Bacterial Meningitis

Bacterial meningitis is an infection of the leptomeninges — the arachnoid and pia mater surrounding the brain and spinal cord — that most often begins when bacteria colonizing the nasopharynx (chiefly Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae) invade the bloodstream and cross the blood-brain barrier.^[1] Once bacteria reach the subarachnoid space, host defenses there are limited, and the resulting cytokine-driven inflammatory cascade — not the bacteria themselves — causes most of the neuronal injury, hearing loss, and long-term neurologic damage seen in survivors.^[1] This is one of the few true pharmacotherapy emergencies in medicine: every hour that empiric antibiotics are delayed measurably worsens the odds of death or permanent disability, which is why treatment must never wait for a lumbar puncture, imaging, or a confirmed diagnosis.^[2]

Classic presentation (older children and adults)

Most adults with bacterial meningitis have at least 2 of the 4 classic features — headache, fever, neck stiffness (nuchal rigidity), and altered mental status — but the complete triad of fever, neck stiffness, and altered consciousness is present in only a minority, so its absence never excludes the diagnosis.^[3]

Other common features include photophobia, vomiting, back pain, and a general sense of being acutely, systemically unwell. Neurologic symptoms — loss of balance, disorientation, confusion, and focal neurologic deficits — can occur at any age. A patient of any age may present in septic shock (decreased level of consciousness, hypotension, poor peripheral perfusion) rather than with the classic fever-and-headache picture, especially with fulminant meningococcemia.^[1]

Meningeal signs

Nuchal rigidity — resistance to passive neck flexion — is the single most useful bedside meningeal sign in older children and adults, though it is frequently absent in neonates and infants with open fontanelles.

Kernig's sign is tested with the patient supine and the hip flexed to 90°: the sign is positive if the examiner cannot passively extend the knee beyond roughly 135° because of hamstring spasm and resistance, or if attempted extension reproduces pain.

Brudzinski's sign is tested with the patient supine: the sign is positive if passive flexion of the neck causes involuntary flexion of the hips and knees.

Both signs have limited sensitivity and can be absent even in confirmed bacterial meningitis — a negative Kernig's or Brudzinski's sign does not rule out the diagnosis and should never be used alone to decide against a lumbar puncture.^[3]

Petechiae or purpura — non-blanching, irregular red-purple spots — strongly suggest meningococcal disease but can also occur with S. pneumoniae. Their presence in a patient with possible meningitis should be treated as a marker of septicemia and escalated accordingly.

• Extremes of age — infants under 12 months and adults over 70 years.
• Recent head or spinal trauma or surgery, cerebrospinal fluid (CSF) leak, or cochlear implant.
• Current or recent immunosuppressive therapy, including long-term prednisone (2 mg/kg/day or more for over 14 days), chemotherapy, and therapeutic monoclonal antibodies — particularly eculizumab and other terminal-complement inhibitors.
• Multiple myeloma, leukemia, or other malignancy.
• Functional or anatomic asplenia (e.g., sickle cell disease, splenectomy) and other hyposplenic states.
• Ventriculoperitoneal shunt, penetrating head trauma, or basilar skull fracture with CSF leak.
• Incomplete or absent immunization against Haemophilus influenzae type b, Streptococcus pneumoniae, or Neisseria meningitidis.
• Close contact (household, daycare, dormitory, or military-unit) with a case of invasive meningococcal or H. influenzae type b disease.
• A neonate born to a parent colonized with group B streptococcus who did not receive intrapartum antibiotic prophylaxis.
• Chronic alcohol use disorder — an independent risk factor specifically for Listeria monocytogenes meningitis.
• Crowded living conditions or travel to a region with a high burden of meningococcal disease (e.g., the sub-Saharan African meningitis belt, or mass gatherings such as the Hajj).

History

Ask about onset and duration of symptoms (most patients present within 24 hours of symptom onset), recent respiratory illness, recent head/spinal trauma or neurosurgery, immunosuppression, asplenia, alcohol use, recent antimicrobial use (which can blunt or mask typical signs and CSF findings), sick contacts, and immunization history.

Examination

Vital signs frequently show tachycardia and tachypnea; blood pressure may be normal or low, especially with septic shock. Look specifically for nuchal rigidity, Kernig's and Brudzinski's signs (see Recognize the Condition), level of consciousness, focal neurologic deficits, cranial nerve palsies, papilledema, and a petechial/purpuric rash. In patients already on antimicrobials, signs may be attenuated or atypical.

