Invasive pneumococcal and meningococcal disease

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

Neisseria meningitidis colonises the nasopharynx and occasionally invades blood, producing endotoxin-driven endothelial injury, capillary leak and disseminated intravascular coagulation. Streptococcus pneumoniae invades after respiratory colonisation and is the leading cause of severe adult bacterial meningitis; capsule impedes phagocytosis and makes splenic function important.

Clinical care has two parallel tracks. The patient needs immediate sepsis, meningitis and organ support, while meningococcal suspicion creates statutory notification and contact prevention. Organism confirmation through culture and PCR guides narrowing, clearance and vaccination, but treatment decisions rest on the syndrome because microbiology can be negative after early antibiotics.

Key points

Meningococcal disease may present as septicaemia, meningitis or both; pneumococcus commonly causes meningitis, bacteraemic pneumonia and overwhelming sepsis.
Absence of rash does not exclude meningococcal disease, and a blanching early rash can evolve into purpura as coagulopathy develops.
Give ceftriaxone immediately for suspected invasive disease after cultures when this causes no material delay; use meningitis dosing when CNS infection is possible.
Take EDTA blood for meningococcal and pneumococcal PCR plus blood cultures because prior antibiotics reduce culture yield but not all molecular yield.
Lumbar puncture is valuable when safe but follows stabilisation and must not precede urgent antibiotics in a deteriorating patient.
Notify suspected meningococcal disease promptly and let the health-protection team define close contacts, prophylaxis and vaccine needs.
Ceftriaxone treatment does not reliably eradicate meningococcal carriage for every regimen; discharge clearance follows specialist advice.
Investigate recurrent invasive encapsulated infection for asplenia, complement deficiency, immunoglobulin disorder, CSF leak or cochlear implant risk.

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

Meningococcal invasion

Nasopharyngeal N meningitidis crosses mucosa and enters blood, with risk shaped by strain, crowding, smoking, complement and immune function.

Pneumococcal invasion

Encapsulated S pneumoniae spreads from airway, sinus, ear or lung into blood and meninges, especially with asplenia, CSF leak or immune deficiency.

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

1
Endothelial toxin injury
Meningococcal lipooligosaccharide triggers cytokines, capillary leak, myocardial depression and disseminated intravascular coagulation during fulminant septic shock.
2
Capsular immune evasion
Bacterial capsules impede opsonisation and phagocytosis, making complement and splenic clearance central to effective bloodstream containment.
3
Meningeal inflammation
Organisms in CSF provoke intense neutrophilic inflammation, cerebral oedema, vasculitis and raised intracranial pressure with neuronal injury.

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

Meningococcal septicaemiaRed flag

Abrupt fever, severe myalgia, limb pain, mottling, purpura, shock and rapid capillary leak may occur before meningism.

Bacterial meningitisRed flag

Headache, fever, neck stiffness, photophobia and altered cognition is a medical emergency even without rash.

Bacteraemic pneumococcal pneumoniaRed flag

Focal consolidation with sepsis, pleuritic pain or hypoxia can accompany pneumococcal bloodstream invasion.

Purpura fulminansRed flag

Expanding ecchymoses, acral ischaemia and coagulopathy indicate severe endothelial and coagulation injury requiring critical care.

Red flags requiring action

A non-blanching rash with fever or toxicity is meningococcal disease until urgent assessment proves otherwise.
Shock, prolonged capillary refill, oliguria, lactate rise or altered consciousness requires immediate critical-care escalation.
Meningism, focal neurology, papilloedema or seizure changes lumbar-puncture safety but never delays antibiotics.
Asplenia, complement deficiency or complement-inhibitor therapy markedly increases risk of overwhelming encapsulated bacterial disease.

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 cultures and EDTA blood PCRFirst step
Why
Confirm viable organism and preserve diagnosis after prior antibiotics.
Interpretation and limitations
Take before treatment only when this causes no delay. PCR can remain positive when cultures are sterilised and supports health-protection typing.
02
Lumbar puncture when safe
Why
Diagnose meningitis and obtain culture, PCR, glucose, protein and cell count.
Interpretation and limitations
Perform after stabilisation unless focal deficit, reduced consciousness, seizure, papilloedema, shock or another contraindication requires imaging or delay.
03
FBC, coagulation, renal, liver and lactate
Why
Grade shock, DIC and organ injury and provide treatment baselines.
Interpretation and limitations
Thrombocytopenia, prolonged clotting, acidosis, rising creatinine or lactate indicates severity and repeated resuscitation assessment.
04
Chest imaging and source assessment
Why
Identify pneumococcal pneumonia, empyema or another invasive focus.
Interpretation and limitations
A lobar infiltrate supports pneumonia but does not exclude concurrent meningitis; drain pleural infection when present.

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

Viral meningitis

Lymphocytic CSF and preserved physiology may favour viral disease, but early bacterial infection cannot be excluded clinically or by rash absence.

