Acute Bacterial Meningitis

Benjamin P. Sneed, MDa,*, William Michael Scheld, MDb

KEYWORDS

� Acute � Bacterial � Meningitis � Cerebrospinal fluid

HOSPITAL MEDICINE CLINICS CHECKLIST

1. Suspect acute bacterial meningitis (ABM) in patients who present with somecombination of fever, neck stiffness, headache, and/or encephalopathy.

2. In suspected ABM, obtain blood cultures immediately and perform lumbarpuncture emergently unless delay for imaging is indicated.

3. Delay lumbar puncture for computed tomography of the head only when riskfactors or signs of intracranial lesion are present (immunocompromise, historyof central nervous system disease, papilledema, seizure, focal neurologicdeficit, or altered level of consciousness).

4. Start antibiotics as soon as possible on diagnosis of ABM by cerebrospinalfluid (CSF) analysis, which reveals evidence such as neutrophilic pleocytosisor positive Gram stain.

5. Administer empiric antibiotic treatment immediately in cases of suspectedABM if imaging before lumbar puncture is indicated or in cases of difficult orfailed lumbar puncture.

6. Administer adjunctive steroids (initial dose of dexamethasone 0.15 mg/kgintravenous [IV]) in the setting of suspected bacterial meningitis.

7. Direct initial antibiotic therapy at probable pathogens based on age and im-mune status; for example, in immunocompetent adults give ceftriaxone 2 g IVevery 12 hours and vancomycin 15 to 20 mg/kg IV every 8 to 12 hours; addampicillin 2 g IV every 4 hours in patients more than 50 years of age.

8. Tailor antibiotic choice and duration of treatment according to microbiology/culture data.

CONTINUED

a Section of Hospital Medicine, University of Virginia Health System, Box 800909, Room 6554,1176 Hospital Drive, Charlottesville, VA 22908, USA; b Division of Infectious Diseases and Inter-national Health, University of Virginia Health System, Box 801342, Room 2528, Carter HarrisonResearch Building (MR6), 345 Crispell Drive, Charlottesville, VA 22908, USA* Corresponding author.E-mail address: bps3u@hscmail.mcc.virginia.edu

Hosp Med Clin 2 (2013) e358–e369http://dx.doi.org/10.1016/j.ehmc.2013.03.0022211-5943/13/$ – see front matter � 2013 Elsevier Inc. All rights reserved.

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CONTINUED

9. Consider shunt removal with external drainage if ABM is complicated by thepresence of a CSF shunt and intraventricular antibiotics if the shunt cannotbe removed.

10. Transition to outpatient treatment only after 6 or more days of IV antibiotics,absence of fever for 24 to 48 hours, clinical improvement, and if there is nosignificant neurologic deficit or dysfunction.

DEFINITIONS

What is the definition of acute bacterial meningitis?

Acute bacterial meningitis (ABM) is a syndrome involving bacterial infection and theassociated inflammation affecting the central nervous system (CNS) leptomeninges,manifesting over hours to several days. It can be community or hospital acquired. En-cephalitis (encephalopathy early in the course with minimal meningeal signs) has someoverlap with acute meningitis, as does chronic meningitis, which is defined by at least4 weeks of abnormal cerebrospinal fluid (CSF) findings and ongoing signs and symp-toms. Distinguishing ABM from encephalitis and chronic meningitis is important forguiding evaluation and management.1

What is the pathogenesis and pathophysiology of ABM?

