Meningitis in neonates and children

• Meningitis is infection and inflammation of the meninges, the membranes that wrap the brain and spinal cord. Bacterial meningitis is a neurological emergency in a child: it evolves over hours and kills through raised pressure, sepsis and stroke.
• In a newborn the illness is silent. Fever may be absent; the baby feeds poorly, is irritable or limp, has temperature instability, apnoea or a bulging fontanelle. Never expect the classic triad in a neonate. ^[1]
• The organism is predicted by age. Group B streptococcus (GBS, Streptococcus agalactiae), Escherichia coli and Listeria monocytogenes dominate in neonates; Streptococcus pneumoniae and Neisseria meningitidis dominate after the neonatal period, with Haemophilus influenzae type b much reduced but not abolished wherever conjugate vaccination is incomplete. ^[2]
• Lumbar puncture is the diagnostic test and should not be delayed for imaging unless there are specific danger signs. The cerebrospinal fluid (CSF) in bacterial disease is cloudy with a neutrophil count usually above 1000 per microlitre, protein above about 1.0 g/L (some sources use >150 mg/dL), and glucose less than roughly 40% of the blood level. ^[2]
• Treatment is antibiotics within one hour of arrival, plus dexamethasone for children over 3 months, and supportive intensive care. Dexamethasone is not recommended in neonates. ^[1][3]
• Prevention combines maternal intrapartum GBS prophylaxis, timely infant vaccination against pneumococcus, meningococcus and Hib, and antibiotic chemoprophylaxis for close contacts of meningococcal and Hib cases. ^[2][4][5]

By the end of this page you should be able to:

1. Predict the likely organism from the child's age and clinical context, and explain why neonatal disease is different.
2. Recognise bacterial meningitis in a neonate or toddler from its often non-specific features, including the non-blanching rash of meningococcal disease.
3. Decide when lumbar puncture is safe, when imaging must come first, and interpret CSF results by age.
4. Choose empiric antibiotics by age and adjust them once the organism is identified, including duration.
5. Use adjunctive dexamethasone correctly, including when to stop it.
6. Detect and manage complications such as hearing loss, hydrocephalus and seizures, and counsel families.
7. Outline prevention: vaccination, maternal screening and chemoprophylaxis of contacts.

Bacterial meningitis is distinguished from meningoencephalitis (infection of brain tissue itself), from sepsis (a dysregulated body-wide response to infection) and from non-infectious inflammation such as chemical or drug-induced meningitis. In practice the boundaries blur: meningococcal disease is often meningitis plus septicaemia, and bacterial meningitis frequently produces encephalopathy through raised pressure and inflamed vessels rather than through direct invasion of brain tissue.

A useful classification for bedside care is by speed and cause. Acute bacterial meningitis declares itself over hours to a day or two and is the dangerous form. Viral (aseptic) meningitis is usually milder and self-limiting. Tuberculous and fungal meningitis run a subacute or chronic course over weeks and need different tests and treatment. Because the early management differs sharply, the first clinical task is to exclude or treat the bacterial form quickly.

The general, all-age approach to meningitis (including adult doses, CT criteria, and viral, tuberculous and fungal disease) is covered in the Infectious Disease meningitis topic. The material here focuses on what changes when the patient is a neonate or a child.

Bacterial meningitis kills most often at the extremes of age, and children carry a large share of the burden. It remains a serious cause of death and long-term disability worldwide. ^[2] The burden is heaviest in sub-Saharan Africa's "meningitis belt", from Senegal to Ethiopia, with recurrent epidemics of meningococcal disease. ^[1]

Age changes the organism and therefore both incidence and prognosis. Neonates are the highest-risk group for bacterial meningitis in childhood, largely because they have not yet had maternal immunoglobulins and have immature phagocyte function. ^[2] In developed countries neonatal mortality from meningitis is around 10%, but in developing countries it can reach 58%. ^[2] In a recent prospective study of infants under 90 days in the United Kingdom and Ireland, mortality was 9% and 23% of survivors had serious central nervous system complications. ^[2]

