Acute Bacterial Meningitis

Current Review and Treatment Update

Michelle VanDemark, MSN, RN, ANP-BC

KEYWORDS
 Bacterial meningitis  Empiric antimicrobial therapy
 Adjunctive corticosteroids therapy  Petechial rash  Meningeal signs

KEY POINTS
 Acute bacterial meningitis is a life-threatening central nervous system (CNS) infection that
requires prompt diagnosis and treatment.
 Bacterial meningitis is an infection of the meninges (dura mater, arachnoid, and pia mater)
that cover and protect the brain and spinal cord.
 Ninety-five percent of persons with bacterial meningitis present with 2 of the following 4
symptoms: fever, nuchal rigidity, altered mental status, and headache.
 Do not delay initiation of empiric antibiotic therapy; antibiotics should be targeted to
persons age, causative pathogen, local epidemiology trends, and patterns of drug
resistance.
 Perform an immediate lumbar puncture without a prior computed tomography scan in
persons without any risk factors for brain herniation. Risk factors include: age >60 years,
altered level of consciousness, immune status, new-onset seizures, CNS disease, or focal
neurologic deficits.
 Adjunctive dexamethasone therapy is associated with lower mortality, fewer neurologic
sequelae, and fewer hearing deficits, and is recommended for children and adults living
in developed countries with a low prevalence of human immunodeficiency virus.

INTRODUCTION

Acute bacterial meningitis is a life-threatening central nervous system (CNS) infection

that requires prompt diagnosis and treatment. The incidence of bacterial meningitis
has decreased with the widespread use of conjugate vaccines and advances in anti-
microbial therapy. However, there continue to be high mortality rates with bacterial
meningitis and significant long-term neurologic sequelae among survivors, especially
in developing countries.13 This review addresses the incidence, etiology, clinical
features, diagnostic studies, and treatment of bacterial meningitis.

Neurocritical Care, Sanford USD Medical Center, 1305 West 18th Street, Sioux Falls, SD
57117-5039, USA
E-mail address: Michelle.vandemark@sanfordhealth.org

Crit Care Nurs Clin N Am 25 (2013) 351361

http://dx.doi.org/10.1016/j.ccell.2013.04.004 ccnursing.theclinics.com
0899-5885/13/$ see front matter 2013 Elsevier Inc. All rights reserved.
352 VanDemark

Bacterial meningitis is an infection of the meninges (dura mater, arachnoid, and pia
mater) that cover and protect the brain and spinal cord. The meninges can be infected
by bacteria, virus, or fungus. Bacterial meningitis may be a community-acquired or
nosocomial infection. Nosocomial bacterial meningitis may result from a neurosurgical
procedure such as a craniotomy, spinal surgery, lumbar drain, ventriculostomy, pene-
trating head trauma, or basal skull fractures.4 The incidence of bacterial meningitis in
the United States is approximately 1.3 to 1.9 cases per 100,000 persons annually.2 In
developing countries the incidence of bacterial meningitis is much higher, with
approximately 2.6 to 6.0 cases per 100,000 persons annually.58 There is a meningitis
belt in Sub-Saharan Africa where several epidemics of meningococcal meningitis have
occurred, and where the rates have exceeded 100 cases per 100,000 persons during
an outbreak.6,9