Most community-acquired cases of ABM involve mucosal colonization with the caus-ative pathogen, development of bacteremia, and invasion across the blood-brain bar-rier.2 The physiology of meningeal invasion is incompletely understood. Sustained orhigh-level bacteremia is necessary but not sufficient to develop meningitis, becausesome bacteria (such as viridans streptococci) commonly cause infective endocarditisbut are rarely associated with meningitis.1 Entry into the CNS may occur via transcel-lular traversal, paracellular traversal, and/or the Trojan horse mechanism involvingparacellular travel within monocytes.3

Once bacteria cross the blood-brain barrier, survival is favored by inadequate hostdefenses stemming from low CSF concentrations of both complement and immuno-globulins.4 Complex inflammatory responses play a major role in the brain injury fromABM. Bacterial antigens lead to immune cell cytokine release, which in turn contrib-utes to subarachnoid inflammation, vasogenic and cytotoxic edema, and ultimatelycompromised cerebral perfusion and cerebrovascular autoregulation.2

EPIDEMIOLOGY

How common is ABM and what are the most common causative pathogens?

The incidence of ABM decreased significantly over the last 3 decades. Surveillance inthe United States in the 1970s and 1980s revealed that more than 80% of cases werecaused by 5 pathogens:Haemophilus influenzae, Streptococcus pneumoniae,Neisse-ria meningitidis, group B streptococcus, and Listeria monocytogenes.5,6 Publishedestimates of incidence accordingly are often based on data involving these 5 causa-tive bacteria. In 1986, the annual incidence (combined adult and pediatric cases) was5.5/100,000.6 A 55% reduction to 2.4/100,000 was seen in 1995 after the introduction

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of H influenzae type b (Hib) vaccine for infants in 1990; there was a concurrent shift inthe average age from 15months to 25 years.7 From 1998 to 1999 and 2006 to 2007 theincidence declined further from 2 to 1.4 with an increase in median age from 30 to42 years. These more recent changes are likely the result of the heptavalent pneumo-coccal conjugate vaccine, which was introduced in 2000. Approximately 4100 casesof bacterial meningitis caused by the 5 common pathogens occurred in the UnitedStates each year between 2003 and 2007, with a fatality rate of about 12%. Therate per 100,000 adults increases with age from 0.66 cases for ages 18 to 34 years,up to 1.92 cases in persons aged 65 years and older.8

Although the order of relative incidence has changed, the 5 most common patho-gens remain the same. The epidemiologic data from 2006 to 2007 show total (adultand pediatric) bacterial meningitis incidence (cases/100,000) (Table 1)8:Among adults the order of pathogens by percent of total cases is shifted as follows:

S pneumoniae (%) 71

N meningitidis (%) 12

Group B Streptococcus (%) 7

H influenzae (%) 6

L monocytogenes (%) 4

What are the less common causes of ABM?

Gram-negative bacilli such as Escherichia coli, Klebsiella spp and Pseudomonas spp,and Staphylococcus (Staphylococcus aureus and coagulase-negative spp such asStaphylococcus epidermidis) rarely cause community-acquired ABM but are com-monly responsible for cases of nosocomial ABM. Risk factors for nosocomial menin-gitis include craniotomy, internal and external ventricular catheters, and head trauma.Most cases of ABM following basilar skull fractures are caused by nasopharyngealcolonizing bacteria such as S pneumoniae.9

What risk factors are associated with ABM?

From epidemiologic studies, factors associated with increased risk of ABM include animmunocompromised state (including but not limited to human immunodeficiencyvirus [HIV], cancer, immunosuppressive drugs, and splenectomy) and the presenceof chronic medical conditions such as chronic obstructive lung disease, congestive

Table 1Total (adult and pediatric) bacterial meningitis incidence: 2006 to 2007 (cases/100,000)

Organism Incidence

S pneumoniae 0.81

Group B Streptococcus 0.25

N meningitidis 0.19

H influenzae 0.08

L monocytogenes 0.05

Data from ThigpenMC,Whitney CG,Messonnier NE, et al. Bacterial meningitis in the United States,1998–2007. N Engl J Med 2011;364:2016–45.

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heart failure, diabetes, alcohol abuse, and cirrhosis.8,10 As noted earlier, age is a riskfactor for ABM, particularly for ABM caused by Listeria, which also disproportionatelyaffects patients with immunocompromise.11,12

What are the common nonbacterial causes of meningitis in immunocompetent individ-uals that should be considered when evidence does not support a bacterial cause?