Vaccination has transformed the picture. Before conjugate vaccines, H. influenzae type b, S. pneumoniae and N. meningitidis were the three overwhelmingly common causes of childhood meningitis; their incidence has fallen sharply wherever the vaccines are used, leaving pneumococcus and meningococcus as the main remaining vaccine-preventable threats and GBS as the leading problem in the first weeks of life. ^[2][5]

Five bacteria cause most childhood bacterial meningitis: GBS, E. coli, L. monocytogenes, S. pneumoniae and N. meningitidis, with H. influenzae type b still relevant where vaccination is incomplete. ^[2] The likely organism changes systematically with age, which is the central fact for choosing empiric antibiotics.

Risk factors span the whole age range and are worth asking about in every child:

• missed or incomplete immunisations (meningococcal, Hib or pneumococcal) ^[1]
• reduced or absent splenic function, or congenital or acquired complement deficiency ^[1]
• a household or nursery contact with meningococcal or Hib disease, or residence in or travel to the meningitis belt ^[1]
• a previous episode of bacterial meningitis, a CSF leak, or a cochlear implant ^[1]
• in neonates: prematurity, maternal rectovaginal colonisation with GBS, prolonged rupture of membranes, chorioamnionitis and invasive devices such as shunts or reservoirs. ^[2]

Viral meningitis (most often enteroviruses), tuberculous meningitis, fungal meningitis (especially cryptococcal in immunocompromised children), non-infectious inflammation and sepsis of another source all enter the differential, but the most useful comparison for the acute bedside decision is between bacterial and viral disease, summarised in the CSF table.

The story is the same across ages, with age-specific variations at the beginning and the end.

Most bacteria reach the meninges through the bloodstream. Meningococci colonise the nasopharynx; pneumococci and Hib live in the upper airway and enter blood after a viral upper respiratory infection. Neonatal organisms come instead from the mother's genital tract, swallowed or aspirated during birth, and cross into blood once the gut or lungs breach. ^[2] Direct spread across a breached dura (head injury, neurosurgery, a CSF leak) and spread from a parameningeal focus (otitis, sinusitis, mastoiditis) are the other routes at any age.

Once bacteria are in the subarachnoid space they multiply and release cell-wall components that trigger an intense inflammatory cascade: cytokines (interleukin-1, tumour necrosis factor-alpha, interleukin-6), a rush of white cells, breakdown of the blood-brain barrier, cerebral oedema and raised intracranial pressure. Vasculitis and thrombosis of cerebral vessels complicate severe disease.

This mechanism explains every common feature:

• Fever and headache come from inflammation of pain-sensitive meninges and raised pressure.
• Neck stiffness is reflex spasm of neck muscles against inflamed, pain-sensitive meninges.
• Photophobia comes from meningeal inflammation around the optic pathways.
• Altered mental state follows oedema, ischaemia and toxins.
• Seizures are common early, especially in children, and are usually generalised and easily controlled; focal or late seizures suggest complications.
• Hearing loss, particularly after pneumococcal and Hib disease, follows inflammatory damage to the cochlea or the auditory nerve.
• Hydrocephalus develops when thick basal exudate obstructs CSF drainage, especially in tuberculous disease.

Neonates have the same process but very little of it shows. Their open fontanelle buffers pressure, their immature immunity produces a muted inflammatory response, and they cannot report headache or neck stiffness. Instead the warning signs are systemic: temperature instability, apnoea, tachypnoea, grunting, irritability, a weak high-pitched cry, poor feeding, vomiting and lethargy. A bulging fontanelle is a late and serious sign of raised intracranial pressure. ^[1][2]

The presentation is non-specific and is a common trap. Fever may be absent; some babies are hypothermic. Look for irritability, a weak high-pitched or continuous cry, lethargy, reduced feeding, vomiting, temperature instability, apnoea, grunting or tachypnoea. A bulging fontanelle, focal neurological signs or seizures may occur but are not reliable. ^[1] In one UK prospective study of infants under 90 days, mortality was driven by prematurity, coma on admission and pneumococcal infection. ^[2]

The older the child, the more the picture resembles adult meningitis, modified by age. Headache, fever, neck stiffness, photophobia, vomiting, altered behaviour or consciousness, and seizures are the components. Neck stiffness is harder to identify in infants and in children with communication or cognitive difficulties. ^[1] Seizures in bacterial meningitis are common, usually generalised, and occur early; fever may make a young child sleepy and irritable, which easily masks the diagnosis.

