Bacterial menigitis in children

Section Editor
Morven S Edwards, MD
Deputy Editor
Carrie Armsby, MD, MPH
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2021. | This topic last updated: Nov 11, 2020.
INTRODUCTION — Children with suspected bacterial meningitis require urgent evaluation and
management, including prompt administration of appropriate antimicrobial therapy (table 1). The
mortality rate of untreated bacterial meningitis approaches 100 percent. Even with optimal therapy,
morbidity and mortality may occur. Neurologic sequelae are common among survivors.
The clinical features, evaluation, and diagnosis of bacterial meningitis in infants and children older than
one month will be reviewed here. The treatment and prognosis of bacterial meningitis in infants and
children are discussed separately. (See "Bacterial meningitis in children older than one month:
Treatment and prognosis".)
Other aspects of bacterial meningitis in pediatric patients are discussed separately:
●Bacterial meningitis in neonates (see "Bacterial meningitis in the neonate: Clinical features and
diagnosis" and "Bacterial meningitis in the neonate: Treatment and outcome" and "Bacterial meningitis
in the neonate: Neurologic complications")
●Neurologic complications (see "Bacterial meningitis in children: Neurologic complications" and
"Bacterial meningitis in children: Dexamethasone and other measures to prevent neurologic
complications")
●Pathophysiology (see "Pathogenesis and pathophysiology of bacterial meningitis")
●Pneumococcal meningitis (see "Pneumococcal meningitis in children")
EPIDEMIOLOGY
Incidence — In a population-based surveillance study from the United States (2006 to 2007), the
annual incidence of bacterial meningitis in children varied with age as follows [1]:
●<2 months – 81 per 100,000 population
●2 months to 2 years – 7 per 100,000 population
●2 through 10 years – 0.6 per 100,000 population
●11 through 17 years – 0.4 per 100,000 population
After the introduction of the Haemophilus influenzae type b (Hib) and pneumococcal conjugate vaccines
to the infant immunization schedule (which occurred in the United States in 1990 and 2000,
respectively), the incidence of bacterial meningitis declined in all age groups except infants <2 months
old [1-3]. The median age shifted from <5 years to approximately 30 to 40 years, though the incidence
remains highest among infants <2 months old [1,3,4].
Causative organisms — The relative frequency of different causative pathogens varies by age and by
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geographic region. In addition, certain pathogens may be more likely depending upon the route of
acquisition and underlying host factors (table 2). (See 'Predisposing factors' below.)
●Age – The most frequent pathogens vary according to age as follows [1-3,5-7]:
•Infants <3 months old – Group B streptococcus (GBS) and Escherichia coli are the most common
pathogens in neonates and young infants. Other enteric gram-negative bacilli, Streptococcus
pneumoniae, and Neisseria meningitidis are less common in this age group. Other uncommon pathogens
include Enterococcus, Staphylococcus aureus, Listeria monocytogenes, group A streptococcus, and
Haemophilus influenzae. (See "Bacterial meningitis in the neonate: Clinical features and diagnosis",
section on 'Etiology'.)
•Older infants and children – S. pneumoniae and N. meningitidis are the most common pathogens in
this age group, together accounting for approximately 60 to 70 percent of cases [1,3,5,8]. As discussed
below, the relative frequencies of these two pathogens vary somewhat in different geographic regions.
Less common pathogens in this age group include group A streptococcus and GBS, H. influenzae, and
other gram-negative organisms.
•Adolescents – N. meningitidis is the most common pathogen in adolescents, accounting for more than
one-half of all cases [1,3,5,8].
●Geographic region – The most frequent pathogens vary somewhat from region to region [9]:
•North America – In North America, S. pneumoniae is the most frequent pathogen, accounting for 35 to
60 percent of cases, followed by N. meningitidis (15 to 25 percent), H. influenzae (15 to 20 percent,
predominantly non-type B in the post-Hib vaccine era), GBS (10 to 15 percent), E. coli (7 percent), and
L. monocytogenes (2 to 3 percent) [1,5,8,10-12].
•Europe – In the United Kingdom and Europe, N. meningitidis is more common than in North America,
accounting for approximately 30 to 50 percent of cases, followed by S. pneumoniae, (20 to 40 percent),
GBS (10 to 15 percent), and H. influenzae (5 to 15 percent) [3,9,13,14].
•Sub-Saharan Africa – In the meningitis belt in sub-Saharan Africa (figure 1), N. meningitidis accounts
for approximately 50 to 60 percent of cases [15]; however, S. pneumoniae and H. influenzae are also
important causes in this region [15,16]. In a systematic review and meta-analysis of the global burden
of bacterial meningitis, S. pneumoniae accounted for 41 percent of cases among children in the entire
African region; H. influenzae accounted for 13 percent and N. meningitidis 7.5 percent [9].
S. pneumoniae remains among the most common causes of bacterial meningitis in children, though the
overall incidence of pneumococcal meningitis in children in the United States declined by 50 to 60
percent after widespread pneumococcal vaccination [1,5,17-19]. (See "Pneumococcal meningitis in
children", section on 'Epidemiology'.)
Before widespread vaccination for Hib in the United States, Hib was the major cause of bacterial
meningitis in children [20]. In developing countries that do not routinely immunize against Hib, Hib
continues to be a frequent cause of meningitis [21].
Mechanisms of infection — There are three major mechanisms for developing meningitis (see
"Pathogenesis and pathophysiology of bacterial meningitis"):
●Colonization of the nasopharynx, with subsequent bloodstream invasion followed by central nervous
system (CNS) invasion
●Direct entry of organisms into the CNS from one of these sources:
•Contiguous infection (eg, sinusitis, mastoiditis) (see "Acute bacterial rhinosinusitis in children: Clinical
features and diagnosis", section on 'Complications' and "Acute mastoiditis in children: Clinical features
and diagnosis", section on 'Complications')

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•Trauma, neurosurgery, or cerebrospinal fluid (CSF) leak (see "Skull fractures in children: Clinical
manifestations, diagnosis, and management", section on 'Complications')
•Medical devices (eg, CSF shunts, cochlear implants) (see "Infections of cerebrospinal fluid shunts and
other devices" and "Cochlear implant infections")
●Invasion of the CNS following bacteremia from another localized source (eg, infective endocarditis)
(see "Infective endocarditis in children")
Predisposing factors — Risk factors for bacterial meningitis include:
●Congenital or acquired immunodeficiency (eg, asplenia, complement deficiency,
hypogammaglobulinemia, HIV infection, glucocorticoid use, diabetes mellitus)
●Anatomic defects of the spinal cord (eg, dermal sinus (picture 1)), brain, or inner ear (see "Cutaneous
developmental anomalies in the newborn and infant", section on 'Cranial dermoid cysts and dermal
sinus tracts')
●Acquired cranial defects due to basilar skull fracture or surgery (see "Skull fractures in children:
Clinical manifestations, diagnosis, and management", section on 'Basilar skull fractures')
●Presence of a medical device (eg, CSF shunt, cochlear implant) (see "Infections of cerebrospinal fluid
shunts and other devices" and "Cochlear implant infections")
●Parameningeal infections (eg, sinusitis, mastoiditis) (see "Acute bacterial rhinosinusitis in children:
Clinical features and diagnosis", section on 'Complications' and "Acute mastoiditis in children: Clinical
features and diagnosis", section on 'Complications')
●Recent infection (especially respiratory and ear infections) (see "Acute otitis media in children: Clinical
manifestations and diagnosis", section on 'Complications of AOM')
●Recent exposure to someone with meningitis
●Recent travel to an area with endemic meningococcal disease, such as sub-Saharan Africa (figure 1)
CLINICAL FEATURES
Course — Acute bacterial meningitis has two patterns of presentation [22,23]:
●Gradually progressive course – Most children with meningitis have a preceding febrile illness and then
develop signs and symptoms of meningeal inflammation progressively over one to several days.
●Fulminant course – Patients with acute and fulminant meningitis present with manifestations of sepsis
and meningitis that develop rapidly over several hours. The fulminant presentation is often complicated
by severe brain edema.
