Central Nervous System Infection in Infants and Children


CNS infection, meningitis, encephalitis, encephalopathy, myelitis, abscess

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Related Conditions

Subarachnoid space infection (meningitis), CSN parenchyma (encephalitis, myelitis, abscess)

1. Description of the problem

What every clinician needs to know

Infections of the CNS are among the most devastating infectious diseases and a major cause of death and disability worldwide. These infections often present as medical emergencies.

Etiology: bacterial (organisms are age-dependent), viral (can be seasonal), fungal (most common in immunocompromised population), parasitic (rare) and aseptic.

CNS infection can present as infection of the subarachnoid space, as in meningitis, or as infection of the parenchyma, as in encephalitis, myelitis or abscess. Most commonly spread hematogenously but can be a direct spread from adjacent structures (otitis, sinusitis, dental abscess), invasive and noninvasive trauma with skull fractures and foreign body (ventricular shunt).

Clinical syndromes of CNS infection

1. Acute meningitis: seen in bacterial and viral infections with acute onset of fever, headache, vomiting, meningismus, altered mental status; rapid progression over hours to days

2. Subacute or chronic meningitis: seen in tuberculous or fungal infections with gradual onset, low-grade fever; progression over weeks

3. Acute encephalitis: caused by viruses with 2 forms of clinical presentation: a) Diffuse: altered mental status and b) Focal: tropism of virus for specific location

4. Encephalopathy with systemic infection: rare infections associated with Shigella, typhoid, malaria, Rickettsia, endocarditis. Symptoms are varied, often associated with altered mental status with choreal movement.

5. Post infectious: associated with viruses/vaccines; symptoms are varied depending on the lesions: acute disseminated encephalomyelitis, transverse myelitis, optic neuritis, multiple sclerosis

2. Emergency Management

Key emergency management steps
  • Neuro assessment: airway protection for severe altered mental status (GCS below 8). Take precautions for increased intracranial pressure during intubation. Consider ICP monitoring for evidence of elevated ICP. Treat seizure activity: 50% of patients who presented with seizures progress to status epilepticus, which is hard to control and correlates with poor neuro outcomes.

  • Cardiovascular support as needed; cerebral perfusion pressure is directly affected by mean blood pressure.

  • Antibiotics early; do not withhold antibiotics awaiting lumbar puncture. Start antiviral if high suspicion of herpes infection.

Management points not to be missed

Electrolyte and fluid derangements are common:

  • Diabetes insipidus: monitor urine output and check sodium level for spike in UOP (Na in the 150s-160s).

  • SIADH: late onset of electrolyte derangements with oliguria and relative hyponatremia (Na can be below 125), increased risk of seizure activity. Correct hyponatremia acutely to bring Na level above 125 with 3% saline if necessary (seizure threshold), then slow correction to normal level (Na 140-145) over the next 36-48 hrs.

  • At risk of hypokalemia secondary to GI losses, hemodilution, osmotherapy, diuretics, sepsis.

  • At risk for cerebral edema.

3. Diagnosis

Diagnostic criteria and tests
  • A complete and detailed history and physical examination with details of length of illness and details of presenting symptoms, preceding illness, past medical history. Also history of exposure: travel, sick contact, insect bites, sexual activities, animal contacts.

  • Initial labs: CBC, CMP, CPR, UA, blood cultures; CSF: with opening pressure, cultures, cytology, serology

  • Initial imaging: CT head without contrast to rule out space-occupying lesions, hemorrhage or trauma. MRI of brain and spine if concern for myelitis/encephalitis

Normal lab values

See Table I.

Table I.n

Confirmatory tests
  • CSF culture is the gold standard in diagnosis of CNS infection.

  • Imaging can be added to evaluate for abscess, inflammation but is not necessarily sensitive to make diagnosis. Cerebral edema is often not demonstrated on scans.

4. Specific Treatment

1. Acute meningitis

See Table II.

Table II.n

2. Subacute or chronic meningitis:

a. TB: 3- or 4-drug therapy.

3. Acute encephalitis:

Primary potentially treated condition would be herpex simplex virus encephalitis. Treatment is IV acyclovir at appropriate dosages.

4. Encephalopathy with systemic infection: rare infections associated with Shigella, typhoid, malaria, Rickettsia, endocarditis. Symptoms are varied, often associated with altered mental status with choreal movement.

5. Post infectious: associated with viruses/vaccines; symptoms are varied depending on the lesions: acute disseminated encephalomyelitis, transverse myelitis, optic neuritis, multiple sclerosis.

Drugs and dosages

Ampicillin 50-100 mg/kg Q6 hrs; max 12 gm/day.