The classic triad of fever, neck stiffness and altered mental state is often absent, and its absence never excludes the disease. ^[1] A more reliable bedside trigger is the red-flag combination of fever, headache, neck stiffness and altered consciousness. ^[1]

Meningococcal disease is the form most likely to kill a child within hours, and it can occur with or without meningitis. The organism seeds the bloodstream, producing septic shock, disseminated intravascular coagulation and a characteristic rash.

Suspect meningococcal disease strongly in any child with a haemorrhagic, non-blanching rash with lesions larger than 2 mm (purpura), a rapidly progressing or spreading non-blanching petechial or purpuric rash, or any feature of bacterial meningitis together with a non-blanching petechial or purpuric rash. ^[1] Also remember that some children with meningococcal disease never develop a rash; its absence does not exclude the diagnosis. ^[1] When looking for the rash, check the whole body including nappy areas, and look for petechiae in the conjunctivae; the rash can be hard to see on brown, black or tanned skin. ^[1] A blanching rash can become non-blanching as the illness evolves, so re-examine. ^[1]

Other clues to meningococcal septicaemia are cold hands and feet, capillary refill of 3 seconds or longer, tachycardia or bradycardia, hypotension, vomiting, diarrhoea, leg pain, and early progression to shock. ^[1]

A thorough but rapid examination includes:

• Temperature, heart rate, blood pressure, capillary refill, and oxygen saturation.
• Fontanelle tension and head circumference in infants.
• Conscious level (for example a Glasgow Coma Scale score or AVPU), and a check for focal neurological signs or cranial nerve palsies.
• Meningism: neck stiffness, and a cautious check of Kernig's and Brudzinski's signs (these are specific but not sensitive, so a negative test means very little). ^[1]
• Skin and conjunctivae for petechiae and purpura.
• A search for a focus: otitis, sinusitis, mastoiditis, a CSF leak, or a cochlear implant site.

Fundoscopy for papilloedema should be attempted but never used to delay treatment.

The differential is wide and includes migraine, viral upper respiratory infection with fever and headache, influenza, sepsis from another focus, subarachnoid haemorrhage, stroke, intracranial mass, encephalitis, intracranial abscess and drug-induced aseptic meningitis. ^[1] Bacterial meningitis can masquerade as a viral illness in its first hours.

A useful bedside screen for children is the meningococcal rash combined with any systemic illness, and a useful investigation discriminator is the CSF, because bacterial and viral meningitis differ sharply.

In suspected bacterial meningitis, take blood cultures (two sets) before antibiotics if this does not delay them, together with a full blood count, C-reactive protein or procalcitonin, glucose and a throat swab for meningococcal culture. ^[1] Whole-blood diagnostic PCR for meningococcus and pneumococcus is valuable when antibiotics have already been given.

Test for HIV in adults with bacterial meningitis, and consider it in babies, children and young people with signs of immunodeficiency or relevant risk factors. ^[1] Children with pneumococcal meningitis should be referred to a paediatric immunology and infectious disease specialist to assess for primary immunodeficiency. ^[1]

Lumbar puncture is the diagnostic test and should be performed as soon as it can be done safely. ^[1] The fluid should be sent for opening pressure, appearance, red and white cell counts with differential, protein, glucose (with a paired blood glucose taken immediately before the procedure), lactate, Gram stain, culture, and PCR for the relevant pathogens. ^[1]

Lumbar puncture is contraindicated and imaging or stabilisation comes first when there is:

• an unprotected airway, respiratory compromise, shock, uncontrolled seizures or a bleeding risk;
• an evolving space-occupying lesion;
• new focal neurological features including posturing, abnormal pupillary reactions, or a Glasgow Coma Scale score of 9 or less, or a progressive, sustained or rapid fall in consciousness. ^[1]

Do not perform a routine cranial CT before lumbar puncture. Imaging is used only for those specific raised-pressure or focal signs; the CT often shows generalised oedema even when it is reported as normal, and performing it must not delay antibiotics. ^[1][2] In neonates and infants with an open fontanelle, cranial ultrasound can be a useful preliminary study. ^[2]

Treat and stabilise the child first when lumbar puncture must wait, but give antibiotics; if the puncture happens after antibiotics, it should still be performed as soon as safely possible, because the organism may still be identifiable by PCR. ^[1]

Bacterial and viral meningitis produce different CSF pictures, and neonates have different normal thresholds from older children. In a term neonate the normal CSF may contain a mean of about 5 white cells per microlitre, protein around 70 mg/dL and glucose around 46 mg/dL, so mildly abnormal values are harder to interpret than in older children. ^[2] Normal thresholds for white cell count and protein are higher in babies under 3 months. ^[1]

Two cautions prevent harm. First, bacterial meningitis can present with a low or almost normal CSF cell count early in illness or after antibiotics, so it is not excluded by counts alone. ^[1] A normalish cell count therefore does not exclude bacterial disease. Second, antibiotic pretreatment sterilises CSF quickly (meningococcus within about 2 hours, pneumococcus by 4 hours), so cultures and Gram stain lose sensitivity; PCR on CSF and blood preserves the diagnosis. ^[2]

Gram stain is rapid and more often positive in pneumococcal (about 90%) and meningococcal (about 80%) disease than in H. influenzae (about 50%) or Listeria (about 30%), and its sensitivity is about 60% in neonates and 50-63% in children. ^[2] CSF lactate above about 54 mg/dL has reported sensitivity 90% and specificity 100% for bacterial meningitis in untreated cases. ^[2]

Bacterial meningitis is a clinical and microbiological diagnosis rather than a score. A useful working definition for acute community-acquired disease is CSF pleocytosis with neutrophil predominance plus at least one of raised protein or a low CSF:serum glucose ratio, supported by a positive Gram stain, culture or PCR. ^[1] When the child is critically ill, treat first and confirm later. Severity is tracked clinically (conscious level, seizures, focal defects, need for ventilation) and on imaging (hydrocephalus, cerebral oedema, infarction). There is no routine staging score.

1. Isolate with droplet precautions until meningococcal disease is excluded. ^[1]
2. Establish airway, breathing and circulation; give oxygen and fluids to reach adequate blood pressure and cerebral perfusion.
3. Take two pairs of blood cultures, throat swab and routine labs, and a paired blood glucose.
4. Perform lumbar puncture now if there is no contraindication, ideally before antibiotics; never delay antibiotics for imaging.
5. Give empiric intravenous antibiotics within 1 hour of arrival.
6. Give dexamethasone with or before the first antibiotic dose in children over 3 months.
7. Arrange paediatric intensive care early: about a third of infants and children develop markedly reduced cerebral blood flow from oedema and raised pressure. ^[2]

The rules are age-based, because the organisms are age-based.

Neonates (including late-onset disease) are covered for GBS, E. coli and Listeria with ampicillin plus an aminoglycoside or a third-generation cephalosporin. AAP, IDSA and ESCMID recommend ampicillin plus cefotaxime or gentamicin; cefotaxime is often preferred because of increasing ampicillin resistance in E. coli and better central nervous system penetration than gentamicin. ^[2] Where no resistant pneumococci are locally expected, some low-resource protocols use ceftriaxone alone, with ampicillin added whenever Listeria is plausible.