Presentation — The characteristic presentation of meningitis is a triad of fever, neck stiffness, and
abnormal mental status (eg, lethargy, confusion, irritability) [23,24]. However, this triad occurs in only
44 percent of affected adults [19] and in even fewer children. The presentation in children varies with
age:
●Infants – In infants, manifestations may include [24,25]:
•Fever or hypothermia
•Lethargy
•Poor feeding
•Irritability
•Bulging fontanel

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•Vomiting
•Diarrhea
•Respiratory distress
•Jaundice
•Seizures
●Children and adolescents – In children and adolescents, clinical manifestations may include [23,25]:
•Fever
•Headache
•Neck stiffness
•Photophobia
•Nausea/vomiting
•Confusion
•Lethargy
•Irritability
Upper respiratory infection symptoms often precede development of meningeal signs [23]. However, the
clinical manifestations of bacterial meningitis are variable and nonspecific; no single sign is
pathognomonic [24]. The symptoms and signs depend, to some extent, upon the duration of illness,
host response to infection, and age of the patient [22,25]. Previous receipt of oral antibiotics does not
affect the clinical presentation of acute bacterial meningitis.
Clinical findings
●General appearance – Children with bacterial meningitis generally appear uncomfortable. In one
study of 103 children with bacterial meningitis, three-quarters of the children were toxic-appearing at
the time of admission [25].
Vital sign abnormalities (eg, tachycardia, tachypnea) are often present, particularly in young children.
Patients with acute and fulminant presentation may present with hypotension and shock.
●Meningeal signs – Meningeal signs (nuchal rigidity, headache, photophobia, irritability) are present
at the time of admission in the majority of patients.
Nuchal rigidity is manifest by the inability to place the chin on the chest, limitation of passive neck
flexion, and Kernig and Brudzinski signs.
•Kernig sign – Kernig sign is present if the patient, in the supine position with the hip and knee flexed
at 90°, cannot extend the knee more than 135° and/or there is flexion of the opposite knee (movie
1A).
•Brudzinski sign – Brudzinski sign is present if the patient, while in the supine position, flexes the lower
extremities during attempted passive flexion of the neck (movie 1B).
Signs of meningeal irritation are present at the time of presentation in approximately 60 to 80 percent
of affected children and can be elicited at some point during the hospital course in >90 percent of
affected children [22,26-28]. Nuchal rigidity may not be elicited in comatose patients or those with
focal or diffuse neurologic deficits [23]. In addition, nuchal rigidity may occur late in the course,
particularly in young children.

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While nuchal rigidity is highly suggestive of meningitis, it can occur in many other conditions, as
summarized in the table (table 3) and discussed separately. (See 'Differential diagnosis' below and
"Approach to neck stiffness in children".)
●Neurologic findings – Neurologic abnormalities may include depressed or altered mental status (eg,
irritability, lethargy, confusion, somnolence), seizures, signs of elevated intracranial pressure (ICP), and
other focal neurologic findings.
•Abnormal mental status – Most affected patients have an abnormal mental status at the time of
presentation, which can range from irritability or confusion, to lethargy, to coma.
In a review of 235 children with bacterial meningitis, approximately three-quarters were irritable or
lethargic, 7 percent were somnolent, and 15 percent were semicomatose or comatose at the time of
admission [23]. In another study of 103 pediatric patients with bacterial meningitis, 28 percent had a
Glasgow Coma Scale score (table 4) ≤10 at the time of admission [25].
The level of consciousness at the time of admission has prognostic significance [29]; patients who are
obtunded, semicomatose, or comatose at the time of admission are more likely to have an adverse
outcome [30]. (See "Bacterial meningitis in children older than one month: Treatment and prognosis",
section on 'Prognostic factors'.)
•Seizures – Approximately 20 to 30 percent of patients with meningitis experience seizures prior to
presentation or within the first 48 hours of admission [23,31,32]. Seizures are typically generalized.
Focal seizures can occur later in the course, which may indicate cerebral injury [31,33,34]. (See
"Bacterial meningitis in children: Neurologic complications", section on 'Seizures'.)
•Increased ICP – In infants, signs of increased ICP may include bulging fontanel or diastasis of the
cranial sutures. In older children, signs of increased ICP may include headache, vomiting, and altered
mental status [24]. The constellation of systemic hypertension, bradycardia, and respiratory depression
(Cushing triad) is a late sign of increased ICP. Papilledema on funduscopic examination is suggestive of
increased ICP at any age, but it is an uncommon finding in acute bacterial meningitis. The finding of
papilledema should prompt evaluation for venous sinus occlusion, subdural empyema, or brain abscess.
(See 'Neuroimaging' below and "Elevated intracranial pressure (ICP) in children: Clinical manifestations
and diagnosis".)
Other signs of increased ICP that may occur in bacterial meningitis include palsies of the third (figure
2), fourth (picture 2), and sixth (most common) cranial nerves. (See "Third cranial nerve (oculomotor
nerve) palsy in children" and "Fourth cranial nerve (trochlear nerve) palsy" and "Sixth cranial nerve
(abducens nerve) palsy", section on 'Clinical manifestations'.)
•Focal neurologic findings – Focal neurologic findings may include motor abnormalities (eg,
hemiparesis, quadriparesis), asymmetric or absent tendon reflexes, or cranial nerve palsies (eg,
abnormal pupillary light response, visual field defects, eye deviation or abnormal extraocular
movements, facial asymmetry). (See "Detailed neurologic assessment of infants and children".)
In one review of 235 children with bacterial meningitis, 10 percent had focal neurologic findings at the
time of admission [35]. The presence of focal neurologic signs at the time of admission was associated
with increased risk of persistent neurologic abnormalities and cognitive impairment one year after
discharge.
Focal neurologic findings also may occur as a late complication of meningitis. (See "Bacterial meningitis
in children: Neurologic complications", section on 'Motor deficits'.)
●Cutaneous findings – Petechiae (picture 3) and purpura (picture 4) may occur with any of the
bacterial pathogens but are most commonly seen in N. meningitidis. The lesions are usually more
pronounced on the extremities and can be preceded by an erythematous maculopapular eruption. (See
"Clinical manifestations of meningococcal infection", section on 'Rash'.)

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●Systemic findings – Children with bacterial meningitis frequently present with systemic
manifestations, which can range from fever and chills to septic shock, disseminated intravascular
coagulation, acute respiratory distress syndrome, pericardial effusion, and septic or reactive arthritis.
Most of these systemic complications are consequences of the bacteremia that frequently accompanies
meningitis.
Arthritis is most common with meningococcal disease but may occur with other infections [23]. Early in
the course of meningitis, arthritis may be related to direct invasion of the joint, whereas arthritis that
develops late in the course is considered an immune complex-mediated event. (See "Clinical
manifestations of meningococcal infection", section on 'Arthritis'.)
Pericardial effusions also may develop in patients with disseminated illness. They usually resolve during
the course of antibiotic therapy [23]. In some cases, pericardial effusions are the cause of persistent
fever and pericardiocentesis or an open drainage procedure may be required. (See "Clinical
manifestations of meningococcal infection", section on 'Arthritis' and "Clinical manifestations of
meningococcal infection", section on 'Pericarditis'.)
EVALUATION
Pace of evaluation — Suspected bacterial meningitis is a medical emergency, and immediate
diagnostic steps must be taken to establish the specific cause (table 1). Ideally, a careful history,
physical examination, blood tests, and lumbar puncture (LP) should be performed before the initiation
of therapy for meningitis.
However, in fulminant cases with hypotension and end-organ failure, rapid intervention is particularly
necessary; administration of antibiotics may precede complete history, examination, and LP. In such
cases, blood culture should be obtained before administration of antibiotics and LP performed as soon as
is feasible. (See "Bacterial meningitis in children older than one month: Treatment and prognosis",
section on 'Empiric therapy'.)
History and physical examination
●History – Important aspects of the history in the child with suspected bacterial meningitis include:
•History of present illness, including the course of illness (see 'Course' above), preceding illness,
symptoms consistent with meningeal inflammation, and history of seizures. (See 'Clinical findings'
above and 'Presentation' above.)