Clinical prediction tools

Several clinical prediction models exist to help distinguish bacterial from viral meningitis, but guidance is mixed on their use — some sources support them as an adjunct, others recommend against routinely relying on them. Clinical judgment, not a scoring tool, should drive the decision to start empiric antibiotics; no validated score is precise enough to safely withhold treatment from a patient who otherwise looks unwell.^[2]

Lumbar puncture and cerebrospinal fluid analysis

Examination of the CSF is essential to the diagnosis and should be obtained whenever meningitis is clinically suspected, unless a specific contraindication is present.

Lumbar puncture is contraindicated in the presence of: raised intracranial pressure (suggested by focal neurologic signs, new-onset seizure, altered or deteriorating consciousness, or papilledema), active seizures, shock, coagulopathy, or infection at the proposed puncture site. When raised intracranial pressure is strongly suspected clinically, obtain a CT scan before the LP — but draw blood cultures and give antibiotics (plus dexamethasone, if indicated) before sending the patient for imaging, not after.^[4]

Neuroimaging (CT or MRI) is also indicated, though not routinely required in every patient, for: focal neurologic signs, clinical evidence of brain herniation, a decreased or fluctuating level of consciousness, clinical deterioration, or persistent fever. Repeat imaging is indicated after starting therapy if any of these develop, or if the patient fails to improve as expected.

Molecular/PCR testing on CSF is increasingly available and particularly useful when antibiotics were given before the LP, or when Gram stain and culture are negative despite significant CSF pleocytosis — involve an infectious diseases specialist to guide further testing in this situation.

Blood investigations

Draw blood cultures (weight-based volumes) before giving antimicrobials whenever possible, but never delay antibiotics to obtain them — draw them immediately before or alongside the first antibiotic dose. Also send a CBC and differential, a blood glucose level near the time of the LP (for comparison with CSF glucose), and total blood protein.

Patients over 60 years of age, and those with underlying neurologic disease or immunosuppression, are at higher risk of Listeria monocytogenes; neuroimaging in this group may show cerebritis or other findings that support that diagnosis.

• Start empiric antibiotic therapy that penetrates the central nervous system as soon as bacterial meningitis is suspected clinically — do not wait for confirmatory testing.
• Modify therapy once a pathogen and its susceptibilities are identified.
• Eradicate the causative bacteria from the CSF.
• Decrease mortality and the risk of permanent neurologic disability.
• Identify, prevent, and manage acute complications — raised intracranial pressure, seizures, septic shock, hydrocephalus — before they cause permanent damage.
• Provide postexposure prophylaxis to close contacts, and eradicate nasopharyngeal carriage in the index patient, when the causative organism is N. meningitidis or H. influenzae type b.

• Manage as a medical emergency in an acute care setting with immediate access to laboratory and imaging support — do not manage suspected bacterial meningitis in a primary-care or community setting.
• Continuous monitoring of airway, breathing, circulation, and neurologic status (level of consciousness, pupils, focal signs) — decompensation can be rapid, especially in meningococcemia.
• Seizure precautions, and prompt treatment of any seizure that occurs.
• Careful fluid management — avoid both under-resuscitation in septic shock and over-aggressive free-water administration, since the syndrome of inappropriate antidiuretic hormone secretion is a recognized complication that can worsen cerebral edema.
• Elevate the head of the bed and involve neurosurgery/critical care early if there are signs of raised intracranial pressure.
• Droplet precautions for the first 24 hours of effective antibiotic therapy in any patient with suspected or confirmed N. meningitidis meningitis.
• Notify public health promptly — invasive meningococcal disease and H. influenzae type b disease are reportable, and contact tracing needs to happen quickly given the short postexposure-prophylaxis window.
• Involve infectious diseases, neurology, and (when relevant) neurosurgery early, particularly for resistant organisms, complications, or lack of improvement.
• Arrange an audiology assessment before or shortly after discharge, given the real risk of sensorineural hearing loss.

