Bacterial meningitis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

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.

The diagnostic sequence is governed by safety and time. Blood culture, full blood count, inflammatory markers, renal and liver tests, clotting, glucose, lactate and whole-blood PCR can be collected rapidly. Lumbar puncture provides crucial cell count, protein, paired glucose, Gram stain, culture and PCR, but antibiotics take precedence whenever imaging, stabilisation or transfer would delay it. Ongoing care includes intracranial, seizure, fluid and organ support, organism-directed narrowing, infection-control advice, notification and audiological or neurocognitive follow-up.

Key points

Fever, headache, neck stiffness and altered consciousness form a high-risk combination, but presentations are incomplete and can evolve over hours; absence of one feature cannot safely exclude meningitis.
Non-blanching petechiae or purpura supports meningococcal disease, yet meningococcal meningitis and sepsis often present before a rash appears and the rash can be subtle on darker skin.
Take blood cultures and diagnostic blood samples promptly, but administer empirical antibiotics within one hour of hospital arrival and sooner in shock; investigations must not create treatment delay.
Lumbar puncture should occur before antibiotics only when it is immediately safe and will not materially delay therapy; CT is not a routine prerequisite.
Signs suggesting raised intracranial pressure, focal neurological findings, uncontrolled seizures, severe coagulopathy, cardiorespiratory instability or local spinal infection make immediate lumbar puncture unsafe.
For most adults, NICE recommends intravenous ceftriaxone while the organism is unknown; use cefotaxime if ceftriaxone is contraindicated and follow local antimicrobial dosing and allergy pathways.
Add intravenous amoxicillin when Listeria monocytogenes is a meaningful risk, including older age, pregnancy or immunocompromise, as defined by current guidance and local microbiology advice.
Give intravenous dexamethasone with or before the first antibiotic where possible in strongly suspected bacterial meningitis, but never delay antimicrobial treatment to obtain or administer it.
Cerebrospinal fluid usually shows neutrophils, high protein and low glucose relative to blood, but prior antibiotics, early disease and immunosuppression can alter the pattern; PCR and culture remain important.
In England, report every suspected acute meningitis case urgently to the local UKHSA health-protection team by telephone within 24 hours and through the online notification service within 3 days; do not wait for laboratory confirmation. For suspected meningococcal disease, the team also directs contact prophylaxis and vaccination. Use the equivalent statutory route in devolved nations.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

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.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Meningeal entry
Bacteria cross mucosal, bloodstream or anatomical barriers and enter cerebrospinal fluid, where limited local immune defences permit rapid multiplication.
2
Inflammatory amplification
Bacterial components trigger intense neutrophilic cytokine responses, increasing blood–brain barrier permeability, disrupting cerebrospinal-fluid circulation and raising intracranial pressure.
3
Pressure and vascular injury
Cerebral oedema, hydrocephalus and vasculitic or thrombotic injury reduce perfusion, while systemic inflammation can produce shock and multi-organ failure.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Red-flag combination

Fever, headache, neck stiffness and altered cognition together are strongly concerning, although each can be absent and clinical deterioration may be rapid.

Meningococcal sepsis

Tachycardia, prolonged capillary refill, limb pain, cold hands or feet, hypotension and a spreading non-blanching rash indicate invasive disease and shock risk.

Neurological severityRed flag

Reduced Glasgow Coma Scale, focal deficit, cranial-nerve palsy, repeated seizure or papilloedema suggests complication and influences airway, imaging and lumbar-puncture decisions.

Listeria context

Older age, pregnancy and immunocompromise increase Listeria probability and should trigger addition of active empirical cover under the current protocol.

Post-neurosurgical pattern

A shunt, recent cranial procedure, penetrating injury or cerebrospinal-fluid leak changes likely organisms and requires a specialist device-associated regimen.