•Presence of predisposing factors, such as immunodeficiency, anatomic defects, prior neurosurgery,
medical devices (eg, cerebrospinal fluid [CSF] shunt, cochlear implant), travel to an area with endemic
meningococcal disease (figure 1), or exposure to someone with bacterial meningitis. (See 'Predisposing
factors' above.)
•Immunization history (particularly the H. influenzae type b [Hib] conjugate vaccine, pneumococcal
conjugate or polysaccharide vaccine, and meningococcal conjugate or polysaccharide vaccine); receipt
of a full series of any of these vaccines does not alter the need for CSF examination or initial empiric
antibiotic therapy but, depending upon age, may affect the need for chemoprophylaxis or evaluation of
the immune system. (See 'Assessment of immune function' below.)
•History of drug allergies, particularly anaphylactic reactions to antibiotics, which, if present, may affect
the choice of antimicrobial therapy. (See "Penicillin allergy: Immediate reactions" and "Immediate
cephalosporin hypersensitivity: Allergy evaluation, skin testing, and cross-reactivity with other
beta-lactam antibiotics" and "Vancomycin hypersensitivity".)
•Recent use of antibiotics, which may affect the yield of blood and/or CSF culture. (See 'Interpretation'
below.)
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●Examination – Important aspects of the examination of a child with suspected bacterial meningitis
include vital signs, general appearance, presence of meningeal signs, neurologic examination, and
cutaneous examination.
•The vital signs are an important part of the assessment of volume status and detection of shock and/or
elevated intracranial pressure (ICP). The constellation of systemic hypertension, bradycardia, and
respiratory depression (Cushing triad) is a late sign of increased ICP. (See "Elevated intracranial
pressure (ICP) in children: Clinical manifestations and diagnosis".)
•Elicitation of meningeal signs (movie 1A-B) and important aspects of the neurologic and cutaneous
examinations are discussed above. (See 'Clinical features' above.)
•Patients with acute bacterial meningitis may also have clinical manifestations of another focal source
of infection (eg, facial cellulitis, sinusitis, otitis media, arthritis, pneumonia).
Laboratory evaluation
Blood tests — Initial blood tests should include (table 1):
●Blood culture – Blood cultures are positive in approximately 60 to 85 percent of patients with bacterial
meningitis [34,36,37].
●Complete blood count with differential.
●Inflammatory markers (eg, C-reactive protein, procalcitonin) – When used in isolation, C-reactive
protein and procalcitonin are not sufficiently specific to accurately discriminate between viral and
bacterial meningitis [38-43]. However, these tests can be helpful when used in conjunction with other
variables (eg, as part of a clinical prediction rule as discussed separately). (See "Viral meningitis in
children: Management, prognosis, and prevention", section on 'Assessing risk of bacterial meningitis'.)
●Serum electrolytes, glucose, blood urea nitrogen, and creatinine – These are helpful in assessing
volume status and planning fluid administration. Serum glucose level is necessary for determining the
CSF-to-blood glucose ratio.
●Coagulation studies (prothrombin time [PT], international normalized ratio [INR], activated partial
thromboplastin time [aPTT]), particularly in patients with petechiae or purpuric lesions.
●Lactate level if there is concern for septic shock. (See "Septic shock in children: Rapid recognition and
initial resuscitation (first hour)", section on 'Obtain laboratory studies'.)
Lumbar puncture
Indications and contraindications — An LP should be performed in all children with suspected
meningitis, unless specific contraindications to LP are present [23]. The threshold for CSF examination
should be fairly low in patients with underlying conditions that may predispose them to bacterial
meningitis. (See 'Predisposing factors' above.)
LP also should be considered in children with bacteremia and persistent fevers, even if meningeal signs
are absent, since bacteremia can progress to meningitis [44].
Indications for performing neuroimaging prior to LP are listed below (see 'Neuroimaging' below).
Additional contraindications to LP include cardiopulmonary compromise and skin infection over the LP
site. (See "Lumbar puncture: Indications, contraindications, technique, and complications in children",
section on 'Contraindications'.)
It is essential that antimicrobial therapy not be delayed if there is a contraindication to or inability to
perform an LP or if the LP is delayed by the need for neuroimaging. In any of these situations, blood
cultures should be obtained and empiric antibiotics administered as soon as is possible (before the
imaging study in children who require imaging) (table 1). (See 'Initiation of empiric therapy' below and
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'Neuroimaging' below.)
Tests to perform — CSF should be sent for:
●Cell count and differential
●Glucose and protein concentration
●Gram stain and culture
Additional testing for unusual pathogens may be warranted in special circumstances (eg, in
immunocompromised hosts) [45]. It is helpful to reserve a tube of CSF for further testing, which may
be necessary if the patient fails to improve as expected.
Interpretation — Characteristic CSF findings in bacterial meningitis include (table 5 and table
6):
●CSF pleocytosis with a predominance of neutrophils
●Elevated CSF protein
●Decreased CSF glucose
●Positive Gram stain
The following sections provide additional details on CSF cell count, CSF chemistries, interpretation of
CSF studies in patients with traumatic LPs and those pretreated with antibiotics, and the approach to
differentiating between bacterial and aseptic meningitis:
●Cell count – A CSF white blood cell (WBC) count >9 WBCs/microL is considered abnormal for infants
<3 months of age, and CSF WBC >6/microL is abnormal in children ≥3 months old [23,46,47]. The CSF
WBC count in acute bacterial meningitis is typically >1000 WBC/microL, with a predominance of
neutrophils (table 5) [23]. However, early in the course (after bacterial invasion but before the
inflammatory response), few or no WBCs may be present [48]. Neither the presence nor quantity of
bands (immature neutrophils) in the CSF helps to distinguish bacterial from viral meningitis [49]. (See
"Viral meningitis in children: Clinical features and diagnosis", section on 'Cerebrospinal fluid studies'.)
●Glucose and protein – The CSF glucose level in bacterial meningitis is typically low, usually <60
percent of the blood glucose level [50]. In more than one-half of cases, CSF glucose is <40 mg/dL
(table 5) [23]. The CSF protein in acute bacterial meningitis typically ranges from 100 to 500 mg/dL
(table 5) [23].
●Traumatic LP – When the LP is traumatic, small amounts of blood enter into the CSF, which can
impact the CSF cell count and protein measurements:
•"Corrected" WBC count – Various formulas have been used to account for blood in the interpretation of
the CSF cell count. These methods can help provide a rough estimate of the CSF WBC count when the
LP is traumatic, but they cannot be used to exclude meningitis with complete confidence [51,52]. In
most cases when the LP is traumatic, it is appropriate to treat presumptively for meningitis pending
results of CSF culture. (See "Bacterial meningitis in children older than one month: Treatment and
prognosis", section on 'Empiric therapy'.)
Our approach to estimating the "corrected" CSF WBC, which we apply only if the CSF is not grossly
bloody, is to subtract 1 WBC for every 1000 red blood cells (RBCs)/microL. Others subtract 1 WBC for
every 500 RBCs/microL
•"Corrected" CSF protein – The CSF protein concentration may be increased in children with traumatic
LP because of the increased protein concentration in plasma and the release of proteins from lysed
RBCs [53]. A "corrected" CSF protein concentration can be estimated by subtracting 1 mg/dL for every

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1000 RBCs/microL [53].
●Pretreated patients – Prior administration of antimicrobial agents, particularly oral antibiotics,
generally has minimal effect on CSF cytology [54-58]. However, pretreatment with antibiotics may alter
CSF chemistry results. In a study examining CSF chemistry results in 85 children with bacterial
meningitis who received antibiotics ≥12 hours before LP compared with 146 children who had not
received antibiotics, pretreated children had higher CSF glucose concentration (median 48 versus 29
mg/dL [2.66 versus 1.6 mmol/L], respectively) and lower CSF protein concentration (median 121
versus 178 mg/dL [1.21 versus 1.78 g/L], respectively) [58].