Pregnancy

Manage suspected bacterial meningitis in pregnancy with the same urgency as in a non-pregnant patient, with combined obstetric/infectious diseases involvement. Ceftriaxone or cefotaxime plus ampicillin form a safe empiric backbone; vancomycin and gentamicin are used when indicated with the same monitoring as any pregnant patient on these agents. For postexposure prophylaxis, ceftriaxone is the drug of choice in pregnancy — rifampin and ciprofloxacin are both avoided. Dexamethasone use in pregnancy is individualized, weighing maternal benefit against the more limited safety data in this population. Intrapartum antibiotic prophylaxis (typically penicillin) for a birthing parent colonized with group B streptococcus meaningfully reduces the risk of early-onset neonatal GBS disease, including neonatal meningitis, and should be confirmed as part of the newborn's risk assessment.^[5]

Breastfeeding

Ceftriaxone, cefotaxime, vancomycin, ampicillin, gentamicin, and dexamethasone are all considered compatible with breastfeeding at standard treatment doses — confirm specifics against each drug's own Drug Database entry. Rifampin and ciprofloxacin, used for prophylaxis rather than pregnancy, are generally compatible with breastfeeding even though both are avoided in pregnancy itself.

Neonates and children

Cefotaxime, not ceftriaxone, is preferred in neonates under 6 weeks given the theoretical risk of bilirubin displacement and kernicterus. All antibiotic doses in neonates and infants should follow current age/weight-banded neonatal dosing protocols, ideally with neonatology or pediatric infectious diseases involvement. Arrange developmental and audiology follow-up after recovery, since neurologic and hearing sequelae are more common — and more consequential for long-term development — in this age group.

Renal impairment

Vancomycin and the aminoglycosides (gentamicin, tobramycin) require dose adjustment and therapeutic drug monitoring in renal impairment; sulfamethoxazole/trimethoprim also requires adjustment. Confirm dosing against each drug's own product-specific renal-adjustment guidance and monitor renal function closely throughout therapy.

Immunocompromised, asplenic, and eculizumab-treated patients

Add ampicillin for Listeria coverage in this group. Prioritize catch-up meningococcal, pneumococcal, and Hib vaccination once the acute illness has resolved. Patients starting eculizumab or another terminal-complement inhibitor should receive both the quadrivalent meningococcal ACYW conjugate vaccine and a meningococcal group B vaccine series at least 2 weeks before the first eculizumab dose whenever possible, since these patients carry a markedly elevated risk of meningococcal disease even when fully vaccinated.^[9] In this high-risk group, give the pneumococcal conjugate vaccine first, followed by the 23-valent pneumococcal polysaccharide vaccine at least 8 weeks later if it has not already been given.^[11] Confirm Hib immunization status as well — the Hib conjugate series does not fully eliminate risk in an unvaccinated or incompletely vaccinated high-risk adult, and catch-up dosing may be appropriate on specialist advice.^[12]

Older adults (over 60)

Add ampicillin for Listeria coverage. Older adults carry a higher overall risk of death and disability from bacterial meningitis and need closer monitoring for medication-related adverse effects (renal function, drug interactions, corticosteroid effects) throughout therapy.

Perform neurologic checks (level of consciousness, pupils, focal signs) and vital signs frequently in the first 24–48 hours, then per unit protocol as the patient stabilizes. Reassess clinically at 48–72 hours — failure to improve, or new deterioration, needs repeat neuroimaging and consideration of repeat lumbar puncture.

Repeat LP is specifically indicated for: failure to improve clinically, cephalosporin-resistant pneumococcal meningitis, or meningitis caused by enteric Gram-negative bacilli or other unusual pathogens.

Monitor vancomycin trough concentrations (target 15–20 mg/L) and aminoglycoside levels closely, along with renal function, throughout therapy. Discontinue vancomycin once the isolate is confirmed penicillin- or ceftriaxone/cefotaxime-susceptible, or at 36–48 hours if cultures remain negative.

Arrange a formal audiology assessment before or shortly after discharge — sensorineural hearing loss is one of the most common permanent sequelae, particularly with S. pneumoniae and H. influenzae type b.

Before discharge, confirm the index patient has received chemoprophylaxis if ceftriaxone or cefotaxime was not used as empiric therapy, and confirm public health has been notified for contact tracing and close-contact prophylaxis for N. meningitidis and H. influenzae type b cases.

Arrange longer-term follow-up for neurologic and developmental sequelae — ataxia, behavioural changes, epilepsy, hydrocephalus, intellectual deficit, sensorineural hearing loss, and visual problems including cortical blindness can all emerge or persist after the acute illness, particularly in children, and warrant referral to neurology, audiology, and/or developmental follow-up as appropriate.