Viruses cause most cases of aseptic meningitis (meningitis with negative CSF stainsand cultures, typically with a lymphocytic CSF pleocytosis). Enteroviruses and herpesviruses are typical causes.1 Enterovirus polymerase chain reaction (PCR) is rapid,sensitive, and reliable. Herpes simplex virus (HSV) PCR also provides a rapid diag-nostic tool to confirm suspected cases of HSV meningitis, and presumptive treatmentwith acyclovir is indicated in case of suspected HSV meningitis/encephalitis. In pa-tients with clinical clues and/or history that suggest rickettsial or ehrlichial infection,doxycycline is advised as empiric treatment pending diagnosis by CSF or serum anal-ysis.13 A myriad of drugs may also cause aseptic meningitis, as can mycobacteria andfungi, although they generally do so in immunocompromised individuals.1 A recentoutbreak of fungal meningitis caused by contamination of steroids used in epiduralinjections showed the possibility of atypical pathogens even in immunocompetent pa-tients and the importance of a thorough history for the evaluation of suspectedmeningitis.14

HISTORY AND EXAMINATION

What key symptoms should prompt concern for ABM? What is the classic triad?

Patients with ABM typically present feeling acutely ill, soon after symptom onset. Aclassic triad of signs/symptoms is often mentioned in references and includes fever,neck stiffness, and either altered mental status (AMS) or headache, depending onthe source. A 1999 meta-analysis found a 7-study pooled sensitivity for headacheof only 50% (95% confidence interval 32–68%, n5 303) with a range between studiesof 27% to 81%.15 This same meta-analysis reviewed 11 studies and found pooledsensitivities of 85% for fever, 70% for neck stiffness, 67% for AMS, and 46% forthe triad of all three. A 2004 study of nearly 700 patients found that less than 50%of cases had the combination of fever, neck stiffness, and AMS; headache was pre-sent in 87% of patients.10 Both studies found that more than two-thirds of patientshad at least 1 of fever, neck stiffness, or AMS. Although the sensitivity of combiningall 4 findings would be low, 95% of the 2004 study patients had at least 2 of the 4parameters of fever, stiff neck, headache, and AMS.

What examination findings suggest ABM? How reliable are they?

Bedside tests for meningeal inflammation have limited usefulness. A study of morethan 200 cases of suspected meningitis revealed a sensitivity of 5%, specificity95%, positive predictive value (PPV) 27%, and negative predictive value (NPV) 72%for both Kernig and Brudzinski signs, and thus poor discrimination regarding the pres-ence or absence of meningitis.16 In the same study, nearly 300 patients with sus-pected meningitis tested for nuchal rigidity revealed a sensitivity of 30%, specificity68%, PPV 26%, and NPV 73%. The absence of these signs cannot be used to excludethe diagnosis of ABM, but their presence should increase the clinical suspicionfor ABM.

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In a study of 54 patients with fever and headache who underwent lumbar puncture(LP) for suspicion of meningitis, jolt accentuation of headache (worsening of the head-ache with periodic horizontal head motions at 2–3 cycles per second) was present in33 of 34 patients with CSF pleocytosis (sensitivity of 97%). Among the 20 patientswithout pleocytosis, 12 had no jolt accentuation (specificity of 60%).17

Which patients ultimately require further evaluation for ABM?

The differential diagnosis in patients with only 1 or 2 of the 4 classic signs and symp-toms of meningitis is broad, but any of them combined with recognized risk factorsand absence of another identified source to account for them is an indication toconsider ABM. Clinicians should use their clinical judgment and consider the patient’spresentation and risk factors for ABM, as well as the relative safety of LP and theconsequences of delaying therapy for possible ABM.

EVALUATION AND DIAGNOSIS OF ABM

Which patients with suspected ABM require neuroimaging?