Infants and children beyond the neonatal period are covered with a third-generation cephalosporin (ceftriaxone or cefotaxime) plus vancomycin wherever the local incidence of ceftriaxone-resistant pneumococcus exceeds about 1%. ^[2] NICE advises using the highest ceftriaxone dose in the formulary and, when ceftriaxone is contraindicated (for example in preterm babies under 41 weeks corrected gestational age), considering cefotaxime. ^[1] Give intravenous amoxicillin in addition for any child with risk factors for Listeria (older or immunocompromised adults, or any immunocompromised child, depending on the guideline). ^[1]

Outside hospital, if transfer is likely to be delayed, give intramuscular or intravenous ceftriaxone or benzylpenicillin for a child with strongly suspected bacterial meningitis, and for meningococcal disease give it as soon as possible, provided it does not delay transfer. ^[1]

Once the organism is identified, switch to directed therapy. Representative durations in uncomplicated disease are: ^[2]

• GBS: 14 days
• L. monocytogenes: 14 to 21 days, with ampicillin or penicillin; add co-trimoxazole on specialist advice
• E. coli and other Gram-negative bacilli: 21 days, until CSF is sterilised
• S. pneumoniae: 10 to 14 days (longer if complicated)
• N. meningitidis: 5 to 7 days ^[2]
• H. influenzae: 7 to 10 days

H. influenzae and pneumococcal meningitis in children are treated with ceftriaxone or cefotaxime, with penicillin-based therapy only when the isolate is fully susceptible. Uncomplicated meningococcal disease is treated with ceftriaxone, typically 80-100 mg/kg once daily for 4 days in children, while penicillin requires about 5 days. ^[1][2] Listeria requires at least 21 days of ampicillin. ^[1]

Repeat lumbar puncture is not routinely needed if the child responds, except when the pneumococcus is cephalosporin-nonsusceptible (repeat at 48-72 hours), in neonatal Gram-negative disease, or when symptoms persist or recur. ^[2]

Dexamethasone helps children but not (as far as current evidence shows) neonates.

• Children over 3 months with strongly suspected or confirmed bacterial meningitis receive 0.15 mg/kg intravenously every 6 hours for 4 days (0.6 mg/kg daily), begun before or with the first antibiotic dose; the BNFC maximum is 10 mg per dose. If the dose is missed by less than 12 hours, give it as soon as possible; do not delay antibiotics to wait for it. ^{[1][3] [2]}
• Neonates: routine dexamethasone is not recommended or used in clinical practice; its role has not been well studied, and better evidence is lacking. ^[2]
• Meningococcal disease: high-dose dexamethasone may increase mortality in children and is not recommended routinely. ^[1]

Adjunctive dexamethasone reduces hearing loss and short-term neurological sequelae in high-income settings, particularly in H. influenzae type b meningitis, and the evidence for pneumococcal disease supports a benefit when it is given early. ^[2] Continue it only when S. pneumoniae or H. influenzae type b is confirmed; stop it for every other organism. ^[1] Some guidelines (for example AAP/IDSA) suggest 2 days for H. influenzae rather than 4, so local protocol should govern duration. ^[2]

Two safety points:

• Start dexamethasone before or with antibiotics; later dosing is much less effective, and delayed administration beyond about 12 hours is generally not given. ^[1]
• Dexamethasone may reduce vancomycin penetration into CSF, so where resistant pneumococci are being covered and dexamethasone is given, replace vancomycin with rifampicin.

Care in a setting with neurological and intensive care expertise is essential. Manage raised intracranial pressure (elevate the head, then mannitol, intubation and hyperventilation if late signs appear), hydrocephalus (ventricular drainage if indicated), seizures, hyponatraemia and circulatory failure. ^[2] Most seizures are focal or generalised, early and controllable; focal, difficult-to-control or late seizures raise the possibility of an abscess, empyema or vascular infarction. Look for a source (otitis, sinusitis, mastoiditis, endocarditis) and treat it promptly; ENT infection often needs surgery within 24 hours. ^[1] Fluid resuscitation is used to reach adequate blood pressure; in a recent Cochrane review maintenance fluids were not worse than restricted fluids. ^[2]

Complications of bacterial meningitis in children include hearing loss (most common), hydrocephalus, seizures, cerebral infarction from vasculitis, brain or subdural abscess, venous sinus thrombosis, cerebral oedema with herniation and death. Hearing loss is the most common sequela in children. ^[2] Many survivors leave hospital with some disability. ^[2]