EPIDEMIOLOGY

Common causative pathogens of bacterial meningitis include Streptococcus pneu-

monia, Neisseria meningitides, Haemophilus influenzae, group B streptococcus
(GBS), Listeria monocytogenes, and Streptococcus agalactiae. The most common
causative pathogens of bacterial meningitis are S pneumonia and N meningitides.6,10
The epidemiology of bacterial meningitis has dramatically changed in the past few de-
cades. In 1986, H influenzae was the leading cause of bacterial meningitis in the United
States, accounting for approximately 45% of cases with the median age of
15 months.6,11 With the introduction and widespread use of the H influenzae type b
conjugate vaccine in infants and children in the 1990s, H influenzae infections have
declined significantly, accounting for approximately 7% of cases of bacterial meningi-
tis.6 In 2007, the median age of persons with bacterial meningitis had increased to
41.9 years.2 The heptavalent pneumococcal conjugate vaccine was introduced in
the United States in 2000, and a tetravalent meningococcal conjugate vaccine was
introduced in 2005. At present the leading cause of bacterial meningitis is S pneumo-
niae, accounting for approximately 60% of community-acquired meningitis.2,6,10
Approximately 40% of persons with pneumococcal meningitis had a preceding sinus-
itis, otitis media, or respiratory infection.6,10 The very young and the very old are most
vulnerable for acquiring bacterial meningitis. Neonates younger than 2 months have an
immature immune system and are still at high risk for developing bacterial meningitis,
especially GBS.2 Special risk groups such as neonates, the elderly, immunocompro-
mised individuals, alcohol abusers, and pregnant women have a higher incidence of L
monocytogenes.11 Nosocomial infections following neurosurgical procedures are
often caused by staphylococci, gram-negative bacilli, or anaerobic pathogens, result-
ing in bacterial meningitis.12

PATHOPHYSIOLOGY

The pathogenesis of bacterial meningitis begins with colonization of the nasopharyn-

geal mucosa or bacteremia from a systemic infection.7,12 There are several different
routes by which bacteria enter the CNS. First, bacteria can spread hematogenously
and overcome the host defenses such as physical barriers, complement system,
and blood-brain barrier, and invade the meninges. An alternative route is direct exten-
sion through emissary veins from a localized infection in the vicinity of the subarach-
noid space such as sinusitis, otitis media, and mastoiditis. Finally, the bacteria can
directly enter the subarachnoid space by way of a nosocomial infection following a
neurosurgical procedure or a penetrating head wound.1214 The bacteria invade the
meninges through the endothelium of choroid plexus and meningeal capillaries,
 Acute Bacterial Meningitis 353

resulting in hyperemia of blood vessels that increase the permeability of the blood-
brain barrier.8,15 Once past the blood-brain barrier, bacteria proliferate because the
cerebrospinal fluid (CSF) contains low levels of immunoglobulins and complement
components with which to combat an invasion, resulting in poor opsonization and
phagocytosis. Replication and lysis of the bacteria trigger an inflammatory cascade
in the CSF and subarachnoid space.8 Meningeal inflammation develops, causing
fever, meningismus, and altered mental status. Meningeal inflammation also increases
the permeability of the blood-brain barrier, causing vasogenic edema.9 The inflamma-
tion and breakdown of bacterial products can lead to neuronal injury resulting in
hydrocephalus, vasculitis, abscess formation, and/or increased intracranial pressure
(ICP) from cerebral edema.8,12 Increased ICP can then cause decreased cerebral
perfusion pressure and ischemia.16
The earlier the infection and inflammation is treated, the better the clinical outcome.
When treatment is delayed bacteria can proliferate in the CSF, resulting in a higher
density of bacterial-breakdown products and leading to increased inflammation.
The cerebral damage results primarily from the immune response rather than the
infection of the bacteria, so neurologic injury may continue even after the completion
of antibiotic therapy.8

