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Meningococcal disease

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Created by CD Gomersall

Updated on November 2006

by Thomas Li


  • at least 13 serogroups with most cases due to infection with A, B or C serogroups of Neisseria meningitides.
  • highest rates of disease amongst infants but this may be altered by the introduction of vaccination. About 50% of cases occur in children under 4 years. Small increases in incidence in late teenage years and above age of 65 years.

Risk factors

  • deficiency of antibody-dependent, complement mediated immune lysis
    • functional or anatomical asplenia
    • properdin deficiency
    • deficiency of terminal complement components
  • household contacts of patient with invasive meningococcal disease
  • tobacco smoke
  • upper respiratory tract infection (probably diminshes barrier properties of respiratory mucosa)


  • respiratory droplet spread and direct mucosal contact results in colonization of upper respiratory tract
  • small minority of patients who are colonized with virulent strains develop invasive disease. Usually occurs 2-4 days after colonization.
  • bacteria migrate across epithelium into submucosal tissue and capillaries resulting in bacteraemia
  • may be followed by meningeal invasion
  • bacterial proliferation and inflammatory response may occur predominantly in subarachnoid space causing meningitis or in circulation causing meningococcaemia

Clinical syndromes

Invasive disease presents as:

  • meningitis without shock
  • shock without meningitis
  • meningitis and shock
  • meningococcaemia without shock or meningitis
  • respiratory tract infection
    • pneumonia
    • epiglottitis
    • otitis media
  • focal infection
    • conjunctivitis
    • endophthalmitis
    • septic arthritis
    • Osteomyelitis
    • urethritis
    • purulent pericarditis

Septic shock without meningitis

Characterised by:

  • persistent circulatory failure
  • severe DIC leading to:
    • thrombosis and extensive haemorrhage of skin
    • thrombosis and gangrene of extremities
    • impaired renal, adrenal and lung function
  • very rapid deterioration over hours

Clinical features

Classical features are fever, non-blanching rash and a sick child

  • fever
  • diarrhoea common in first few hours
  • non-blanching rash
    • haemorrhagic skin lesions
    • initially bluish petechiae (larger than in idiopathic thrombocytopaenic purpura)
    • rapidly increase in size and number
    • if non-blanching rash is more than 2 mm in diameter in a sick febrile child, meningococcal disease is highly likely
    • all over body but often more pronounced and appear early on extremities
    • occasionally on mucous membranes
    • up to 30% of children with meningococcal disease may have non-specific maculopapular rash, but most will have non-blanching element
  • shock
    • initially high cardiac output, although extremities often cold and cyanotic with poor capillary refill
    • Tachycardia
    • Widened central-peripheral temperature gradient
    • later cardiac output falls
    • oliguria
    • hypotension is a late sign in children
  • neck stiffness usually absent and Kernig's sign -ve. Many patients alert at time of hospital admission
  • consumptive coagulopathy associated with inhibition of fibrinolysis by release of plasminogen activator inhibitor 1 from activated endothelial cells and platelets
    • thrombosis occurs particularly in the skin, kidneys, adrenals, muscles and limbs. Reduced concentrations of antithrombin III and protein C (natural inhibitors of coagulation).
  • ± multiple organ failure
    • ARDS
    • renal failure
    • rhabdomyolysis

Clinical course

Rapid deterioration is common and death often occurs within 48 hours


  • Full blood count: low WCC with marked left shift
  • blood cultures usually +ve
  • Blood for polymerase chain reaction for meningococci
  • Aspirate, smear or punch biopsy may show meningococci
  • metabolic acidosis
  • raised creatinine and urea
  • glucose may be high, low or normal
  • hypokalaemia, hypomagnesaemia, hypocalcaemia
  • slightly raised AST and ALT but normal GGT
  • CPK rises after 1-3 days due to rhabdomyolysis
  • platelets, fibrinogen low
  • fibrinogen degradation products elevated
  • lumbar puncture contraindicated because of coagulopathy