Once recovered, confirm the patient is up to date on meningococcal, pneumococcal, and (if age-appropriate) H. influenzae type b vaccination, since a first episode does not protect against future disease from other serotypes or serogroups.

1. Reassess the whole clinical picture if the patient is not improving as expected by 48–72 hours — repeat neuroimaging to look for a complication (subdural empyema, hydrocephalus, venous sinus thrombosis, cerebral infarction, abscess).
2. Repeat the lumbar puncture if there is failure to improve clinically, if the isolate is cephalosporin-resistant S. pneumoniae, or if the organism is an enteric Gram-negative bacillus or other unusual pathogen.
3. Confirm the antibiotic regimen, dose, and timing were actually correct for the patient's age/risk group, and that vancomycin was dosed to a therapeutic trough — inadequate CNS penetration or underdosing is a common, correctable cause of apparent treatment failure.
4. For confirmed S. pneumoniae with a penicillin MIC of 0.12 mg/L or higher and a cephalosporin MIC of 1.0 mg/L or higher, add vancomycin (with high-dose cefotaxime/ceftriaxone) with or without rifampin, and obtain an infectious diseases consultation — cephalosporins alone, even at high doses, may be inadequate at this level of resistance.
5. If resistant pneumococci are isolated in a patient who has already received dexamethasone, strongly consider adding rifampin to the regimen, since dexamethasone may theoretically delay CSF sterilization when vancomycin is also required.
6. If Listeria is confirmed and dexamethasone was started, discontinue it — dexamethasone has been associated with worse outcomes in listerial meningitis.
7. For confirmed resistance to ceftriaxone, cefotaxime, and meropenem, or true anaphylaxis to available agents, moxifloxacin may be an option if the isolate is susceptible — use only with infectious diseases input, since fluoroquinolones are not standard meningitis therapy and resistance can develop quickly.
8. Involve neurosurgery for any drainable complication (empyema, abscess, or hydrocephalus needing CSF diversion).

• Waiting for a CT scan, lumbar puncture, or confirmed diagnosis before giving antibiotics — give empiric antibiotics within 1 hour of suspicion regardless of what workup has or has not happened yet.
• Withholding antibiotics because the Gram stain is negative — a negative Gram stain does not rule out bacterial meningitis.
• Giving vancomycin before or at the same time as the cephalosporin, rather than giving the cephalosporin first and vancomycin about 2 hours later.
• Forgetting to add ampicillin for Listeria coverage in patients over 60, immunocompromised patients, pregnant patients, or those with alcohol use disorder.
• Using ceftriaxone in a neonate under 6 weeks of age — use cefotaxime instead, given the theoretical risk of bilirubin displacement and kernicterus.
• Continuing empiric vancomycin beyond 36–48 hours once cultures are negative or the isolate is confirmed penicillin/ceftriaxone-susceptible.
• Using penicillin G as empiric, rather than culture-directed, therapy — current resistance rates no longer support this for empiric use.
• Starting dexamethasone after the antibiotic course is already well underway — it needs to be given before or with the first antibiotic dose to have benefit, not added later.
• Continuing dexamethasone in a patient with confirmed or strongly suspected Listeria meningitis.
• Using imipenem instead of meropenem when a carbapenem is needed — imipenem carries a higher seizure risk in this setting.
• Missing a non-blanching petechial or purpuric rash as a marker of meningococcemia requiring an even more urgent, aggressive response.
• Discharging an index patient with N. meningitidis or H. influenzae type b meningitis without chemoprophylaxis when ceftriaxone/cefotaxime was not used empirically, or failing to notify public health for contact tracing.

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

IV Antibacterial Therapy — Empiric and Culture-Directed

Adjunctive Corticosteroid Therapy

Give before or with the first dose of antibiotics; giving it later loses most of the benefit.

Duration of Therapy by Pathogen, Once Susceptibilities Are Known

Uncomplicated bacterial meningitis in a patient responding appropriately to therapy; complications or delayed clinical response may require a longer course.

Postexposure Chemoprophylaxis for Close Contacts

Start within 24 hours of identifying the index case.

Vaccines for Prevention of Bacterial Meningitis

Public funding and eligibility vary by province/territory — confirm with the local public health authority.