Several studies have examined the usefulness of obtaining brain computed tomogra-phy (CT) in patients with suspected meningitis and signs that were concerning for amass lesion or increased intracranial pressure. These studies show that historicaland physical examinations are good predictors of abnormalities on brain CT, andthat most patients with suspected ABM do not need neuroimaging as part of theirevaluation.18,19 A prospective study of 113 adults needing urgent LP who had brainCT identified 3 predictors of brain lesions: AMS (likelihood ration [LR] 2.2, 95% CI1.5–3.2), focal neurologic examination (LR 4.3, 95% CI 1.9–10), and papilledema(LR 11.1, 95% CI 1.1–115).19 A study of 301 patients with suspected meningitis, inwhich 78% underwent brain CT before LP, found that 24% of those scans wereabnormal, but only 5% showed evidence of mass effect. A negative clinical screeningthat included theModified National Institutes of Health Stroke Scale assessment had aNPV of 97%. Three patients were misclassified; only 1 had mild mass effect and toler-ated LP without complications.18 The current Infectious Disease Society of America(IDSA) guidelines for management of ABM suggest neuroimaging in patients with 1or more of the following20:

� Immunocompromised state (HIV, chronic immunosuppression such as in trans-plant patients)

� History of CNS disease (mass lesions, stroke)� Recent seizure� Papilledema� Abnormal level of consciousness� Focal neurologic deficit

As addressed later, delay for CT imaging should not delay the administration oftherapy.

How should hospitalists prioritize LP and therapy in suspected ABM?

LP provides crucial diagnostic data in suspected ABM, and, given the seriousness ofthe diagnosis, it should be performed emergently. Many clinicians worry that empirictherapy alters LP results and complicates the diagnosis. However, because LPmay be

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difficult or require preprocedural neuroimaging, withholding therapy until LP isobtained can be dangerous. Several studies have examined the relationship betweentiming of antibiotic administration and outcomes in ABM. Themost recent studies sup-port early treatment. One retrospective cohort study of 286 cases of community-acquired ABM found that early antibiotic treatment was independently associatedwith favorable outcome (mild or no disability) with an odds ratio (OR) of 11.2(CI 4.4–32.6, P<.001).21 Another retrospective study of 119 adult patients with ABMshowed an incremental time-to-treatment relationship with increased mortality, withan adjusted mortality OR of 8.4 (95% CI 1.7–40.9) with door-to-antibiotic time greaterthan 6 hours.22

LP should be delayed only if preprocedure CT imaging is required. Therapy (antibi-otics and possibly steroids) should be given immediately after LP if it is performedwithout delay. If LP is delayed for imaging, therapy should be initiated immediately af-ter blood cultures, prior to CT.1 Likewise, if LP is unsuccessful, therapy should be initi-ated immediately rather than delaying therapy for a repeat LP attempt.

What is the proper technique for performing LP?

LP is a sterile procedure typically performed at the bedside with patients lying on theirsides with positioning for maximum flexion of the lumbar spine. Upright positioningmay also be used but does not permit the measurement of opening pressure. A spinalneedle is passed through the midline intervertebral disc space of L3/4 or L4/5 and intothe thecal sac to obtain CSF. The superior-most aspects of the iliac crests that coin-cide with the L4 vertebral body are used to determine the vertebral level, and palpationof spinous processes allow localization of the intervertebral disc spaces. Ultrasoundhas been shown to reduce the rate of failed LP and increase the ease of the procedurein obese patients.23

What diagnostic tests should be performed on CSF and blood samples?

Routine blood analysis including a metabolic profile, complete blood count, and bloodculture should be collected as soon as possible during assessment. Crucial CSF testsinclude the following24:

� Cell count with differential� Gram stain and culture� Protein� Glucose� Opening pressure

PCR should be performed for enteroviruses and HSV when the tests discussedearlier do not support a bacterial pathogen and/or findings are consistent with viralmeningitis.

How does CSF analysis confirm the diagnosis of ABM?