The impact of pretreatment on CSF culture results is discussed below. (See 'Cerebrospinal fluid culture'
below.)
●Distinguishing between bacterial and aseptic meningitis – The clinical and laboratory findings of
bacterial meningitis overlap with those of aseptic or viral meningitis (table 5 and table 6). In patients
with CSF pleocytosis, clinical prediction rules can be used in conjunction with clinical judgment to
identify patients with a very low risk of bacterial meningitis. The approach is summarized in the
algorithm and discussed in greater detail separately (algorithm 1). (See "Viral meningitis in children:
Management, prognosis, and prevention", section on 'Assessing risk of bacterial meningitis'.)
Initiation of empiric therapy — Once the results of the LP are available, empiric antibiotics
should be initiated immediately if the findings suggest bacterial meningitis. If there is a high level of
concern based upon clinical findings, empiric antibiotics should be administered immediately after the
LP is performed without waiting for results. Empiric treatment is summarized in the table and discussed
in greater detail separately (table 1). (See "Bacterial meningitis in children older than one month:
Treatment and prognosis", section on 'Empiric therapy'.)
Microbiologic tests
Cerebrospinal fluid Gram stain — The presence of an organism on CSF Gram stain can suggest
the bacterial etiology one day or more before culture results are available. The absence of organisms on
Gram stain does not exclude the diagnosis [59]. The likelihood of detecting bacteria on Gram stain
depends upon the number of organisms present and is enhanced by cytocentrifugation [60].
The likelihood of detecting bacteria also depends on the pathogen. CSF Gram stain is positive in
approximately 80 to 90 percent of children with pneumococcal meningitis [31] and 70 to 80 percent of
children with meningococcal meningitis [61]. In contrast, the Gram stain is positive in only one-half of
patients with gram-negative bacillary meningitis and one-third of patients with Listeria meningitis
[62,63].
Characteristic morphologic features of the common pathogens for bacterial meningitis in children are as
follows:
●Gram-positive diplococci suggest S. pneumoniae (picture 5)
●Gram-negative diplococci suggest N. meningitidis (picture 6)
●Small pleomorphic gram-negative coccobacilli suggest Hib (picture 7)
●Gram-positive cocci or coccobacilli suggest group B streptococcus (GBS) (picture 8)
●Gram-positive rods and coccobacilli suggest L. monocytogenes (picture 9)
Gram stain results are subject to observer misinterpretation, and, therefore, broad-spectrum
antimicrobial therapy should be continued until CSF culture results are available [64]. (See "Bacterial
meningitis in children older than one month: Treatment and prognosis", section on 'Empiric therapy'.)
Cerebrospinal fluid culture — CSF cultures should be performed in all cases of suspected
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bacterial meningitis, regardless of the CSF cell count. Early in the disease process, the CSF culture may
be positive in the absence of pleocytosis [48].
Isolation of a bacterial pathogen from the CSF culture confirms the diagnosis of bacterial meningitis.
However, CSF culture may be negative in children pretreated with antibiotics prior to LP [48,65,66].
This is particularly true of meningococcal meningitis, in which the CSF is rapidly sterilized following
administration of parenteral antibiotics [65,66]. CSF cultures can also be negative if bacteria are
sequestered in pockets adjacent to, but not directly communicating with, the CSF (eg, epidural or
subdural abscess).
In one review of 128 children with bacterial meningitis, CSF cultures were positive in 97 percent of
patients who hadn't received any antibiotics, 67 percent of those pretreated with oral antibiotics, and
56 percent of those pretreated with parenteral antibiotics [65]. The likelihood of isolating an organism
in CSF culture in pretreated patients depends in part upon the causative pathogen and the time interval
between administering antibiotics and performing the LP. The study described above demonstrated this
by reviewing CSF culture results of 55 children with bacterial meningitis who underwent serial LPs
before and after administration of parenteral antibiotics [65] Among the nine children with
meningococcal meningitis, all had sterile CSF cultures within two hours of receiving antibiotics (three
were sterile within one hour). Sterilization of the CSF was slower with pneumococcal meningitis. The
first negative culture was obtained four hours after administration of antibiotics, and five of seven were
negative by 10 hours.
Other cultures — Culture of other sites should be obtained as indicated:
●Blood culture should be obtain in all patients, as discussed above. (See 'Blood tests' above.)
●Urine culture – Urine cultures should be obtained in infants (<12 months of age) who present with
fever and nonspecific symptoms and signs of meningitis since a urinary tract infection may be the
primary source of the meningitis pathogen in such patients [67]. However, a CSF pleocytosis can be
seen in infants with urinary tract infection and sterile CSF cultures [67-70]. In such cases, the CSF
pleocytosis may be related to a viral meningitis or an innate response to bacteria or bacterial products
[71-73].
Urine cultures also should be obtained in children with anomalies of the urinary tract and in
immunocompromised patients.
If possible, urine for culture should be obtained before antimicrobial therapy is administered. However,
therapy should not be withheld if an adequate specimen cannot be promptly obtained.
●Skin biopsy – Gram stain and culture of purpuric lesions may have some use in the diagnosis of
suspected meningococcal disease [74]. (See "Diagnosis of meningococcal infection", section on 'Skin
biopsy'.)
●Middle ear fluid – In patients with concomitant otitis media or mastoiditis, a tympanocentesis can be
performed to obtain middle ear fluid for Gram stain and culture, which may be helpful, particularly if
CSF culture is negative. (See "Acute mastoiditis in children: Treatment and prevention", section on
'Drainage'.)
●No role for throat or nasopharyngeal cultures – Cultures of the nose and throat are not helpful in
identifying the etiology of bacterial meningitis.
Molecular methods — Molecular methods (ie, polymerase chain reaction [PCR] and other
nucleic acid amplification test [NATs]) are increasingly used to assist in the diagnosis of central nervous
system (CNS) infections. (See "Molecular diagnosis of central nervous system infections".)
●Multiplex (panel-based) testing – Multiplex or panel-based NATs are now available that test for
multiple bacterial and viral pathogens simultaneously in a single CSF sample (eg, FilmArray

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meningitis/encephalitis panel [BioFire]) [75-78]. These tests are highly sensitive and specific, though
false-positive and false-negative results can occur. If a multiplex panel is performed, it should be used
in conjunction with standard microbiologic tests (eg, cultures of CSF and blood). Multiplex panels do not
detect all causes of CNS infection nor do they provide any information on antimicrobial susceptibility.
●Meningococcal PCR – PCR of CSF and blood can be helpful for documenting meningococcal disease in
the patient with negative cultures [79]. (See "Diagnosis of meningococcal infection", section on
'Polymerase chain reaction'.)
●Loop-mediated isothermal amplification (LAMP) – LAMP is another promising nucleic acid
amplification method for rapid detection of meningococcus in respiratory and blood samples of infected
children, but it is not yet commercially available [80].
Bacterial antigen tests — CSF latex agglutination tests add little to conventional testing with
Gram stain and culture [81,82]. These tests are rarely used in the current era, given the availability of
molecular tests, which are more sensitive and specific. However, in settings where molecular testing is
not available, latex agglutination tests may play a role, particularly in children with negative bacterial
cultures.
Assessment of immune function — The possibility of an immune deficiency or anatomic
predisposition should be considered in the following settings:
●Hib meningitis or pneumococcal meningitis – For children who develop Hib meningitis or
pneumococcal meningitis with a serotype contained in the pneumococcal vaccine despite having
received at least three doses of the respective conjugate vaccines, it is reasonable to screen for
underlying immune deficiency. This is particularly warranted if there are additional concerning features
in the history or physical examination (eg, recurrent infections, poor growth). The initial evaluation
may include measuring quantitative immunoglobulins, antibody titers to vaccine antigens, and
complement activity. In addition, examining the peripheral blood smear may be helpful because the
presence of Howell-Jolly bodies (picture 10) may indicate splenic hypofunction. The approach to
evaluating immune function in children is discussed in greater detail separately. (See "Approach to the
child with recurrent infections" and "Primary humoral immunodeficiencies: An overview" and "Assessing
antibody function as part of an immunologic evaluation".)