• Hearing loss is particularly frequent after pneumococcal and H. influenzae disease, which is why every child who has had meningitis should have audiological follow-up, even if the hearing seemed normal before discharge. ^[2]
• Hydrocephalus is more common after tuberculous and, in neonates, Gram-negative meningitis, and may need a ventricular drain or shunt.
• Seizures can be early and benign or late and a warning of complications.
• Waterhouse-Friderichsen syndrome (adrenal haemorrhage, purpura, shock) is the catastrophic form of meningococcal disease.
• Neurodevelopmental sequelae (cognitive and behavioural problems, motor disorder, cerebral palsy) are a major long-term concern after neonatal disease.
• Relapse can occur after inadequate duration or undrained foci.

In one UK prospective study of infants under 90 days, 23% of survivors had serious central nervous system complications, including seizures, motor disorder, hydrocephalus with or without a shunt, hearing loss or extradural collection requiring neurosurgery. ^[2]

Prognosis depends on age, organism, speed of treatment and setting. Neonatal mortality ranges from about 10% in developed countries to 58% in developing countries; in children older than the neonatal period it ranges from under 5% to 15%. ^[2] S. pneumoniae carries the worst outcome among common pathogens, with about 10% mortality and 20 to 30% morbidity. ^[2] Other predictors of death and long-term neurological sequelae include a Glasgow Coma Scale score under 8 on admission, cranial nerve palsy, seizures, a low CSF white cell count, a positive Gram stain or culture, and abnormal imaging. ^[2] Treatment is started within 1 hour of arrival; delays of more than about 3 hours in pneumococcal disease and more than about 6 hours in bacterial meningitis generally are associated with worse outcomes. ^[1][2]

Vaccination is the single most effective way to prevent the common meningeal pathogens of childhood. Timely childhood immunisation against Hib, pneumococcus and meningococcus, with boosters in adolescence, has driven down the incidence of meningitis and provides herd protection for unvaccinated infants. ^[2][5] In the United States, CDC recommends MenACWY vaccination for all adolescents and for children from 2 months to 10 years who are at increased risk, together with serogroup B and pentavalent meningococcal vaccines where indicated. ^[5] BCG vaccination protects infants against disseminated tuberculosis, including TB meningitis. ^[1]

Maternal intrapartum antibiotic prophylaxis has cut early-onset GBS disease dramatically but does not protect against late-onset disease, which is why GBS vaccine development is an active priority. ^[2]

Close contacts of a confirmed meningococcal case, and of Hib disease where it is used locally, should receive prophylactic antibiotics to eradicate carriage and prevent secondary cases. Secondary cases occur soon after exposure, so prophylaxis should be given promptly. ^[4]

Typical regimens are: ^[4]

• Ciprofloxacin: 20 mg/kg orally as a single dose (maximum 500 mg) in children 1 month and older; an adult single dose is 500 mg. ^[4]
• Ceftriaxone: 125 mg intramuscularly as a single dose for children under 15 years and 250 mg for adults, which is the preferred option in pregnancy. ^[4]
• Rifampicin: 10 mg/kg orally every 12 hours for 2 days for children 1 month and older (maximum 600 mg) and for adults; for infants under 1 month use 5 mg/kg every 12 hours. Rifampicin is avoided in pregnancy. ^[4]

These regimens are about 90 to 95% effective at eradicating nasopharyngeal carriage. ^[4] Close contacts are household members, childcare contacts and anyone with direct exposure to the patient's oral secretions. The index patient should also receive eradication therapy before discharge if the treatment antibiotic (for example penicillin) does not reliably clear carriage. ^[4]

Children with cochlear implants are 30 times more likely than age-matched peers to develop pneumococcal meningitis, so they should be fully immunised against pneumococcus. ^[2]

As above: cover GBS, E. coli and Listeria; do not give routine dexamethasone; consider repeat lumbar puncture and longer courses for Gram-negative disease; look for a sinus tract and consider urinary tract infection or congenital anomalies with recurrence. ^[1][2]