Analysis of CSF parameters is the key to diagnosis in patients with suspected ABM(Table 2).CSF findings that do not support a diagnosis of ABM but show an inflammatory pro-

cess point to aseptic meningitis, most of which is has viral causes such as enterovirusand HSV2. Other causes include varicella-zoster virus, HIV, and West Nile virus. HSV1is more commonly associated with encephalitis. As mentioned earlier, nonviral causesalso include tick-borne pathogens, mycobacteria, and fungi.

Table 2Typical CSF findings in ABM

Opening pressure (mm H2O) 200–500

White blood cell count (per mL) 1000–5000 (range <100 to >10,000)

Neutrophil percentage (%) �80

Protein (mg/dL) 100–500

Glucose (mg/dL) �40

CSF/serum glucose ratio �0.4

Gram stain (% positive) 60–90

Culture (% positive) 70–85

PCR Helpful to identify viral cause

Data from Tunkel AR, Van de Beek D, Scheld WM. Acute meningitis. In: Mandell GL, Bennett JE,Dolin R, editors. Principles and practice of infectious disease, 7th edition. Philadelphia: ChurchillLivingstone/Elsevier; 2010. p. 1189–229.

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MANAGEMENT

What is appropriate initial or empiric antibiotic treatment?

In patients with suspected meningitis who undergo emergent LP for CSF analysis,initial antibiotic therapy should be chosen according to Gram stain results if it is sug-gestive (Table 3).20

An empiric antibiotic regimen is indicated if the Gram stain is negative. In cases ofpostponed LP, initiation of empiric antibiotics must not be delayed. Empiric antibiotictherapy should reflect the predisposition for specific pathogens particular to thepatient’s age and underlying health status.1,20

Empiric Antibiotic Therapy for Suspected Community-acquired Bacterial Meningitisin Adults

Ceftriaxone 2 g intravenous (IV) every 12 hours or cefotaxime 2 g IV every 4 to6 hours

Plus:Vancomycin 15 to 20 mg/kg IV every 8 to 12 hours (goal trough 15–20 mg/mL)Plus (if age >50 years):Ampicillin 2 g IV every 4 hours

Table 3Antibiotic therapies

GramStain

ProbableMicroorganism Antibiotic Alternative Antibiotic

GPC S pneumoniae Vancomycin 1 third-generation ceph

Meropenem or fluoroquinolone

GNC N meningitidis Third-generation ceph Pen G or ampicillin or fluoroquinolone

GPR L monocytogenes Ampicillin TMP-SMX or meropenem

GNR E coli, H influenzae,Klebsiella spp

Third-generation ceph Cefepime, meropenem

Fluoroquinolone 5 moxifloxacin.Abbreviations: ceph, ceftriaxone or cefotaxime; GNC, gram-negative cocci; GNR, gram-negative

rod; GPC, gram-positive cocci; GPR, gram-positive rod; Pen, penicillin; TMP-SMX, trimethoprim-sulfamethoxazole.

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In cases of known or suspected immunocompromise, a anti-Pseudomonal cepha-losporin (eg, cefepime 2 g IV every 8 hours or ceftazidime 2 g IV every 8 hours) or anti-Pseudomonal carbapenem (eg, meropenem 2 g IV every 8 hours) should besubstituted for the third-generation cephalosporin and ampicillin should be givenregardless of age.Immunocompromise is defined in this instance as a patient with diagnosed or sus-

pected HIV/acquired immunodeficiency syndrome, immunosuppressive therapy, aftertransplantation, lymphoma, neutropenia (absolute neutrophil count <500).Suspected health care–associated/nosocomial (after neurosurgery or CSF shunt) or

trauma-associated ABM (penetrating head wound or basilar skull fracture) is an indi-cation to include antibiotic coverage for Staphylococci and potentially resistant gram-negative organisms.9,20

Empiric Antibiotic Therapy for Suspected Health Care–associated or Trauma-relatedMeningitis

Cefepime 2 g IV every 8 hours, or ceftazidime 2 g IV every 8 hours, or meropenem2 g IV every 8 hours

Plus:Vancomycin 15 to 20 mg/kg IV every 8 to 12 hours (goal trough 15–20 mg/mL)

How should therapy be tailored to culture results?