●Unusual pathogens – If an unusual organism, such as S. aureus or another organism that commonly
colonizes the skin, is isolated, a direct connection to the skin via a sinus tract should be sought [83].
Neuroimaging — In select children, it is appropriate to delay the LP while performing neuroimaging
(typically with computed tomography) to exclude an intracranial process that would contraindicate an
LP.
Indications for neuroimaging before LP in children with suspected bacterial meningitis include (table 1)
[64]:
●Coma
●Papilledema
●Focal neurologic deficit (with the exception of palsy of cranial nerve VI [abducens nerve] or VII [facial
nerve])
●CSF shunt in place
●History of hydrocephalus
●Recent CNS trauma or neurosurgery
In children who require neuroimaging before LP, blood cultures should be obtained and empiric

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antibiotics administered before imaging (table 1) [64]. LP should be performed as soon as possible after
neuroimaging, provided that neuroimaging has not revealed any contraindications.
In patients with confirmed bacterial meningitis, herniation following LP is uncommon in the absence of
focal neurologic findings or coma [84].
DIAGNOSIS — Acute bacterial meningitis should be suspected in children who present with fever and
signs of meningeal inflammation. (See 'Presentation' above.)
The diagnosis of bacterial meningitis is confirmed by any of the following:
●Isolation of a bacterial pathogen from the cerebrospinal fluid (CSF) culture (see 'Cerebrospinal fluid
culture' above)
●Isolation of bacteria from blood cultures in a patient with CSF pleocytosis (see 'Blood tests' above)
●Detection of a bacterial pathogen in the CSF by molecular methods (see 'Molecular methods' above)
The CSF culture may be negative in children who received antibiotic therapy before CSF examination.
In such children, increased CSF cell count with a predominance of neutrophils, elevated CSF protein
concentration, and/or decreased CSF glucose concentration usually are sufficient to establish the
diagnosis of bacterial meningitis [54-57]; blood cultures and/or molecular tests may help to identify the
specific pathogen [78]. (See 'Interpretation' above and 'Molecular methods' above.)
A negative culture of the CSF does not preclude the development of meningitis hours or days after
lumbar puncture (LP); if clinical signs strongly suggest meningitis, repeat LP may be warranted. (See
"Bacterial meningitis in children older than one month: Treatment and prognosis", section on 'Repeat
lumbar puncture'.)
DIFFERENTIAL DIAGNOSIS
Fever, neck stiffness, and abnormal mental status — The characteristic presentation of meningitis
is a triad of fever, neck stiffness, and abnormal mental status (eg, lethargy, confusion, irritability). Many
other conditions can present with similar manifestations. The cerebrospinal fluid (CSF) examination and
bacterial cultures differentiate bacterial meningitis from other causes:
●Febrile illness – Children with other infectious conditions can present with a constellation of
symptoms that mimic meningitis. In a review of 650 children (ages 0 to 12 years) who underwent
lumbar puncture (LP) for evaluation of possible meningitis, CSF findings were normal in 57 percent of
patients [28]. Indications for LP included fever; headache; vomiting; nuchal rigidity; first episode of
convulsion with fever; and encephalopathic, toxic, or septic appearance. Common conditions among
children with normal CSF findings included:
•Right-sided pneumonia
•Otitis media presenting with fever and irritability
•Pharyngitis/tonsillitis
•Upper respiratory infection with cervical adenopathy
•Viral infection/herpangina (predominantly in children <5 years)
•Gastroenteritis
●Nuchal rigidity – While nuchal rigidity is highly suggestive of meningitis, it can occur in other
conditions, such as retropharyngeal abscess, cervical spine injury or infection, and many others, as
summarized in the table (table 3). The approach to evaluating neck stiffness in children is discussed
separately. (See "Approach to neck stiffness in children".)

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●Depressed mental status – Important causes of altered depressed mental status in children include
head trauma, seizure, and ingestions (table 7). (See "Evaluation of stupor and coma in children" and
"Approach to the child with occult toxic exposure".)
Cerebrospinal fluid pleocytosis — The clinical and laboratory findings of bacterial meningitis overlap
with those of aseptic or viral meningitis (table 5 and table 6). In patients with CSF pleocytosis, clinical
prediction rules can be used in conjunction with clinical judgment to identify patients with a very low
risk of bacterial meningitis. The approach is summarized in the algorithm and discussed in greater
detail separately (algorithm 1). (See "Viral meningitis in children: Management, prognosis, and
prevention", section on 'Assessing risk of bacterial meningitis'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected
countries and regions around the world are provided separately. (See "Society guideline links: Bacterial
meningitis in infants and children".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The
Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at
the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview and who
prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more
sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and
are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or
email these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on "patient info" and the keyword[s] of interest.)
●Basics topics (see "Patient education: Meningitis in children (The Basics)" and "Patient education:
Bacterial meningitis (The Basics)")
●Beyond the Basics topic (see "Patient education: Meningitis in children (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Streptococcus pneumoniae and Neisseria meningitidis are the most common causes of bacterial
meningitis in infants and children older than one month of age. Risk factors for bacterial meningitis
include anatomic defects of the spinal cord, brain, or inner ear; acquired cranial defects due to basilar
skull fracture or surgery; medical device (eg, cerebrospinal fluid [CSF] shunt, cochlear implant);
congenital or acquired immunodeficiency; parameningeal infections (eg, sinusitis, mastoiditis); recent
infection (especially respiratory and ear infections); recent exposure to someone with meningitis; and
recent travel to an area with endemic meningococcal disease, such as sub-Saharan Africa. (See
'Epidemiology' above.)
●Most patients with bacterial meningitis present with fever and symptoms and signs of meningeal
inflammation, such as nuchal rigidity (movie 1A-B), headache, photophobia, and irritability. However,
the clinical manifestations of bacterial meningitis are variable and nonspecific; no single sign is
pathognomonic. (See 'Clinical features' above.)
●The laboratory evaluation of children with suspected meningitis includes (see 'Evaluation' above):
•Blood tests (see 'Blood tests' above):
-Aerobic blood culture
-Complete blood count with differential
-Inflammatory markers (eg, C-reactive protein, procalcitonin)

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-Serum electrolytes, glucose, blood urea nitrogen, and creatinine
-Coagulation studies (prothrombin time [PT], international normalized ratio [INR], activated partial
thromboplastin time [aPTT])
-Lactate level if there is concern for septic shock
•CSF studies (see 'Lumbar puncture' above):
-Cell count and differential
-Glucose and protein concentration
-Gram stain and culture
If there is a contraindication to or inability to perform the lumbar puncture (LP) or if the LP is delayed
by the need for neuroimaging, blood cultures should be obtained and empiric antibiotics administered as
soon as possible (table 1). (See 'Neuroimaging' above and 'Initiation of empiric therapy' above.)
●Laboratory findings characteristic of bacterial meningitis include CSF pleocytosis with a predominance
of neutrophils, elevated CSF protein, decreased CSF glucose, and presence of an organism on CSF Gram
stain (table 5 and table 6). (See 'Interpretation' above.)
●The diagnosis of bacterial meningitis is confirmed by any of the following (see 'Diagnosis' above):
•Isolation of a bacterial pathogen from the CSF culture (see 'Cerebrospinal fluid culture' above)
•Isolation of bacteria from blood cultures in a patient with CSF pleocytosis (see 'Blood tests' above)
•Detection of a bacterial pathogen in the CSF by molecular methods (see 'Molecular methods' above)
●Conditions that can present with symptoms similar to those of bacterial meningitis include other febrile
illnesses (eg, pneumonia, otitis media), other conditions associated with neck stiffness (table 3), and
other causes of altered depressed mental status (table 7). The CSF examination and bacterial cultures
differentiate bacterial meningitis from other causes. (See 'Differential diagnosis' above.)
●The clinical and laboratory findings of bacterial meningitis overlap with those of aseptic or viral
meningitis (table 5 and table 6). In patients with CSF pleocytosis, clinical prediction rules can be used
in conjunction with clinical judgment to identify patients with a very low risk of bacterial meningitis.
