Overview
Treat suspected bacterial meningitis as a time-critical emergency, obtain microbiology without unsafe delay, add age- and risk-appropriate therapy, and coordinate complications, prophylaxis and follow-up.
Bacterial meningitis is inflammation of the meninges caused by invasive bacterial infection and carries high risks of death and neurological disability. Streptococcus pneumoniae and Neisseria meningitidis are leading adult causes; Listeria becomes important with age, pregnancy and impaired cellular immunity. Recent neurosurgery, cerebrospinal-fluid shunts, skull fracture and cochlear implants change the likely pathogens and empirical regimen, so these cases need immediate microbiology and neurosurgical input rather than an unmodified community-acquired pathway.
Clinical recognition is probabilistic. Fever or hypothermia, severe headache, neck stiffness, photophobia, vomiting, confusion, reduced consciousness and seizures may occur, while infants and older or immunosuppressed adults can present non-specifically. Meningococcal bloodstream infection may cause limb pain, cold peripheries, prolonged capillary refill and shock. Examine the entire skin surface in good light and reassess, but do not use a negative tumbler test or absence of rash as reassurance when physiology is concerning.
Aetiology
Community-acquired bacterial invasion
Streptococcus pneumoniae and Neisseria meningitidis are major adult causes, reaching the meninges after nasopharyngeal colonisation, bacteraemia or disruption of protective barriers.
Listeria and host susceptibility
Listeria becomes more relevant with older age, pregnancy or impaired cellular immunity, so host factors change the likely organism and empirical treatment pathway.
Healthcare and anatomical routes
Recent neurosurgery, cerebrospinal-fluid shunts, skull fracture, cochlear implants and contiguous ear or sinus infection introduce different organisms and require microbiology or neurosurgical input.
Pathophysiology
- 1Meningeal entry
Bacteria cross mucosal, bloodstream or anatomical barriers and enter cerebrospinal fluid, where limited local immune defences permit rapid multiplication.
- 2Inflammatory amplification
Bacterial components trigger intense neutrophilic cytokine responses, increasing blood–brain barrier permeability, disrupting cerebrospinal-fluid circulation and raising intracranial pressure.
- 3Pressure and vascular injury
Cerebral oedema, hydrocephalus and vasculitic or thrombotic injury reduce perfusion, while systemic inflammation can produce shock and multi-organ failure.
Clinical features and red flags
Fever, headache, neck stiffness and altered cognition together are strongly concerning, although each can be absent and clinical deterioration may be rapid.
Tachycardia, prolonged capillary refill, limb pain, cold hands or feet, hypotension and a spreading non-blanching rash indicate invasive disease and shock risk.
Reduced Glasgow Coma Scale, focal deficit, cranial-nerve palsy, repeated seizure or papilloedema suggests complication and influences airway, imaging and lumbar-puncture decisions.
Older age, pregnancy and immunocompromise increase Listeria probability and should trigger addition of active empirical cover under the current protocol.
A shunt, recent cranial procedure, penetrating injury or cerebrospinal-fluid leak changes likely organisms and requires a specialist device-associated regimen.
Infants, frail older people and immunosuppressed patients may lack fever or marked meningism, so altered behaviour, feeding, alertness or unexplained sepsis matters.
Investigations
- 01
Blood culturesFirst step - Why
- Identify the organism when cerebrospinal-fluid culture may later be sterilised.
- Interpretation and limitations
- Collect before antibiotics when this causes no meaningful delay; a positive result enables narrowing and public-health characterisation.
- 02
Blood count, CRP, renal, liver, clotting, glucose and lactate - Why
- Assess inflammation, organ dysfunction, procedure safety and antimicrobial dosing.
- Interpretation and limitations
- Normal inflammatory markers early do not exclude meningitis; paired blood glucose is required to interpret the cerebrospinal-fluid glucose ratio.
- 03
Lumbar puncture - Why
- Obtain cerebrospinal fluid for cells, protein, glucose, microscopy, culture and molecular testing.
- Interpretation and limitations
- Neutrophilic pleocytosis, raised protein and a low CSF-to-blood glucose ratio support bacterial infection, but pretreatment and host factors can blur the pattern.
- 04
Whole-blood and cerebrospinal-fluid PCR - Why
- Detect meningococcal, pneumococcal or other pathogen DNA after antibiotics reduce culture yield.