Microbiologic data including pathogen identification and antibiotic susceptibilitypattern should be used to determine the optimal treatment regimen in ABM.IDSA guidelines provide recommended antibiotic regimens based on culture and

susceptibility data (Table 4).20

What is the role of adjunctive corticosteroids in the management of ABM?

The role of steroids in ABM has been controversial because of inconsistent resultsamong studies done in both undeveloped and developed countries and includingboth adult and pediatric patients. A 2010 meta-analysis of 24 studies and morethan 4000 participants (adult and pediatric) concluded that, in high-income countries,corticosteroids significantly reduced severe hearing loss (relative risk [RR] 0.51, 95%CI 0.35–0.73), any hearing loss (RR 0.58, 95% CI 0.45–0.73), and short-term neuro-logic sequelae (RR 0.64, 95% CI 0.48–0.85), but not mortality. There was a trend to-ward reduced mortality among adults (RR 0.74, 95% CI 0.53–1.05, P 5 .09), andsubgroup analysis revealed that steroids reduced mortality in adults and childrenwith ABM caused by S pneumoniae (RR 0.84, 95% CI 0.72–0.98).25 The 2004 IDSAguidelines recommend that dexamethasone be given in cases of suspected or provenpneumococcal meningitis before or at the time of antibiotics. The recommendeddose/schedule of dexamethasone is 0.15 mg/kg every 6 hours for 2 to 4 days.20

Because of the improvement in mortality in pneumococcal meningitis and the reduc-tion in hearing loss and neurologic complications shown in recent data, someexperts26 and the authors of the comprehensive 2010 review25 recommend dexa-methasone be used routinely in cases of suspected ABM in developed countries.

What duration of antibiotics is appropriate for ABM?

Rigorous studies regarding optimal duration of antibiotics are lacking and most pub-lished recommendations are based on historical data. In general, short courses are

Table 4Recommended antibiotic regimens

Microorganism andSusceptibility Standard Antibiotic Alternative

S pneumoniae

Penicillin MIC

<0.1 mg/mL Penicillin G or ampicillin Third-generation cephalosporin

0.1–1.0 mg/mL Third-generation cephalosporin Cefepime, meropenem

�2.0 mg/mL Vancomycin 1 third-generationcephalosporin

Fluoroquinolone

Cefotaxime/ceftriaxone MIC

�1.0 mg/mL Vancomycin 1 third-generationcephalosporin

Fluoroquinolone

Streptococcus agalactiae Ampicillin or penicillin G Third-generation cephalosporin

H influenzae

b-Lactamase negative Ampicillin Third-generation cephalosporin,cefepime, fluoroquinolone

b-Lactamase positive Third-generation cephalosporin Cefepime, fluoroquinolone

N meningitidis

Penicillin MIC

<0.1 mg/mL Penicillin G or ampicillin Third-generation cephalosporin

0.1–1.0 mg/mL Third-generation cephalosporin Fluoroquinolone, meropenem

L monocytogenes Ampicillin or penicillin G TMP-SMX, meropenem

E coli and otherEnterobacteriaceae

Third-generation cephalosporin Aztreonam, fluoroquinolone,meropenem, TMP-SMX

P aeruginosa Cefepime or ceftazidime Aztreonam, ciprofloxacin,meropenem

S aureus

Methicillin susceptible Nafcillin or oxacillin Vancomycin, meropenem

Methicillin resistant Vancomycin TMP-SMX, linezolid*

S epidermidis Vancomycin Linezolid*

Enterococcus species

Ampicillin susceptible Ampicillin 1 gentamicin —

Ampicillin resistant Vancomycin 1 gentamicin —

Vancomycin resistant Linezolid* —

Abbreviation: MIC, minimum inhibitory concentration.* daptomycin.

