL) — the MOST COMMON sequela → all children need a hearing (BERA/audiometry) test after recovery.
• Developmental delay, intellectual disability, cerebral palsy, epilepsy, hydrocephalus, visual impairment.

High-yield: Subdural effusion → think H. influenzae / pneumococcus in infants. Persistent or recurrent fever during treatment should prompt evaluation for subdural effusion, inadequate therapy, nosocomial infection or drug fever.

High-yield: Sensorineural hearing loss is the commonest long-term sequela — every survivor needs formal audiological assessment before discharge/follow-up.

Key differentials

• Viral (aseptic) meningitis — enteroviruses commonest; CSF lymphocytic, normal glucose, milder course.
• Tuberculous meningitis — subacute, cranial nerve palsies (esp. CN VI), basal exudates on imaging, very high CSF protein, low glucose, lymphocytic; CBNAAT/ADA help.
• Viral encephalitis (HSV) — altered behaviour, focal seizures, temporal lobe changes on MRI; CSF PCR; treat empirically with aciclovir.
• Partially treated bacterial meningitis — prior oral antibiotics → sterile culture but CSF still shows neutrophils/low glucose; use antigen/PCR.
• Febrile seizure — but a child with meningism needs LP; do LP especially in infants <12 months with febrile seizure where signs may be subtle.
• Brain abscess, cerebral malaria, leptospirosis, fungal meningitis (Cryptococcus in immunocompromised).

Recently asked / exam angle

• Age → organism → empirical drug matching: neonate = ampicillin + cefotaxime (the "ampicillin for Listeria" point is a near-guaranteed distractor question).
• Why cefotaxime over ceftriaxone in neonates — bilirubin displacement/kernicterus and calcium precipitation.
• CSF picture single-best-answer: low glucose + high protein + neutrophils = bacterial.
• Timing and indication of dexamethasone — before/with first antibiotic; biggest benefit = reduced deafness in Hib.
• Commonest sequela = sensorineural hearing loss; mandatory hearing screen.
• Subdural effusion association with H. influenzae.
• Waterhouse–Friderichsen syndrome and adrenal haemorrhage with meningococcaemia.
• Chemoprophylaxis = rifampicin (meningococcus and Hib); ceftriaxone in pregnancy.
• Conjugate vs polysaccharide vaccine immunology (T-dependent, works in infants).
• SIADH causing hyponatraemia as a complication and fluid management nuance.

Rapid revision

1. Neonatal "GEL": Group B Strep, E. coli, Listeria → empirical ampicillin + cefotaxime.
2. Children >3 months → ceftriaxone + vancomycin (vanco for resistant pneumococcus).
3. Cephalosporins do NOT cover Listeria — hence ampicillin in neonates.
4. Ceftriaxone avoided in neonates (kernicterus + calcium precipitation) → use cefotaxime.
5. LP/CSF analysis is the investigation of choice; culture is the gold standard.
6. Bacterial CSF = turbid, neutrophils, high protein, LOW glucose (ratio <0.4), high lactate.
7. Never delay antibiotics for CT/LP; give CT-before-LP only if raised ICP signs.
8. Dexamethasone before/with first antibiotic — reduces hearing loss, best evidence in Hib.
9. Sensorineural hearing loss = commonest long-term sequela → screen every survivor.
10. Subdural effusion ↔ H. influenzae / pneumococcus in infants; SIADH → hyponatraemia.
11. Waterhouse–Friderichsen = meningococcaemia + adrenal haemorrhage + DIC + shock.
12. Chemoprophylaxis = rifampicin (meningococcus & Hib); conjugate vaccines work in infants <2 yrs.