Vancomycin15-20 mg/kg Q8 hrs; max 1 gm/dose; follow level, adjust dose for renal insufficiency.

Gentamycin 2.5 mg/kg Q8 hrs; max 120 mg/dose; follow level, adjust dose with renal insufficiency.

Cefotaxime 50 mg/kg Q6 hrs; max 2 gm/dose.

Ceftriaxone 100 mg/kg Q24 hrs; max 4 gm/day.

Acyclovir10-20 mg/kg Q8 hrs.

5. Disease monitoring, follow-up and disposition

Expected response to treatment
  • With appropriate treatment: CSF culture and gram stain will become negative in 24-48 hours, glucose will normalize in 72 hrs. Cell counts and proteins will take days to normalize.

  • Clinical symptoms: Fever and headaches may persist for 7-10 days,


Invasion of the CNS via 5 steps:

  • Colonization of the nasopharynx by adhesion to the mucosa. Method depends on organisms: Neisseria uses fimbriae on the cell wall, Strep pneumo uses surface adhesion proteins. Host defense is interrupted with secreted endopeptidases that cleave host IgA.

  • Invasion of the mucosa and penetration into the bloodstream between or through epithelial cells

  • Circulation in bloodstream and invasion of blood-brain barrier (BBB): polysaccharide capsule protects the bacteria from host defense. Crossing BBB with similar mechanism as crossing mucosa at the choroid plexus and cerebral capillaries into the ventricular fluid.

  • Multiplication in the CSF: LPS and cell wall fragments trigger an inflammatory response in the CNS via cytokines IL-1b, IL-6 and TNF, resulting in increased permeability of the BBB.

  • End results: cerebral edema, derangements of cerebral metabolism, neuronal damage, strokes


Bacterial meningitis etiologyvaries by region and age

  • Streptococcus pneumoniae: small, non-motile GPC in pairs or chains. Virulence depends on capsular polysaccharide. Also associated with CSF leak (skull fractures), asplenia, HIV, cochlear implants.

  • Haemophilus influenzae: smal GN, pleomorphic coccobacilli; Type B caused almost all invasive disease; incidence decreased by 97% after vaccination.

  • Neisseria meningiditis: GN diplococci; invasive disease caused by encapsulated organism. Virulence depends on many factors: capsular polysaccharide, LPS (endotoxin), pili, IgA protease and ompS gene.

  • Gram-negative bacilli: E. coli is a common cause in neonatal sepsis/meningitis. Beyond neonatal period, GN bacilli associated with GI infections, head trauma, neurosurgical procedures, immune deficiency (Klebsiella, Salmonella, Enterobacter, and Pseudomonas).

  • Group B strep: common cause of invasive neonatal disease. 6 types, with Type III causing most neonatal meningitis cases. Prenatal screening and treatment help to decrease incidence of infection in developed countries. Can be early or late onset.

  • Listeria monocytogenes: GP rod, important neonatal infection associated with maternal consumption of unpasteurized cheese or contaminated meats

  • Anaerobes:

    Bacteroides fragilis, Fusobacterium spp., Clostridium spp. Infection occurs in only certain conditions: ruptured brain abscess, chronic otitis, mastoiditis, sinusitis; head trauma, NS procedures; congenital dural defects; GI infections, suppurative pharyngitis; CSF shunts; immune suppression.


Bacterial infection: early recognition, diagnosis and start of treatment are associated generally with better outcomes. HIB, pneumococcal and meningococcal vaccines decreases the incidence of meningitis.

Special considerations for nursing and allied health professionals.

  • Early start of treatment: antibiotic. Treatment should not be delayed for lumbar puncture.

  • Monitor for electrolyte abnormalities.

  • Monitor for seizure activity.

What's the evidence?

Feigin & Cherry. Textbook of Pediatric Infectious Diseases.

Behrman, RE, Kliegman, RM, Jenson, HB. Nelson Textbook of Pediatrics.

Nichols, DG. Rogers' Textbook of Pediatric Intensive Care.

Thigpen, MC. “Bacterial meningitis in the United States, 1998-2007”. N Engl J Med. vol. 3654. 2011;May 26. pp. 2016-25. (Updated CDC information on prevalence.)

Agrawal, S, Nagel, S. “Acute Bacterial meningitis in Infants and Children: Epidemiology and Management”. Peaediatr Drugs. 2011. (Good review of antibiotic choices.)

National Institute for Health and Clinical Excellence: Guidance. National Collaborating Centre for Women's and Children's Health (UK). 2011. (Excellent evidence based review.)