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appropriate forNeisseria andHaemophilus infections, whereas streptococcal, Listeria,and gram-negative infections require longer courses. IDSA guidelines give recommen-dations for duration based on the historical data, with the caveat that, given the lack ofevidence-based information, individualization based on clinical response is appro-priate. IV therapy is advised throughout the course of treatment (Table 5).

How does presence of a CSF shunt affect management of ABM?

In patients who develop ABM complicated by presence of a CSF shunt, IDSA guide-lines recommend shunt removal and external drainage in addition to appropriateantibiotics, based on findings of more rapid clearing of ventriculitis and lower success

Table 5Duration of antibiotic treatment of select bacterial causes of meningitis

Pathogen Duration (d)

S pneumoniae 10–14

N meningitidis 5-7

H influenzae 7

L monocytogenes �21

Aerobic gram-negative bacilli 21

S agalactiae 14–21

Data from Tunkel AR, Hartman BJ, Kaplan SL, et al. Practice guidelines for the management ofbacterial meningitis. Clin Infect Dis 2004;39:1267–87.

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rates of treatment without removal of the shunt.27 Although rigorous evidence is lack-ing and accepted dosing is based on historical data, the guidelines advise the use ofintraventricular antibiotics in cases of poor treatment response or the inability toremove the shunt. The timing of shunt replacement should be guided by the combina-tion of negative cultures and duration of antibiotic therapy, which in general is 7 daysfor coagulase-negative staphylococci, 10 days for S aureus, and 10 to 14 days forgram-negative infections.27,28

When can a patient diagnosed with ABM be safely transitioned to outpatienttreatment?

A review of 68 cases of outpatient IV antibiotic therapy for CNS infections showed thattreatment outside the hospital can be effective and safe.29 All cases resulted in cure,and although there was a 16% rate of admission to the hospital during outpatient ther-apy, all readmissions were caused by issues that would also have occurred in an inpa-tient setting. Seizures occurred in 2 patients, leading the investigators to recommend asupport system out of the hospital for close observation. This review produced a set ofcriteria that the IDSA endorses for use in consideration of hospital discharge inpatients with ABM.

Criteria for Discharge and Treatment as Outpatient for Bacterial Meningitis

� Inpatient antibiotics for a minimum of 6 days� Afebrile >24 to 48 hours� Clear clinical improvement and stability� No limiting neurologic dysfunction, focal findings, or seizures� Infusion venous catheter and home health support for infusions� Established plan for postdischarge monitoring, follow-up visits, and contingencyavailability of physician

� Safe home environment with support for compliance

How can ABM be prevented?

Childhood vaccines for H influenzae type B (introduced in 1990) and S pneumoniae(introduced in 2000) produced significant reductions in the incidence of bacterial men-ingitis, as previously detailed. More recently, the US Centers for Disease Control andPrevention has included recommendations for the conjugate vaccine forNmeningitidis

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for children aged 11 to 18 years, students entering college dormitories, travelers toendemic areas, and those with complement deficiencies. Patients with asplenia (func-tional or anatomic) should receive these three vaccines. N meningitidis infection(proven or suspected) requires droplet precautions for 24 hours after the initiation oftherapy, and chemoprophylaxis of contacts in proven cases is recommended.30

What performance improvement standards apply to ABM evaluation andmanagement?

The authors know of no specific regulatory standards that apply to ABM care. How-ever, quality and performance measures for ABM could include education and trainingwithin a group of hospitalists or an institution to ensure a uniform and evidence-basedapproach to diagnosis and treatment. Data collection and analysis regarding sus-pected or confirmed cases, antibiotic use, and outcomes may or may not be illumi-nating because of the low incidence of ABM. However, neuroimaging is overused atmany centers, and the use of CT for suspected ABMmay be amenable to intervention.

What clinical guidelines exist to guide ABM evaluation and management?

The IDSA guidelines for themanagement of bacterial meningitis offer a comprehensiveresource for clinicians.20 An update to these guidelines is in process and is expectedto be published in 2014. The recommendations made in this article are consistent withthose of the IDSA.

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