CLINICAL PRESENTATION

The clinical presentation of bacterial meningitis may range from an insidious progres-
sive course over 3 to 5 days of malaise, fever, irritability, or vomiting, to a rapid fulmi-
nating course.12 The classical triad of bacterial meningitis consists of fever, neck
stiffness, and altered mental status; headache is also another common symptom. A
prospective study of 696 adults with bacterial meningitis found that only 44% of cases
presented with the classic triad, whereas 95% of cases presented with at least 2 of the
4 symptoms: fever, nuchal rigidity, altered mental status, and headache.10 Fever is the
most common and nonspecific symptom.11 Meningeal irritation consists of headache,
nuchal rigidity, and photophobia. The meningeal irritation can be demonstrated by the
presence of a positive Kernigs sign or Brudzinskis sign. A positive Kernigs sign is
produced by flexing both the hip and knee then extending the leg, which elicits pain
in the hamstrings. A positive Brudzinskis sign is produced when the person is supine
and the neck is passively flexed, resulting in involuntary flexion of the legs.11 A meta-
analysis of prospective studies found that neck stiffness was 51% sensitive, the
Kernigs sign was 53% sensitive, and the Brudzinskis sign was 66% sensitive for
the diagnosis of bacterial meningitis in children.6,17 In adults, these diagnostic tests
have less sensitivity.6,18 A petechial rash can appear as tiny red or purple dots early
in the course of a meningococcal infection. This rash can then progress to nonblanch-
ing purpural blotches in 90% of children and 60% of adults with N meningitides.6 The
petechial rash can develop under elastic waist bands or stockings, or in dependent
areas such as the back of a supine person.7 Other symptoms of bacterial meningitis
may include aphasia, lethargy, malaise, vomiting, focal neurologic deficits, ataxia,
and seizures.10
Neonates and infants may not present with the classic findings of bacterial menin-
gitis, and instead may present with vague nonspecific symptoms such as a high-
pitched or moaning cry, fever, lethargy, irritability, poor feeding, vomiting, diarrhea,
respiratory distress, seizures, and bulging fontanels.14,19 These vague symptoms
make the diagnosis of meningitis challenging. In addition, health care providers should
consider the diagnosis of bacterial meningitis in any immunocompromised individual
who presents with an infectious disease and a decrease in mental status.14,16,20
354 VanDemark

DIAGNOSIS

Diagnosis of bacterial meningitis begins with a complete medical history and compre-
hensive physical examination. During the medical history one must inquire about the
persons recent illnesses, travel history, vaccinations, immunosuppressed conditions,
illicit drug use, or exposure to persons with bacterial meningitis. However, the medical
history and physical examination are not always sufficient to diagnose bacterial men-
ingitis; a lumbar puncture for CSF analysis is necessary for a definitive diagnosis.
Blood cultures should be drawn immediately. Blood cultures identify the causative or-
ganism in 50% to 80% of cases of bacterial meningitis, and should be obtained before
the initiation of antimicrobial therapy. If the person was pretreated with antibiotics, the
yield of blood cultures decreases by 20%.6,21 Controversy exists regarding whether a
computed tomography (CT) scan of the brain should be performed before a lumbar
puncture. A CT scan of the brain would determine if the person has cerebral edema.
Cerebral edema can increase the risk of brain herniation during a lumbar puncture. The
Infectious Diseases Society of America (IDSA) recommends proceeding to immediate
lumbar puncture without a prior CT scan in persons without any of the following risk
factors: age greater than 60 years; altered level of consciousness or immunocompro-
mised state (human immunodeficiency virus [HIV]/AIDS, posttransplant, receiving
immunosuppressive therapy, asplenia, cancer); new-onset seizures (within 1 week);
history of CNS disease (brain lesion, stroke, or focal infection); focal neurologic deficits
such as papilledema, dilated nonreactive pupil, gaze, or facial palsy; abnormal lan-
guage; inability to answer 2 questions or follow 2 commands; visual field abnormal-
ities; and arm or leg drift (Box 1).11,20,22,23 People identified as high risk for a lumbar
puncture should have blood cultures and initiation of empiric antibiotic therapy before
undergoing a CT scan. In the absence of any of these findings, blood cultures and a
lumbar puncture should be immediately performed, followed by administration of
empiric antibiotic therapy.22
Lumbar puncture provides for CSF analysis that identifies the organism and its sus-
ceptibility to various antibiotics. Ideally the lumbar puncture should be performed
before initiation of antimicrobial therapy to maximize the yield of cultures.7 Studies
have found that complete sterilization of the CSF can occur within 2 to 4 hours after
initiating antibiotics.7,19,24 Analysis of the CSF is the gold standard, essential for the
diagnosis of bacterial meningitis by identifying the causative organism and

Box 1
Clinical conditions that predict the need for head CT prior to a lumbar puncture when
diagnosing bacterial meningitis