Severe sepsis from another source

Pneumonia, endocarditis and abdominal or urinary infection can cause shock and DIC without meningococcal disease being the primary diagnosis.

Thrombotic or inflammatory purpura

TTP, vasculitis and haematological disease can cause petechiae, but fever and shock require infection treatment during evaluation.

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

01ASSESSTreat invasive disease immediatelyFirst stepInvasive meningococcal or pneumococcal disease is clinically suspected.

1Use ABCDE, capillary refill, lactate, urine output and neurological examination and involve critical care early for shock or altered consciousness.
2Take blood culture and PCR quickly, then give ceftriaxone at meningitis dose when CNS infection cannot be excluded.
3Manage hypoglycaemia, seizures, coagulopathy and raised intracranial pressure while using reassessed fluids and vasopressors.
4Perform lumbar puncture only after safety criteria are met and never use CT as a routine prerequisite that delays treatment.

02TREATLink organism to public-health actionMeningococcal infection is possible or confirmed.

1Notify the proper officer or health-protection team on suspicion of meningococcal disease rather than waiting for laboratory confirmation.
2Give the health-protection team names and exposure details securely so they can identify household, intimate and directly exposed airway contacts.
3Provide chemoprophylaxis and group-specific vaccination only to contacts defined by health protection, using pregnancy and allergy modifiers.
4Ensure the index case receives carriage eradication if the treatment course did not provide it and document advice before discharge.

03REVIEWFind susceptibility and host riskThe organism is identified or invasive infection is recurrent.

1Narrow treatment to organism and susceptibility and define duration from meningitis, pneumonia, septic arthritis or another focus.
2Repeat cultures and investigate empyema, endocarditis or occult focus when fever or bacteraemia persists.
3Assess spleen, complement, immunoglobulin, CSF leak and cochlear implant factors after recurrent pneumococcal or meningococcal invasion.
4Arrange hearing, neurological, skin and rehabilitation follow-up after meningitis, shock, limb ischaemia or intensive care.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Provides immediate bactericidal cover for meningococcus, pneumococcus and susceptible H influenzae.

Ceftriaxone for suspected invasive meningitis

Give ceftriaxone 2 g intravenously every 12 hours in adults when bacterial meningitis is suspected.

Check immediate cephalosporin allergy and local resistance; do not delay for CT or lumbar puncture and narrow when organism and susceptibility return.

Treats susceptible meningococcal and pneumococcal bloodstream and focal disease.

Ceftriaxone for non-meningeal invasive infection

Give ceftriaxone 2 g intravenously once daily when invasive disease is severe but meningitis has been excluded.

Dose and duration depend on source, organ function and cultures; search for endocarditis, empyema or joint infection when recovery is slow.

Eradicates meningococcal carriage and reduces secondary cases after defined exposure.

Contact chemoprophylaxis

Use a health-protection-selected regimen such as ciprofloxacin 500 mg orally once for an eligible adult close contact.

Apply pregnancy, allergy, resistance and fluoroquinolone safety modifiers; prophylaxis never treats symptomatic invasive disease.

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

Neurological disability

Infarction, seizures, hydrocephalus, cognitive injury and hearing loss follow meningeal inflammation and require structured multidisciplinary rehabilitation.

Limb and skin necrosis

Purpura fulminans and vasopressor-dependent shock cause acral ischaemia, tissue loss and substantial reconstructive and rehabilitation needs.

Secondary cases

Close contacts can carry and develop meningococcal disease, making rapid prophylaxis and individual vaccine assessment essential for prevention.

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

Repeat haemodynamic, skin, neurological and urine-output assessment frequently through the period of rapid deterioration risk.
Track coagulation, platelets, lactate, renal function and cultures and link abnormalities to bleeding, shock and medicine safety.
Confirm notification, contact risk assessment, prophylaxis, vaccination and index-case carriage clearance are completed and documented.
Arrange hearing testing and neurological, renal, dermatological and psychological follow-up after invasive meningitis or shock.

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

Rash may be absent

Meningococcal meningitis and early septicaemia can occur without purpura, so treatment depends on physiology and syndrome rather than skin alone.

PCR rescues diagnosis

Molecular testing of blood or CSF can retain value after antibiotics have sterilised culture, but samples never justify treatment delay.

Contacts are defined narrowly

Sitting near a case or routine clinical contact does not automatically warrant antibiotics; intensity and direct secretion exposure guide health protection.

Recurrence reveals host risk

Repeated encapsulated bacterial invasion should trigger spleen and complement evaluation rather than being dismissed as bad luck.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for a non-blanching rash before treating a rapidly deteriorating febrile patient.
02
Delaying ceftriaxone for CT or lumbar puncture when bacterial meningitis or shock is credible.
03
Giving prophylaxis to every workplace or healthcare contact without health-protection risk assessment.
04
Discharging after recovery without hearing, neurological, skin, renal and public-health follow-up.