Differential diagnosis


  • may present with cardiac tamponade
  • fever, nausea, epigastric pain
  • blood cultures may be -ve


  • immediate aggressive resuscitation with urgent transfer to the Intensive Care Unit
  • intravenous fluid 20 ml/kg and repeated if necessary
  • high dose ceftriaxone (4g daily) or cefotaxime (2g 6hourly) in countries with a significant risk of penicillin resistant N. meningitidis.
  • high dose benzylpenicillin (2.4g 6 hourly) if penicillin resistance is not a concern
  • the following have been recommended but there are no controlled data demonstrating an improvement in outcome:
    • heparin (10-15 IU/kg/h)
    • antithrombin III (to keep plasma concentration >35-40 IU/ml)
    • protein C (loading dose 100 IU/kg followed by 15 IU/kg/h to keep plasma concentration between 0.8-1.2 IU/ml)
    • recombinant tissue plasminogen activator
      • 0.25-0.5 mg/kg over 1.5-4 h
      • to overcome inhibition of fibrinolysis
      • if used, should be started early
    • plasma exchange

Secondary prophylaxis

Should be offered to household and kissing contacts of patient

  • rifampicin is not recommended for pregnant women. Patients taking oral contraceptives should be warned to use alternative methods while rifampicin is being taken. Patients should also be warned that rifampicin colours all secretions and may stain soft contact lenses
  • ciprofloxacin is not recommended for pregnant or lactating women. Should not be used for prophylaxis in children unless no acceptable alternative is available
  • ceftriaxone, but not benzylpenicillin, eliminates nasal carriage of meningococci. Patients who have not received ceftriaxone should be treated with rifampicin to eliminate nasal carriage prior to discharge from hospital

Prophylaxis for healthcare workers

  • Healthcare workers coming within 3 feet of patients should wear surgical masks
  • Eye protection should be worn when there is a risk of secretions splashing onto face or into eyes
  • Chemoprophylaxis should be offered to healthcare workers whose mouth or nose is directly exposed to respiratory droplets/secretions within a distance of 3 ft from a probable or confirmed case of meningococcal disease who has received <24h appropriate treatment
    • eg staff undertaking airway management during resuscitation without wearing a mask or other mechanical protection or a clear perception of physical contact with droplets/secretions
    • Chemoprophylaxis is not recommended in the absence of a clear history of exposure. General medical or nursing care of cases is not an indication for prophylaxis
    • Exposure of eyes to respiratory droplets is not an indication for chemoprophylaxis but is associated with a low risk of conjunctivitis and subsequent invasive disease. Staff should be counseled about this risk and advised to seek early treatment if conjunctivitis develops within 10 days of exposure


Drug Dose
  Children Adults
Rifampicin <1 month: 5mg/kg 12hrly for 2 days
Others: 10mg/kg 12hrly for 2 days
600 mg 12 hrly for 2 days
Ciprofloxacin Not recommended <18 years 500 mg single dose
Ceftriaxone <15 years: 125mg IM single dose
Others: adult dose
250 mg single dose


  • Most children survive
  • 8% die from septic shock and complications
  • Among survivors
  • 10% have neurodevelopmental consequences like cerebral palsy
  • 10% have deafness

Further reading

Brandzaeg P. Meningococcal infections. In Warrell DA, Cox TM, Firth JD, Benz EJ. Oxford Textbook of Medicine, 4th edition, 2003, Oxford, Oxford University Press, pp 7.11.5

Rosenstein NE et al. Medical Progress: Meningococcal disease. N Engl J Med, 2001; 344(18):1378-1388

Stuart JM et al. Preventing secondary meningococcal disease in health care workers: recommendations of a working group of the PHLS Meningococcus Forum. Communicable Disease and Public Health, 2001; 4:102-5

Hart CA and Thomson APJ. Meningococcal disease and its management in children. BMJ 2006; 333: 685-690

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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