 Age > 60 years

 Altered level of consciousness
 Immunocompromised state (HIV/AIDS, immunosuppressive therapy, transplant recipient)
 History of CNS disease: brain lesion, stroke or focal infection
 New-onset seizures in past week
 Focal neurologic deficits such as papilledema, dilated pupil or visual field abnormalities
 Abnormal language
 Arm or leg drift inability of answer 2 questions or follow 2 commands

Data from Refs.6,7,22,23

 Acute Bacterial Meningitis 355

susceptibility to antimicrobial therapy. CSF Gram stain was found to be positive for
bacterial meningitis in 60% to 80% of cases, with yield decreasing to 7% to 41%
among persons pretreated with antibiotics.6,11,22 If the CSF specimen is obtained
before antibiotics are started, the CSF culture is positive in 80% to 90% of cases
and is diagnostic for bacterial meningitis; however, a time frame up to 48 hours may
be needed for organism identification (Fig. 1).6
In bacterial meningitis the opening pressure of the lumbar puncture is elevated,
greater than 180 mm H2O. The CSF analysis predictive of bacterial meningitis
includes: white blood cell (WBC; leukocyte) count greater than 2000 cells/mm3 or
CSF neutrophil count of more than 1180 cells/mm3; protein concentration of more
than 220 mg/dL; or a CSF glucose concentration of less than 34 mg/dL and a CSF-
to-serum glucose ratio of less than 0.23.6,10,22 Additional CSF studies that aid in the
diagnosis include the latex agglutination antigen test and real-time polymerase chain
reaction (PCR). Real-time PCR amplifies DNA to detect the presence of bacteria. La-
tex agglutination and real-time PCR tests may be especially helpful if lumbar puncture
has been delayed and antimicrobial therapy initiated. CSF lactate concentration has
been found to be more than 90% sensitive and specific in differentiating bacterial
from aseptic meningitis. If antibiotics are administered before the lumbar puncture,
the sensitivity of CSF lactate concentration decreases to 49%, limiting the usefulness
of this test.6,25 In addition, elevated C-reactive protein (20 mg/L) and serum procal-
citonin (0.5 mg/L) concentrations are associated with bacterial meningitis rather than
aseptic meningitis.6,11,22

Fig. 1. Diagnostic algorithm for acute bacterial meningitis. a Includes those associated with
CSF shunts, hydrocephalus, or trauma, those occurring after neurosurgery, or various space-
occupying lesions. b Palsy of cranial nerve VI or VII is not an indication to delay lumbar punc-
ture. c See text for recommendations for use of adjunctive dexamethasone in infants and
children with bacterial meningitis. d See Table 1. e Dexamethasone and antimicrobial ther-
apy should be administered immediately after CSF is obtained. (From Tunkel AR, Hart BJ,
Kaplan SL, et al. Practice guidelines for the management of bacterial meningitis. Clin Infect
Dis 2004;39:1270; with permission.)
356 VanDemark

TREATMENT

Strategies used to improve clinical outcomes from bacterial meningitis include prompt
diagnosis of bacterial meningitis, and initiation of antimicrobial therapy to optimize
bacterial kill and decrease the inflammatory response in the subarachnoid space.5
Persons who present to the emergency department (ED) with a suspicion of bacterial
meningitis should receive empiric broad-spectrum antibiotics immediately until the
causative organism is identified. When selecting the most effective empiric antibiotics,
consideration should be made regarding the most likely causative organism as well as
the persons age, risk factors, immune status, setting of acquisition (community-
acquired vs nosocomial), and local epidemiology.3,6,22 If there is a delay in lumbar
puncture, antibiotic therapy should be promptly initiated. A retrospective study by
Proulx and colleagues26 found that if antibiotics are initiated within 6 hours of presen-
tation to the ED for a person with suspected bacterial meningitis, the case fatality rate
is 5% to 6%. If antibiotic therapy is initiated 6 to 8 hours after arrival the case fatality
rate increases to 45%, and if therapy starts 8 to 10 hours after arrival the case fatality
rate increases to 75%.7 Antimicrobial therapy for meningitis requires higher doses to
penetrate the blood-brain barrier and be metabolized in the CSF.1 Recommendations
by the IDSA for empiric antibiotic therapy may include third-generation cephalospo-
rins such as cefotaxime or ceftriaxone, plus penicillin G or ampicillin, plus vancomycin
(Table 1). Third-generation cephalosporins have excellent CSF penetration and pro-
vide coverage for the most common bacterial pathogens, including S pneumonia
and N meningitis.11 Penicillin G and ampicillin have been shown to be effective against
multiple bacterial pathogens and should be included in the empiric therapy, especially
when L monocytogenes meningitis is suspected.1,11,22 Vancomycin should be added
to the therapeutic regime owing to concern for drug-resistant pathogens.1 The global
emergence of antibiotic-resistant pathogens and the slow development of new antibi-
otics have made bacterial meningitis an evolving therapeutic challenge.3 After the re-
sults of the Gram stain, culture, and susceptibility have become available, and the
causative pathogen has been identified, antibiotic therapy should be de-escalated.
The IDSA guidelines recommend the use of adjunctive dexamethasone in children
or adults with suspected community-acquired bacterial meningitis.22 Corticosteroids