Subtle host response

Infants, frail older people and immunosuppressed patients may lack fever or marked meningism, so altered behaviour, feeding, alertness or unexplained sepsis matters.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

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.
05
CT brain before lumbar puncture
Why
Evaluate suspected mass effect or another lesion only when specific clinical indicators exist.
Interpretation and limitations
Focal deficit, abnormal pupils, markedly reduced or falling consciousness and certain seizure patterns may justify imaging; a normal CT does not guarantee puncture safety.
06
Microbiology susceptibility testing
Why
Refine antibiotics and detect resistance once an isolate is available.
Interpretation and limitations
Narrow therapy in discussion with infection specialists, integrating the organism, minimum inhibitory concentrations, site penetration and clinical response.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

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.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

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.

1Check for focal deficit, abnormal pupils, significant consciousness impairment, ongoing seizure, cardiorespiratory instability, coagulopathy, thrombocytopenia and local infection.
2If no contraindication and no treatment delay will occur, measure opening pressure and send adequate paired samples for cells, protein, glucose, Gram stain, culture and PCR.
3If puncture is deferred, document the reason, treat immediately and reassess later because delayed cerebrospinal-fluid analysis may still provide useful molecular or inflammatory evidence.

03Empirical regimenCover likely community pathogensThe causative organism is not yet known in an adult with community-acquired disease.

1Give intravenous ceftriaxone at the current meningitis dose, or cefotaxime where ceftriaxone cannot be used, following allergy, renal and local antimicrobial guidance.
2Add intravenous amoxicillin when age, pregnancy, immunocompromise or another factor creates Listeria risk, and seek immediate advice for severe beta-lactam allergy.
3Review microscopy, PCR, culture and susceptibility results daily with infection specialists, narrowing agent and duration to the organism and clinical complications.

04After stabilisationPrevent sequelae and protect contactsThe patient survives the acute phase or meningococcal disease is suspected.

1Monitor for raised intracranial pressure, stroke, seizures, hyponatraemia, hydrocephalus and organ failure, obtaining targeted neuroimaging and critical-care support when deterioration occurs.
2Report suspected acute meningitis to the local health-protection team without waiting for confirmation; for suspected meningococcal disease, provide chemoprophylaxis and vaccination only to contacts they define under current national guidance.
3Before and after discharge arrange audiology, neurological and cognitive review, rehabilitation, recurrence safety-netting and investigation of an anatomical or immune predisposition when indicated.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Empirical treatment covering major community-acquired meningitis pathogens except Listeria.

Ceftriaxone

NICE recommends 2 g intravenously twice daily for adults with suspected bacterial meningitis while the organism is unknown; verify the current BNF, allergy status and local protocol.

Give promptly after cultures if feasible; assess severe beta-lactam allergy, biliary issues and interactions, and obtain specialist advice for post-neurosurgical infection or resistant organisms.

Adds empirical Listeria monocytogenes cover in older, pregnant or immunocompromised patients and other defined risk groups.

Amoxicillin

For adult Listeria risk, NICE uses 2 g intravenously every 4 hours as an addition to the cephalosporin; adjust through specialist advice where renal function requires it.

Check immediate and delayed penicillin allergy, renal function and sodium load; rash, cytopenia and liver injury require review, and allergy alternatives need microbiology input.

Reduces inflammatory neurological complications, with continuation guided by the identified or suspected organism.

Dexamethasone

For adults, NICE recommends 10 mg intravenously four times daily for 4 days when bacterial meningitis is strongly suspected, ideally with or before the first antibiotic.

Never postpone antibiotics to give it; review glucose, gastrointestinal risk, delirium and infection context, and seek specialist advice if started more than 12 hours after antimicrobials.

Provides early meningococcal treatment in exceptional prehospital delay, while urgent transfer remains the priority.

Benzylpenicillin before hospital

Use the age-appropriate parenteral dose in the current emergency formulary only when meningococcal disease is strongly suspected and transfer will be substantially delayed.

Do not delay transport or resuscitation, and do not give for a non-blanching rash alone without clinical suspicion; record administration and communicate it to hospital.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

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.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

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.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

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.

11Common pitfallsFrequent interpretation and management errors.

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.