The approach is summarized in the algorithm and discussed in greater detail separately (algorithm 1).
(See "Viral meningitis in children: Management, prognosis, and prevention", section on 'Assessing risk
of bacterial meningitis'.)
Use of UpToDate is subject to the Subscription and License Agreement
Topic 5968 Version 37.0
© 2021 UpToDate, Inc. and/or its affiliates. All rights reserved.

Our suggested approach to determining the need for empiric
antibiotic therapy in children with CSF pleocytosis*
This algorithm summarizes the approach to determining the need for empiric
antibiotic therapy while awaiting bacterial cultures and PCR studies in children with
CSF pleocytosis. It is intended for use in conjunction with other UpToDate content on
viral and bacterial meningitis in children. For guidance on appropriate empiric
antibiotic regimens, refer to UpToDate's topic on bacterial meningitis in children.
CSF: cerebrospinal fluid; LP: lumbar puncture; BMS: bacterial meningitis score; ANC:
absolute neutrophil count; PCR: polymerase chain reaction; WBC: white blood cell; MSE:
meningitis score for emergencies; CRP: C-reactive protein.
* The definition of CSF pleocytosis differs in young infants versus older infants and children.
In young infants (1 to 3 months of age), a CSF WBC count >9/microL is considered
abnormal; in children and infants >3 months of age, a CSF WBC count >6/microL is
abnormal. Refer to separate UpTo Date topics on meningitis in children for additional details
of CSF interpretation, including interpreting traumatic LPs and LPs in children pretreated
with antibiotics.
¶ The BMS [1] is the most well-studied and most commonly used clinical prediction rule for
bacterial meningitis. The MSE[2] is an alternate tool that can be used in conjunction with the
BMS to improve the sensitivity, specificity, and negative predictive value. The MSE assigns
points for the following variables: serum procalcitonin >1.20 ng/mL (3 points), serum CRP
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>40 mg/L (1 point), CSF ANC >1000/mcL (1 point), CSF protein >80 mg/dL (2 points). If
both scores are 0, the patient can be classified as "very low risk". If it is not possible to
determine the MSE (eg, because serum CRP or procalcitonin levels were not measured or
not available), the BMS can be used alone.
Δ Factors that may suggest Lyme meningitis include living in or recent travel to an endemic
area, preceding tick bite and/or erythema migrans, prolonged duration of symptoms (>7
days), and the presence of a facial nerve palsy. Refer to separate UpToDate content on
Lyme meningitis for additional details.
◊ Important considerations include the age and clinical status of the child, season (ie,
likelihood of enteroviral infection), exposure history, and findings of the initial evaluation. In
view of the serious consequences of delayed treatment for bacterial meningitis, the
threshold to initiate empiric antibiotic therapy should be relatively low.
References:
1. Nigrovic LE, Kuppermann N, Macias CG, et al. Clinical prediction rule for identifying
children with cerebrospinal fluid pleocytosis at very low risk of bacterial meningitis.
JAMA 2007; 297:52.
2. Mintegi S, García S, Martín MJ, et al. Clinical Prediction Rule for Distinguishing
Bacterial From Aseptic Meningitis. Pediatrics 2020; 146:e20201126.
Graphic 129845 Version 2.0
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Areas with frequent epidemics of meningococcal meningitis
Disease data source: World Health Organization. International Travel and Health. Geneva, Switzerland: 2012.
Reproduced from: Mbaeyi SA, McNamara LA. Travel-Related Infectious Diseases: Meningococcal Disease. In: CDC Ye
2020, Brunette GW, Nemhauser JB (Eds), Oxford University Press, New York 2019. Available at: https://wwwnc.cdc.g
/yellowbook/2020/table-of-contents (Accessed on August 2, 2019).
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Third nerve palsy of the left eye
Clinical features of third nerve palsy may include ptosis and pupillary dilation (all
images), exotropia and hypotropia in neutral gaze (central image), limited adduction
(left column), limited elevation (top row), and limited depression (bottom row).
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Dermal sinus
Dermal sinus lesions may predispose to meningitis with Staphylococcus
aureus, coagulase-negative staphylococci, and enteric gram-negative
organisms, such as Escherichia coli and Klebsiella species.
Courtesy of Sheldon L Kaplan, MD.
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Bilateral superior oblique palsy
A patient with a bilateral fourth nerve palsy demonstrates a reversing
hypertropia (left hypertropia in right gaze and a right hypertropia in left gaze
in the middle panels right and left). The primary position deviation is not
readily apparent, because of the bilateral palsy (middle row, center panel).
There is underaction of both superior oblique muscles (right lower and left
lower panels). There is overaction of the inferior oblique muscle bilaterally
(right upper and left upper panels).
Reproduced with permission from: Tasman W, Jaeger E. The Wills Eye Hospital
Atlas of Clinical Ophthalmology, 2nd ed, Lippincott Williams & Wilkins, Philadelphia
2001. Copyright ©2001 Lippincott Williams & Wilkins.
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Petechiae
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Courtesy of Leslie Raffini, MD.
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Acute meningococcemia
Skin lesions in acute meningococcemia can begin as papules but quickly
progress to petechiae and purpura. As seen here, the purpuric lesions
can coalesce.
Courtesy of Charles V Sanders. (The Skin and Infection: A Color Atlas and
Text, Sanders CV, Nesbitt, LT Jr [Eds], Williams & Wilkins, Baltimore, 1995).
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Streptococcus pneumoniae in cerebrospinal fluid
Gram stain of cerebrospinal fluid (x1000) shows inflammatory cells and
gram-positive diplococci. Streptococcus pneumoniae grew from this
specimen.
Courtesy of Harriet Provine.
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Neisseria meningitidis in cerebrospinal fluid
kidney-shaped, gram-negative diplococci (arrows). Neisseria
meningitidis grew from this specimen.
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Haemophilus influenzae in cerebrospinal fluid
small, pleomorphic, gram-negative coccobacilli. Haemophilus influenzae
grew from this specimen.
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Group B streptococcus in cerebrospinal fluid
gram-positive coccobacilli. Streptococcus agalactiae (group B
streptococcus) grew from this specimen.
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Listeria monocytogenes in cerebrospinal fluid
small, gram-positive rods and coccobacilli. Culture of this specimen
revealed moderate-sized beta-hemolytic colonies composed of small,
motile gram-positive rods, confirmed to be Listeria monocytogenes.
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Howell-Jolly bodies following splenectomy
This peripheral blood smear shows 2 RBCs that contain Howell-Jolly
bodies (arrowheads). Howell-Jolly bodies are remnants of RBC nuclei
that are normally removed by the spleen. Thus, they are seen in patients
who have undergone splenectomy (as in this case) or who have
functional asplenia (eg, from sickle cell disease). Target cells (arrows)
are another consequence of splenectomy.
RBC: red blood cell.
Courtesy of Carola von Kapff, SH (ASCP).
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Normal peripheral blood smear
High-power view of a normal peripheral blood smear. Several platelets
(arrowheads) and a normal lymphocyte (arrow) can also be seen. The
red cells are of relatively uniform size and shape. The diameter of the
normal red cell should approximate that of the nucleus of the small
lymphocyte; central pallor (dashed arrow) should equal one-third of its
diameter.
Courtesy of Carola von Kapff, SH (ASCP).
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Clinical findings
Infants – Fever, hypothermia, bulging fontanel, lethargy, irritability, seizures, respiratory distress, poor
feeding, vomiting.
Older children – Fever, headache, photophobia, meningismus, nausea/vomiting, confusion, lethargy,
irritability.
Evaluation
Laboratory testing – Initial laboratory testing should include (STAT):
Blood culture.
CBC with differential and platelet count.
Inflammatory markers (CRP, procalcitonin).
Serum electrolytes, BUN, creatinine, glucose.
PT, INR, and PTT.
Lumbar puncture (LP):
LP should be performed in all children with suspected meningitis, unless there is a specific
contraindication to LP.