Recurrent or unusual-organism meningitis should prompt investigation: immunoglobulin levels, complement studies, HIV testing, and imaging for cranial defects and CSF leaks. Pneumococcal meningitis in a child always warrants referral to paediatric immunology. ^[1]

Look for complement deficiency or asplenia, which can produce recurrent disease. ^[1]

In settings where imaging, CSF biochemistry and PCR are limited:

• Treat empirically on clinical suspicion within 1 hour of arrival and start droplet precautions. ^[1]
• Lumbar puncture can proceed without a prior CT if there are no focal deficits, recent seizures, coma, papilloedema or raised-pressure signs. ^[1]
• Basic CSF examination (appearance, crude cell count, protein, and bedside glucose comparison with a glucometer) separates bacterial from viral disease well enough to guide treatment. ^[1]
• Where cephalosporins are unavailable, benzylpenicillin plus chloramphenicol (with ampicillin if Listeria is plausible) is used; ceftriaxone is continued if resistant pneumococci are not locally expected.
• Adjunctive dexamethasone is probably most useful where early care is available; benefit is smaller when presentation is delayed, and in some low-resource trials glycerol did not reduce mortality. ^[2]
• Vaccination (Hib, pneumococcal conjugate, meningococcal A conjugate in the belt, BCG) is the single most cost-effective intervention and should be prioritised. ^[2]

• Meningitis is inflammation of the meninges; bacterial forms are rapidly lethal emergencies in children.
• Presentation is age-dependent. Neonates are quiet: poor feeding, irritability, lethargy, temperature instability, apnoea, grunting and a bulging fontanelle, with fever often absent. ^[1][2]
• The organism is predicted by age: GBS, E. coli and Listeria in neonates; pneumococcus and meningococcus (and H. influenzae type b where unvaccinated) in older children. ^[2]
• The classic triad is often absent; its absence never excludes meningitis. ^[1]
• N. meningitidis commonly presents with septicaemia and a non-blanching petechial or purpuric rash with lesions larger than 2 mm (purpura); a rash is not always present. ^[1]
• Lumbar puncture is the diagnostic test and is safe without routine CT unless focal or raised-pressure signs are present. ^[1][2]
• CSF in bacterial disease: cloudy, over 1000 neutrophils per microlitre, protein above 100-150 mg/dL (threshold varies by source), glucose under half (under 0.4 of) the serum level; neonates have higher normal thresholds. ^[2]
• Bacterial meningitis can occur despite a low or near-normal CSF cell count; interpret CSF with age-appropriate thresholds. ^[1]
• Antibiotics must start within 1 hour: ampicillin plus cefotaxime or gentamicin in neonates; a third-generation cephalosporin plus vancomycin (where resistant pneumococci occur) in older children, with amoxicillin added for Listeria risk. ^[1][2]
• Dexamethasone (0.15 mg/kg intravenously every 6 hours for 4 days) is given before or with antibiotics to children over 3 months but is not recommended in neonates; continue it only for pneumococcal or Hib meningitis. ^[1][3]
• Meningococcal disease is not routinely treated with high-dose dexamethasone. ^[1]
• Complications include hearing loss (most common), hydrocephalus, seizures, infarction and developmental delay; arrange hearing follow-up for every case. ^[2]
• Prevention: maternal GBS prophylaxis, timely Hib/pneumococcal/meningococcal vaccination, and chemoprophylaxis (ciprofloxacin, ceftriaxone or rifampicin) for close contacts of meningococcal disease. ^[4][5]
• Cochlear implants carry a 30-fold increased risk of pneumococcal meningitis; vaccinate these children. ^[2]

The Infectious Disease meningitis topic (bacterial and viral meningitis, CSF criteria, CT rules, adult dosing); neonatal sepsis and infection (NICE NG195); encephalitis; tuberculous meningitis; meningococcal septicaemia; hydrocephalus; hearing loss and vestibular disorders; vaccination schedules and immunisation; fever in children under 5 years; sepsis in children.