Table 1
Empiric antimicrobial therapy based on age and causative pathogen

Age Common Bacterial Pathogens Antimicrobial Therapy

<1 mo Streptococcus agalactiae, Escherichia Ampicillin plus cefotaxime or
coli, Listeria monocytogenes, ampicillin plus an aminoglycoside
Klebsiella spp
123 mo Streptococcus pneumoniae, Neisseria Vancomycin plus a third-generation
meningitidis, S agalactiae, cephalosporina,b
Haemophilus influenzae, E coli
250 y N meningitidis, S pneumoniae Vancomycin plus a third-generation
cephalosporina,b
>50 y S pneumoniae, N meningitidis, L Vancomycin plus ampicillin plus a
monocytogenes, aerobic gram- third-generation cephalosporina,b
negative bacilli
a
Ceftriaxone or cefotaxime.
b
Some experts would add rifampin if dexamethasone is also given.
From van de Beek D, Brouwer MC, Thwaites GE, et al. Advances in treatment of bacterial
meningitis. Lancet 2012;380:1694; with permission.
 Acute Bacterial Meningitis 357

act to decrease the inflammation of the subarachnoid space caused by the bacterial
products responsible for neuronal injury. Moreover, corticosteroids have been shown
to stabilize the blood-brain barrier and reduce CSF outflow resistance, resulting in
decreased ICP. Dexamethasone is the corticosteroid most often recommended for
use in bacterial meningitis because of its ability to penetrate the CSF.8 Reports exist
regarding administration of adjunctive dexamethasone to reduce hearing loss in chil-
dren with H influenzae type b meningitis.6 In 2010, a Cochrane meta-analysis showed
that use of adjunctive dexamethasone in children decreased the incidence of hearing
loss but did not affect mortality.6 The IDSA guidelines advise the administration of
adjunctive dexamethasone before or with the first dose of antibiotics with continuance
every 6 hours for 4 days. However, dexamethasone reduces the permeability of the
blood-brain barrier, decreasing the clinical efficacy of large-molecule antimicrobials
such as vancomycin in penetrating the CSF and thus delaying CSF sterilization.1,3,22,27
Multiple studies have demonstrated conflicting results as to whether adjunctive dexa-
methasone is beneficial in adults with suspected community-acquired bacterial
meningitis.6 A European controlled trial showed that adjunctive dexamethasone was
associated with a favorable outcome, resulting in fewer neurologic sequelae and a
lower mortality rate among people with pneumococcal meningitis.28 The European
Dexamethasone in Adulthood Bacterial Meningitis Study showed that dexamethasone
can provide extended survival benefits of up to 20 years in persons with bacterial
meningitis.29 However, a meta-analysis of more than 2000 persons with bacterial
meningitis showed that adjunctive dexamethasone treatment did not reduce neuro-
logic sequelae or decrease mortality.30 These studies suggest that dexamethasone
treatment is associated with lower mortality, fewer neurologic sequelae, and fewer
hearing deficits in children and adults with pneumococcal meningitis who live in devel-
oped countries.27 Adjunctive dexamethasone therapy is most efficacious for persons
with community-acquired bacterial meningitis living in developed countries with a low
HIV prevalence, whereas there may be no benefit for persons living in developing
countries where the disease burden is highest and there is a high HIV prevalence,
making dexamethasone ineffective.6,8,31