Contraindications to LP include: cardiopulmonary compromise, clinical signs of increased intracranial
pressure, papilledema, focal neurologic signs, and skin infection over the site for LP. If there is a
contraindication to or inability to perform an LP, or if the LP is delayed by the need for cranial
imaging, antimicrobial therapy should not be delayed. Blood cultures should be obtained and empiric
antibiotics administered as soon as is possible.
CSF should be sent for the following (STAT): cell count and differential, glucose and protein
concentration, Gram stain, and culture.
Neuroimaging (eg, head CT):
In children who require neuroimaging before LP, blood cultures should be obtained and empiric
antibiotics administered before imaging. LP should be performed as soon as possible
after neuroimaging is completed, provided that the imaging has not revealed any contraindications.
Indications for neuroimaging before LP include: severely depressed mental status (coma),
papilledema, focal neurologic deficit (with the exception of cranial nerve VI or VII palsy), history of
hydrocephalus and/or presence of a CSF shunt, recent history of CNS trauma or neurosurgery.
Management
Supportive care:
Ensure adequate oxygenation, ventilation, and circulation.
Obtain venous access and initiate cardiorespiratory monitoring while obtaining laboratory studies.
Keep the head of bed elevated at 15 to 20°.
Treat hypoglycemia, acidosis, and coagulopathy, if present.
Antimicrobial therapy – Antibiotic therapy should be initiated immediately following the LP if the clinical
suspicion for meningitis is high:
Administer first doses of empiric antibiotic therapy:
Vancomycin (15 mg/kg IV), PLUS
Ceftriaxone (50 mg/kg IV) or cefotaxime (100 mg/kg IV; where available).
Consider dexamethasone therapy* (0.15 mg/kg IV) in patients with certain risk factors (eg,
unimmunized patients, young children [age ≥6 weeks to ≤5 years], children with sickle cell disease,
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Rapid overview: Emergency management of infants (≥1 month) and children
with suspected bacterial meningitis
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asplenic patients) or if there is known or suspected Haemophilus influenzae infection (eg, based on
Gram stain results).
If dexamethasone is given, it should be administered before, or immediately after, the first dose of
antibiotic therapy.
STAT: intervention should be performed emergently; CBC: complete blood count; CRP: C-reactive protein; BUN:
blood urea nitrogen; PT: prothrombin time; INR: international normalized ratio; PTT: partial thromboplastin time;
LP: lumbar puncture; CT: computed tomography; CSF: cerebrospinal fluid; CNS: central nervous system; IV:
intravenous.
* Decisions regarding the administration of dexamethasone should be individualized. The use of dexamethasone in
children with suspected meningitis is controversial, and the opinions of UpToDate authors regarding this issue differ.
One UpToDate author would administer dexamethasone only to children who are known or highly suspected to have
H. influenzae (Hib) at the time the LP is performed (a fairly uncommon scenario), whereas another UpToDate
author would administer dexamethasone to all young children (age ≥6 weeks to ≤5 years old) with community-
acquired meningitis and to children with sickle cell disease or asplenia with suspected bacterial meningitis. The 2018
Red Book statement on dexamethasone use in pneumococcal meningitis also acknowledges that expert opinion
differs on this issue. Evidence supporting the efficacy of dexamethasone in reducing the risk of hearing loss in
children with meningitis is most clearly established for infections caused by Hib. For other bacterial pathogens (eg,
pneumococcus, meningococcus), the efficacy of dexamethasone is uncertain. For further details, refer to UpToDate
topics on bacterial meningitis in children, pneumococcal meningitis in children, and the use of dexamethasone and
other measures to prevent neurologic complications of pediatric bacterial meningitis.
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Organism Site of entry Age range Predisposing conditions
Neisseria
meningitidis
Nasopharynx All ages Usually none, rarely complement deficiency
Streptococcus
pneumoniae
Nasopharynx, direct
extension across skull
fracture, or from
contiguous or distant foci
of infection
All ages All conditions that predispose to
pneumococcal bacteremia, fracture of
cribriform plate, cochlear
implants, cerebrospinal fluid otorrhea from
basilar skull fracture, defects of the ear
ossicle (Mondini defect)
Listeria
monocytogenes
Gastrointestinal tract,
placenta
Older adults
and neonates
Defects in cell-mediated immunity (eg,
glucocorticoids, transplantation [especially
renal transplantation]), pregnancy, liver
disease, alcoholism, malignancy
Coagulase-
negative
staphylococci
Foreign body All ages Surgery and foreign body, especially
ventricular drains
Staphylococcus
aureus
Bacteremia, foreign
body, skin
All ages Endocarditis, surgery and foreign body,
especially ventricular drains; cellulitis,
decubitus ulcer
Gram-negative
bacilli
Various Older adults
and neonates
Advanced medical illness, neurosurgery,
ventricular drains, disseminated
strongyloidiasis
Haemophilus
influenzae
Nasopharynx,
contiguous spread from
local infection
Adults; infants
and children if
not vaccinated
Diminished humoral immunity
Characteristic features of common causes of bacterial meningitis
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Trauma
Clavicular fracture*
Epidural hematoma of the cervical spine ¶
Fracture of the cervical spine ¶
Muscular contusion or neck spasm*
SCIWORA syndrome¶
Subarachnoid hemorrhage ¶
Subluxation of the cervical spine ¶
Infectious or inflammatory
Bacterial meningitis¶
Branchial cleft or thyroglossal duct cyst abscess
Cervical lymphadenitis*
Collagen vascular disease (eg, systemic JIA, ankylosing spondylitis, psoriatic arthritis)
Infections of the spine – Vertebral osteomyelitis, infectious discitis, epidural abscess¶
Intervertebral disc calcification
Kawasaki disease with cervical lymphadenopathy
Lyme meningitis
Muscle strain*
Otitis media and mastoiditis
Pharyngitis or tonsillitis*
Retropharyngeal abscess¶
Rotary atlantoaxial subluxation as a result of local inflammation or procedure (Grisel syndrome)
Upper lobe pneumonia
Viral meningitis*
Viral myositis
Tumors, other space-occupying and vascular lesions of the central nervous
system
Brain tumor ¶
Other space-occupying lesions of the spinal cord (neurenteric cyst, arteriovenous malformation,
syringomyelia) ¶
Other tumors of the head and neck (osteoid osteoma, eosinophilic granuloma, orbital tumor, acoustic
neuroma, osteoblastoma, metastatic tumor to the spine, nasopharyngeal carcinoma, bone cyst)¶
Spinal cord tumor ¶
Subarachnoid hemorrhage (aneurysm rupture-congenital, sickle cell disease) ¶
Congenital conditions
Causes of neck stiffness in children
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Atlantoaxial instability secondary to congenital conditions (Down syndrome, Klippel-Feil syndrome, os
odontoideum, Morquio syndrome)
Benign paroxysmal torticollis
Congenital muscular torticollis*
Skeletal malformations (Klippel-Feil syndrome, Sprengel deformity, hemiatlas, basilar impression,
occipitocervical synostosis)
Miscellaneous
Dystonic reaction
Guillain-Barre syndrome
Myasthenia gravis
Ophthalmologic, neurologic, and/or vestibular causes (strabismus, cranial nerve palsies, extraocular
muscle palsies, refractive errors, myasthenia gravis, Guillain-Barre syndrome, migraine headaches)
Idiopathic intracranial hypertension
Psychogenic
Sandifer syndrome
Spasmus nutans
Spontaneous pneumomediastinum
SCIWORA: spinal cord injury without radiographic abnormality; JIA: juvenile idiopathic arthritis.
* Common condition.
¶ Life-threatening condition.