- Interpretation and limitations
- A positive validated assay can confirm aetiology and guide notification, while a negative result cannot by itself overturn compelling clinical and biochemical evidence.
Differential diagnosis
Viral meningitis
Preserved cognition and lymphocytic cerebrospinal fluid support viral infection, but early viral disease may be neutrophilic and partially treated bacterial meningitis may become lymphocytic.
Encephalitis
Prominent personality change, focal seizures, aphasia or temporal imaging abnormalities indicate brain parenchymal involvement and require an encephalitis pathway alongside antibacterial cover.
Aneurysmal thunderclap headache
Thunderclap onset, collapse and subarachnoid blood on urgent imaging favour haemorrhage; meningism and photophobia occur in both disorders.
Brain abscess
Focal deficit, seizure, mass effect or a ring-enhancing lesion support localised intracranial infection; lumbar puncture may be hazardous and has poor diagnostic yield.
Management
01First hourResuscitate and treat before certaintyFirst stepBacterial meningitis or meningococcal disease is clinically suspected.+
- 1Use an ABCDE approach, obtain intravenous access, treat hypoxia, shock, hypoglycaemia and seizures, and involve senior emergency, medical and critical-care clinicians early.
- 2Collect blood cultures and time-critical samples immediately if feasible, then give empirical intravenous antibiotics within the emergency standard without waiting for CT or lumbar puncture.
- 3Administer dexamethasone with or just before antibiotics where indicated, record exact times, isolate according to the infection-control policy and notify microbiology.
02Lumbar punctureObtain cerebrospinal fluid without creating harmThe patient is sufficiently stable and the result will refine diagnosis.+
Complications
Sepsis and circulatory shock
Invasive infection can cause profound vasodilatation, capillary leak, coagulopathy and multi-organ hypoperfusion, particularly with meningococcal bloodstream disease.
Raised pressure, infarction and seizure
Oedema, hydrocephalus and vascular inflammation can cause herniation, cranial neuropathy, cerebral infarction or status epilepticus despite antimicrobial treatment.
Hearing and neurocognitive disability
Cochlear, cranial-nerve and cortical injury may leave sensorineural hearing loss, memory difficulty, fatigue, epilepsy or focal neurological disability requiring planned follow-up.
Secondary transmission
Meningococcal infection creates a public-health risk for defined close contacts, making urgent notification, chemoprophylaxis and vaccination decisions important beyond the individual patient.
Monitoring and follow-up
- Record neurological observations, pupils and Glasgow Coma Scale frequently, escalating any decline for airway and intracranial-complication management.
- Trend blood pressure, perfusion, urine output, lactate, oxygenation and organ function through a sepsis pathway, avoiding uncritical fluid restriction.
- Monitor sodium and fluid balance because cerebral salt wasting, inappropriate antidiuresis and resuscitation effects require different interpretation.
- Review seizures clinically and use electroencephalography when persistent encephalopathy raises concern for non-convulsive status.
- Check antibiotic doses, renal and hepatic function, allergy, culture susceptibility and intravenous access every day with antimicrobial stewardship oversight.
- Arrange formal hearing assessment and review cognition, balance, focal neurology, fatigue and psychological effects after the acute illness.
Special situations
CT is not routine
Automatic imaging before lumbar puncture delays antibiotics and rarely improves safety; scan only for clinical indicators and treat first when any delay develops.
Rash absence reassures nobody
Meningococcal disease can be fulminant before petechiae appear, so circulation, limb pain and mental state deserve repeated assessment.
Paired glucose matters
Cerebrospinal-fluid glucose is interpreted against blood glucose collected around the puncture, not as an isolated laboratory number.
Pretreatment changes yield
Antibiotics may sterilise culture quickly, but cell profile, protein, glucose and molecular assays can still support diagnosis and must still be requested.
Public health defines contacts
Exposure duration, household relationship and secretion contact determine prophylaxis; indiscriminate prescribing creates harm and confusion.
Common pitfalls
- 01
Waiting for the complete meningitis triad before treating.
- 02
Delaying antibiotics while arranging CT or lumbar puncture.
- 03
Performing lumbar puncture during instability or signs of mass effect.
- 04
Forgetting Listeria cover in a patient with relevant risk.
- 05
Giving dexamethasone late while postponing the antimicrobial dose.
- 06
Reassuring from an absent rash or normal early inflammatory marker.
- 07
Omitting notification, contact management or post-meningitis audiology.