Nursing Management
Nursing management consists of effective delivery of antibiotic therapy, fluid manage-
ment, and supportive care. Persons with bacterial meningitis should be placed on
droplet isolation precautions until the organism has been identified and they have
completed 24 hours of appropriate antibiotic therapy.32 The neurologic status of pa-
tients with bacterial meningitis should be monitored closely, being alert for signs of
increased ICP, altered level of consciousness, or seizures. Nursing responsibilities
include airway protection, oxygenation monitoring, and administration of supple-
mental oxygen as needed. The temperature of patients should be monitored and
treated aggressively with antipyretic agents, fans, and cooling measures. Fluid bal-
ance and electrolytes should be closely watched and treated as needed. A quiet dark-
ened room to limit stimulation is recommended. Supportive care should be provided
for persons with bacterial meningitis and their family.

PREVENTION

Chemoprophylaxis should be given to individuals who have had close contact with a
person with N meningitidis or H influenzae type b meningitis within 1 week before the
onset of symptoms.16 Bacterial meningitis is caused by spread of the organism
through water droplets from person to person, by intimate personal contact such as
358 VanDemark

through kissing or sneezing, or close contact with an infected person. N meningitidis is

a large droplet that may be transmitted easily through respiratory secretions or saliva.
Persons at risk for acquiring N meningitidis include household members, intimate con-
tacts, active or passive smokers, and/or living in crowded environments such as dor-
mitories, military barracks, and child care centers.7 Chemoprophylaxis includes
antibiotics that reduce nasopharyngeal colonization including rifampin, ciprofloxacin,
or ceftriaxone.16
Vaccinations provide the best protection against bacterial meningitis. Vaccines are
available to protect against 3 common forms: H influenzae type b conjugate vaccine,
heptavalent pneumococcal conjugate vaccine PCV7, and tetravalent meningococcal
conjugate vaccine. Many of the current vaccines for bacterial meningitis do not protect
against all forms of bacterial serotypes, creating a challenge when combating menin-
gitis worldwide. Up to 90% of children in developed countries are protected by PCV7,
but only 50% to 65% of children in developing countries.33 However, the PCV7 does
not cover all of the serotypes of pneumococcal disease. The meningococcal
conjugate vaccine protects against serogroups A, C, W-135, and Y, which account
for the majority of meningococcal disease. However, the vaccine does not cover
serogroup B, which accounts for one-third of meningococcal disease.12 Unfortu-
nately, only 45% of the worlds children have been fully immunized. Effort is needed
to promote immunization programs worldwide, especially in developing countries.33
The development of a universal vaccine with broad protection against pneumococcal
and meningococcal meningitis serotypes would be a great benefit for the worlds
health.