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Sign
Glasgow Coma
Scale[1] Pediatric Glasgow Coma Scale[2] Score
Eye opening Spontaneous Spontaneous 4
To command To sound 3
To pain To pain 2
None None 1
Verbal
response
Oriented Age-appropriate vocalization, smile, or orientation to
sound; interacts (coos, babbles); follows objects
5
Confused, disoriented Cries, irritable 4
Inappropriate words Cries to pain 3
Incomprehensible
sounds
Moans to pain 2
None None 1
Motor
response
Obeys commands Spontaneous movements (obeys verbal command) 6
Localizes pain Withdraws to touch (localizes pain) 5
Withdraws Withdraws to pain 4
Abnormal flexion to pain Abnormal flexion to pain (decorticate posture) 3
Abnormal extension to
pain
Abnormal extension to pain (decerebrate posture) 2
None None 1
Best total score 15
Glasgow Coma Scale and Pediatric Glasgow Coma Scale
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The Glasgow Coma Scale (GCS) is scored between 3 and 15, with 3 being the worst and 15 the best. It is
composed of 3 parameters: best eye response (E), best verbal response (V), and best motor response (M).
The components of the GCS should be recorded individually; for example, E2V3M4 results in a GCS of 9. A
score of 13 or higher correlates with mild brain injury, a score of 9 to 12 correlates with moderate injury,
and a score of 8 or less represents severe brain injury. The Pediatric Glasgow Coma Scale (PGCS) was
validated in children 2 years of age or younger.
Data from:
1. Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet 1974;
2:81.
2. Holmes JF, Palchak MJ, MacFarlane T, Kuppermann N. Performance of the pediatric Glasgow coma scale in
children with blunt head trauma. Acad Emerg Med 2005; 12:814.
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Glucose (mg/dL) Protein (mg/dL)
Total white blood cell count
(cells/microL)
<10¶ 10 to 40Δ 100 to
500◊ 50 to 300§ >1000
100 to
1000
5 to 100
More
common
Bacterial
meningitis
Bacterial
meningitis
Bacterial
meningitis
Viral meningitis
Nervous system
Lyme disease
(neuroborreliosis)
Encephalitis
Bacterial
meningitis
Bacterial or
viral
meningitis
TB
meningitis
Early
bacterial
meningitis
Viral
meningitis
Neurosyphilis Neurosyphilis
TB meningitis¥ TB
meningitis
Less
common
TB
meningitis
Fungal
meningitis
Neurosyphilis
Some viral
infections
(such as
mumps and
LCMV)
Early bacterial
meningitis
Some
cases of
mumps
and LCMV
Encephalitis Encephalitis
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Typical cerebrospinal fluid findings in central nervous system infections*
36 of 39 20-Aug-21 9:33 AM
TB: tuberculosis; LCMV: lymphocytic choriomeningitis virus.
* It is important to note that the spectrum of cerebrospinal fluid values in bacterial meningitis is so wide that the
absence of one or more of these findings is of little value. Refer to the UpToDate topic reviews on bacterial
meningitis for additional details.
¶ <0.6 mmol/L.
Δ 0.6 to 2.2 mmol/L.
◊ 1 to 5 g/L.
§ 0.5 to 3 g/L.
¥ Cerebrospinal fluid protein concentrations may be higher in some patients with tuberculous meningitis;
concentrations >500 mg/dL are an indication of blood-brain barrier disruption or increased intracerebral production
of immunoglobulins, and extremely high concentrations, in the range of 2 to 6 g/dL, may be found in association
with subarachnoid block.

Feature Viral meningitis Bacterial meningitis
Seasonal pattern Enteroviral infections (the most
common cause of viral meningitis)
occur mostly in summer and fall
No characteristic seasonal pattern
Clinical features
Fever, headache, stiff neck,
photophobia
Common Common
Ill appearance Uncommon Common
Petechiae or purpura Absent May be present
Other manifestations of
enteroviral infection (eg, rash,
conjunctivitis, herpangina,
pharyngitis)
Common Uncommon
Symptoms after LP Often, there is improvement No improvement
CSF parameters
WBC count Typically 10 to 500 cells/microL Typically >1000 cells/microL, but
can be lower, particularly early in
the course
Differential Mononuclear predominance Neutrophil predominance
Glucose Normal or slightly reduced
Usually ≥40% of serum value
Usually <60% of serum value
Often <40 mg/dL
Protein Normal to slightly elevated
Usually <150 mg/dL
Typically 100 to 500 mg/dL
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Clinical and laboratory features of viral and bacterial meningitis in children
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This table summarizes the typical findings in viral and bacterial meningitis in children. However, there is
considerable overlap between the two conditions and these features do not reliably distinguish between
them. In addition, there is considerable overlap between viral meningitis and Lyme meningitis, which is also
characterized by lymphocyte-predominant pleocytosis. In Lyme-endemic areas during the summer and fall,
it can be difficult to distinguish Lyme meningitis from enteroviral meningitis unless the patient had a known
tick bite and/or erythema migrans. For additional details, including use of clinical prediction rules to identify
children at low risk of bacterial meningitis, refer to separate UpToDate content on viral, bacterial, and Lyme
meningitis.
LP: lumbar puncture; CSF: cerebrospinal fluid; WBC: white blood cell.

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I. Symmetrical, nonstructural II. Symmetrical, structural
Toxins Supratentorial
Lead Bilateral internal carotid occlusion
Thallium Bilateral anterior cerebral artery occlusion
Mushrooms Sagittal sinus thrombosis
Cyanide Subarachnoid hemorrhage
Methanol Thalamic hemorrhage*
Ethylene glycol Trauma-contusion, concussion*
Carbon monoxide Hydrocephalus
Drugs Infratentorial
Sedatives Basilar occlusion*
Barbiturates* Midline brainstem tumor
Other hypnotics Pontine hemorrhage*
Tranquilizers Central pontine myelinolysis
Bromides III. Asymmetrical, structural
Alcohol
Supratentorial
Opiates
Thrombotic thrombocytopenic purpura¶
Paraldehyde
Disseminated intravascular coagulation
Salicylate
Nonbacterial thrombotic endocarditis (marantic
endocarditis)
Psychotropics
Anticholinergics Subacute bacterial endocarditis
Amphetamines Fat emboli
Lithium Unilateral hemispheric mass (tumor, abscess,
bleed) with herniation
Phencyclidine
Subdural hemorrhage bilateral
Monoamine oxidase inhibitors
Intracerebral bleed
Metabolic
Pituitary apoplexy¶
Hypoxia
Massive or bilateral supratentorial infarction
Hypercapnia
Multifocal leukoencephalopathy
Hypernatremia*
Creutzfeldt-Jakob disease
Hypoglycemia*
Adrenal leukodystrophy
Hyperglycemic nonketotic coma
Cerebral vasculitis
Diabetic ketoacidosis
Cerebral abscess
Lactic acidosis
Subdural empyema
Hypercalcemia
Thrombophlebitis¶
Hypocalcemia
Multiple sclerosis
Hypermagnesemia
Causes of coma
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Hyperthermia
Hypothermia
Reye syndrome
Aminoacidemia
Wernicke encephalopathy
Porphyria
Hepatic encephalopathy*
Uremia
Dialysis encephalopathy
Addisonian crisis
Hypothyroidism
Infections
Bacterial meningitis
Viral encephalitis
Postinfectious encephalomyelitis
Syphilis
Sepsis
Typhoid fever
Malaria
Waterhouse-Friderichsen syndrome
Psychiatric
Catatonia
Other
Postictal seizure*
Diffuse ischemia (myocardial infarction, heart
failure, arrhythmia)
Hypotension
Fat embolism*
Hypertensive encephalopathy
Hypothyroidism
Nonconvulsive status epilepticus
Heat stroke
Leukoencephalopathy associated with
chemotherapy
Acute disseminated encephalomyelitis
Infratentorial
Brainstem infarction
Brainstem hemorrhage
Brainstem thrombencephalitis
* Relatively common asymmetrical presentation.
¶ Relatively symmetrical presentation.
Reproduced with permission from: Berger JR. Clinical Approach to Stupor and Coma. In: Neurology in Clinical
Practice: Principles of Diagnosis and Management, 4th ed, Bradley WG, Daroff RB, Fenichel GM, Jankovic J (Eds),
Butterworth Heinemann, Philadelphia, PA 2004. p.46. Copyright © 2004 Elsevier.
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