Neonatal Meningitis

Meningitis occurring within the first 28 days of life, with a distinct microbiology from meningitis in older children and adults, reflecting the specific exposures and immature immune status of the neonate.

Early-onset disease (within the first 72 hours, sometimes extended to the first week in some classifications) typically results from vertical transmission during delivery, with group B streptococcus (Streptococcus agalactiae) and Escherichia coli as the leading causes.

Late-onset disease (after the first week) reflects a broader range of acquisition routes (nosocomial, environmental, or continued vertical transmission), with group B streptococcus, E. coli, Listeria monocytogenes, and, in the hospitalized or preterm population, coagulase-negative staphylococci and other nosocomial organisms featuring more prominently.

Herpes simplex virus (typically HSV-2 from maternal genital shedding at delivery) is an important cause of neonatal meningoencephalitis carrying particularly high morbidity if treatment is delayed.

Presentation in the neonate is frequently non-specific and subtle, and the classic adult features of neck stiffness and photophobia are often absent or unreliable: fever or, notably, hypothermia (neonates may respond to severe infection with temperature instability in either direction), poor feeding, lethargy or irritability, a bulging fontanelle (a useful but late and insensitive sign), seizures, apnea, and, in the most severe or advanced presentations, signs of septic shock.

Any unwell, non-specifically deteriorating neonate should prompt a low threshold for full septic workup including lumbar puncture, given how easily this diagnosis can be missed on clinical grounds alone.

• Lumbar puncture with CSF analysis is essential in any neonate undergoing a septic workup, given the poor correlation between clinical severity and the presence of meningitis in this age group, and given that CSF findings and normal reference ranges differ from older children and adults (neonates, particularly preterm, normally have somewhat higher CSF protein and a wider range of normal white cell counts, requiring interpretation against age-specific reference ranges)
• Blood cultures, FBC, CRP, and, where facilities allow, PCR-based pathogen panels support diagnosis and pathogen identification
• HSV PCR of CSF (and, where relevant, blood, skin/mucosal lesion swabs, and conjunctival swabs) should be considered in any neonate with a compatible presentation, particularly with seizures, vesicular skin lesions, or a maternal history of genital herpes, given the specific and time-critical treatment implications

• Empirical antibiotics, started promptly on clinical suspicion, typically combine an agent with good gram positive and Listeria cover with a broad gram negative agent: a commonly used regimen is IV ampicillin (weight-based, e.g. 50 mg/kg every 6 to 8 hours depending on age) combined with a third-generation cephalosporin (e.g. cefotaxime, weight and age-based dosing), with gentamicin sometimes added for additional gram negative and synergistic cover per local neonatal protocol; ceftriaxone is generally avoided in neonates, particularly preterm or jaundiced infants, given a risk of displacing bilirubin from albumin and precipitating kernicterus
• Empirical aciclovir (weight-based IV dosing) should be added where HSV meningoencephalitis is a genuine clinical possibility, given the same principle of empirical treatment pending confirmation described in the Herpes Simplex Encephalitis entry, and continued for a prolonged course (commonly 14 to 21 days depending on presentation) if confirmed
• Treatment duration for confirmed bacterial neonatal meningitis is typically longer than in older age groups, commonly 14 to 21 days depending on the organism (gram negative meningitis in particular often requiring the longer end of this range), guided by repeat CSF analysis in some protocols to confirm sterilization before treatment cessation
• Supportive neonatal intensive care, including careful fluid and electrolyte management, seizure control, and monitoring for complications (hydrocephalus, subdural effusion, hearing loss, requiring formal audiological assessment before discharge given the significant risk of sensorineural hearing loss with bacterial meningitis in this age group)
• Prevention: intrapartum antibiotic prophylaxis for maternal group B streptococcus colonization (see the Preterm Labour entry for the specific regimen) substantially reduces early-onset GBS disease incidence

Referral: neonatology and infectious disease input for all cases; neurology for seizures or evolving structural complications; audiology follow-up for all survivors of confirmed bacterial meningitis.