OUTCOME

The incidence of bacterial meningitis has decreased in the past few decades primarily
because of widespread vaccine use and improved antimicrobial therapy. The persons
level of consciousness and the severity of the disease at presentation, plus the time-
liness of antibiotic therapy, affect the prognosis of bacterial meningitis.12 Several
retrospective studies have identified risk factors associated with poor prognosis,
including the causative organism, persons age greater than 60 years, comorbidities,
presence of otitis media or sinusitis, low Glasgow Coma Scale score on admission,
focal neurologic deficits, tachycardia, positive blood culture, absence of rash,
elevated erythrocyte sedimentation rate, thrombocytopenia, and low CSF WBC
count.10,12 Worsened clinical outcomes are associated with tachycardia, hypotension,
seizures, altered mental status, and CSF WBC count less than 1000 (Box 2).11 The
incidence of bacterial meningitis in older adults has remained high, and mortality
increases with increasing age. In the United States, adults 18 to 34 years old had
8.9% mortality rate, whereas mortality rate was 22.7% in adults 65 years and older.2
In developing countries, the mortality rate in adults with bacterial meningitis is 6% to
37% of cases.2,6,27
Neurologic sequelae occur in up to 50% of survivors following bacterial meningitis,
and include hearing loss, seizures, hydrocephalus, developmental disorders, and neu-
ropsychological impairment.5,10 Permanent sensorineural hearing loss occurs in 5%
to 35% of survivors of bacterial meningitis.14 Approximately 27% of persons with
pneumococcal meningitis suffer from neuropsychological sequelae.27,30 Systemic
complications in approximately 44% of survivors include hyponatremia, septic shock,
adult respiratory distress syndrome, and disseminated intravascular coagulation.14
Bacterial meningitis remains a devastating disease, with significant morbidity and
mortality especially in the very young and very old. Bacterial meningitis is an evolving
 Acute Bacterial Meningitis 359

Box 2
Acute bacterial meningitis: indicators of poor prognosis

 Causative organism
 Age greater than 60 years old
 Comorbidities
 Altered mental status
 Low Glasgow Coma Scale score on admission
 Focal neurologic deficits
 Cerebrospinal fluid white blood cell count less than 1000
 Elevated erythrocyte sedimentation rate and thrombocytopenia
 Tachycardia and hypotension
 Seizures

Data from Refs.1012

therapeutic challenge with the global emergence of multidrug-resistant pathogens.

Empiric antibiotics should be administered promptly and be targeted to the persons
age, causative organism, local epidemiology trends, and drug-resistance patterns.
Diagnostic studies should be promptly and efficiently performed. A CT scan of the
head should be done if the person has a decreased level of consciousness, focal
neurologic deficits, or signs of increased ICP. CSF examination is crucial for the diag-
nosis of bacterial meningitis and identification of the causative organism. Medical
treatment remains a challenge with the changing epidemiology of bacterial meningitis
and the emergence of antimicrobial-resistant pathogens. Worldwide prevention mea-
sures and increased availability of vaccines, especially in developing countries, will aid
in eliminating this devastating disease.

REFERENCES

1. Miranda J, Tunkel AR. Strategies and new developments in the management of

bacterial meningitis. Infect Dis Clin North Am 2009;23:92543.
2. Thigpen MC, Whitney CG, Messonnier NE, et al. Bacterial meningitis in the United
States, 1998-2007. N Engl J Med 2011;364:201625.
3. van de Beek D, Brouwer MC, Thwaites GE, et al. Advances in treatment of
bacterial meningitis. Lancet 2012;380:1693702.
4. van de Beek D, Drake J, Tunkel AR. Nosocomial bacterial meningitis. N Engl
J Med 2010;362:14654.
5. van de Beek D, de Gans J, Tunkel AR, et al. Community-acquired bacterial
meningitis in adults. N Engl J Med 2006;354:4453.
6. Brouwer MC, Tunkel AR, van de Beek D. Epidemiology, diagnosis, and antimicro-
bial treatment of acute bacterial meningitis. Clin Microbiol Rev 2010;23:46792.
7. Bhimraj A. Acute community-acquired bacterial meningitis in adults: an evidence
based review. Cleve Clin J Med 2012;79:393400.
8. Prasad K, Rai NK, Kumar A. Use of corticosteroids and other adjunct therapies
for acute bacterial meningitis in adults. Curr Infect Dis Rep 2012;14:44553.
9. Agrawal S, Nadel S. Acute bacterial meningitis in infants and children: epidemi-
ology and management. Paediatr Drugs 2011;13:385400.
360 VanDemark

10. van de Beek D, de Gans J, Spanjaard L, et al. Clinical features and prognostic
factors in adults with bacterial meningitis. N Engl J Med 2004;351:184959.
11. Fitch MT, Abrahamian FM, Moran GJ, et al. Emergency department management
of meningitis and encephalitis. Infect Dis Clin North Am 2008;22:3352.
12. Roos KL, Greenlee JE. Meningitis and encephalitis. Neurology 2011;17:101023.
13. Koedel U, Klein M, Pfister HW. New understanding of the pathophysiology of
bacterial meningitis. Curr Opin Infect Dis 2010;23:21723.
14. Lin AL, Safdieh JE. The evaluation and management of bacterial meningitis:
current practice and emerging developments. Neurologist 2010;16:14351.
15. Gerber J, Nau R. Mechanisms of injury in bacterial meningitis. Curr Opin Neurol
2010;23:3128.
16. Somand D, Meurer W. Central nervous system infections. Emerg Med Clin North
Am 2009;27:89100.
17. Curtis S, Stobart K, Vandermeer B, et al. Clinical features suggestive of meningi-
tis in children: a systematic review of prospective data. Pediatrics 2010;126:
95260.
18. Thomas KE, Hasbun R, Jekel J, et al. The diagnostic accuracy of Kernigs sign,
Brudzinskis sign, and nuchal rigidity in adults with suspected meningitis. Clin
Infect Dis 2002;35:4652.
19. Kim KS. Acute bacterial meningitis in infants and children. Lancet Infect Dis 2010;
10:3242.
20. Ziai WC, Lewin JJ. Update in the diagnosis and management of central nervous
system infections. Neurol Clin 2008;26:42768.
21. Nigrovic LE, Mallery R, Macias CG, et al. Effect of antibiotic pretreatment on ce-
rebrospinal fluid profiles of children with bacterial meningitis. Pediatrics 2008;
122:72630.
22. Tunkel AR, Hart BJ, Kaplan SL, et al. Practice guidelines for the management of
bacterial meningitis. Clin Infect Dis 2004;39:126784.
23. Hasbun R, Abrahams J, Jekel J, et al. Computed tomography of the head before
lumbar puncture in adults with suspected meningitis. N Engl J Med 2001;345:
172733.
24. Kanegaye JT, Soliemanzadeh P, Bradley JS. Lumbar puncture in pediatric bacte-
rial meningitis: defining the time interval for recovery of cerebrospinal fluid path-
ogens after parenteral antibiotic pretreatment. Pediatrics 2001;108:116974.
25. Sakushima K, Hayashino Y, Kawaguchi T, et al. Diagnostic accuracy of cerebro-
spinal fluid lactate for differentiating bacterial meningitis from aseptic meningitis:
a meta-analysis. J Infect 2011;62:25562.
26. Proulx N, Frechette D, Toye B, et al. Delays in the administration of antibiotics are
associated with mortality from adult acute bacterial meningitis. QJM 2005;98:
2918.
27. Borchorst S, Moller S. The role of dexamethasone in the treatment of bacterial
meningitisa systematic review. Acta Anaesthesiol Scand 2012;56(10):121021.
28. de Gans J, van de Beek D. Dexamethasone in adults with bacterial meningitis.
N Engl J Med 2002;347:154956.
29. Fritz D, Brouwer MC, van de Beek D. Dexamethasone and long-term survival in
bacterial meningitis. Neurology 2012;79:13.
30. van de Beek D, Farrar JJ, de Gans J. Adjunctive dexamethasone in bacterial
meningitis: a meta-analysis of individual patient data. Lancet Neurol 2010;9:
25463.
31. Cooper DD, Seupaul RA. Is adjunctive dexamethasone beneficial in patients with
bacterial Meningitis? Ann Emerg Med 2012;59:2256.
 Acute Bacterial Meningitis 361

32. Siegel JD, Rhinehart E, Jackson M, et al, and the Healthcare Infection Control
Practices Advisory Committee, 2007 Guideline for Isolation Precautions: Prevent-
ing Transmission of Infectious Agents in Healthcare Settings, June 2007. http://
www.cdc.gov/ncidod/dhqp/pdf/isolation2007.pdf.
33. Bottomley MJ, Serruto K, Safadi MA, et al. Future challenges in the elimination of
bacterial meningitis. Vaccine 2012;30(Suppl 2):B7886.