Meningitis Medications Medscape

12/3/2017 Meningitis Medication: Sulfonamides, Tetracyclines, Carbapenems, Fluoroquinolones, Antibiotics, Miscellaneous, Glycopeptides, Aminogly
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Meningitis Medication
Updated: Oct 12, 2017
Author: Rodrigo Hasbun, MD, MPH; Chief Editor: Michael Stuart Bronze, MD more...
MEDICATION
Medication Summary
Begin empiric antibiotic coverage according to age and presence of overriding physical conditions.
Empiric therapy also depends on prevalence of cephalosporin-resistant S pneumoniae (DRSP). In
the United States, prevalence is considered high (>2-5%). Patients with severe penicillin (and
presumed cephalosporin) allergies often require alternative therapy.
Sulfonamides
Class Summary
Empiric antimicrobial therapy should cover all likely pathogens in the context of this clinical setting.
Trimethoprim-sulfamethoxazole (TMP-SMX) is effective against many aerobic gram-positive and
gram-negative bacteria, but its use in bacterial meningitis is limited to patients with Listeria
monocytogenes meningitis who have a penicillin allergy.
Trimethoprim-sulfamethoxazole (Bactrim, Bactrim DS, Septra DS, Sulfatrim)
View full drug information
Trimethoprim and sulfamethoxazole work together to inhibit bacterial synthesis of tetrahydrofolic

acid. Trimethoprim prevents the formation of tetrahydrofolic acid by binding to bacterial
dihydrofolate reductase. Sulfamethoxazole inhibits bacterial synthesis of dihydrofolic acid by
competing with para-aminobenzoic acid, inhibiting folic acid synthesis. This results in inhibition of
bacterial replication.
Tetracyclines
Class Summary
Tetracyclines inhibit protein synthesis and, therefore, bacterial growth by binding with 30S and
possibly 50S ribosomal subunits of susceptible bacteria. They are broad-spectrum bacteriostatic
antibiotics that are used to treat infections caused by many gram-positive and gram-negative
bacteria. They are contraindicated in children younger than 8 years of age, because they can
cause tooth discoloration and bone growth retardation.
Doxycycline (Doryx, Adoxa, Doxy 100, Monodox, Oracea)
https://emedicine.medscape.com/article/232915-medication 1/35
Doxycycline can be administered twice daily and is available in both intravenous (IV) and oral
formulations. It is less likely to cause photosensitivity than other tetracyclines are. The maximum
serum concentration of an IV dose of doxycycline occurs within 30 minutes of administration. The
use of doxycycline in meningitis is limited to cases of Brucella or rickettsial meningitis.
Carbapenems
Class Summary
Carbapenems inhibit bacterial cell wall synthesis by binding to penicillin-binding proteins.
Carbapenems, including meropenem, can be used for the treatment of meningitis.
Meropenem (Merrem IV)
A broad-spectrum carbapenem antibiotic, meropenem inhibits cell wall synthesis and has
bactericidal activity. It is effective against most gram-positive and gram-negative bacteria.
Compared with imipenem, meropenem has slightly increased activity against gram-negative
organisms and slightly decreased activity against staphylococci and streptococci. It also has limited
activity against highly-penicillin-resistant S pneumoniae isolates. [43]
Fluoroquinolones
Class Summary
Fluoroquinolones inhibit bacterial DNA synthesis and, consequently, growth by inhibiting DNA
gyrase and topoisomerases, which are required for replication, transcription, and translation of
genetic material. The use of fluoroquinolones is not recommended in patients with myasthenia
gravis.
Second-generation fluoroquinolones, such as gatifloxacin and moxifloxacin, have excellent

cerebrospinal fluid (CSF) penetration, and animal models suggest that they are effective in
penicillin- and ceftriaxone-resistant pneumococcal meningitis. (Clinical trial data are available only
for trovafloxacin, which has been removed from the market.)
Ciprofloxacin (Cipro, Cipro XR)
Quinolones have broad activity against gram-positive and gram-negative aerobic organisms.
Ciprofloxacin has no activity against anaerobes. Ciprofloxacin has an off-label indication for
prophylaxis against Neisseria meningitidis meningitis after close contact with an infected person.
Moxifloxacin (Avelox)
Quinolones have broad activity against gram-positive and gram-negative aerobic organisms.
Infectious Diseases Society of America guidelines recommend moxifloxacin plus vancomycin as an
alternative to third-generation cephalosporins in meningitis caused by penicillin- and ceftriaxone-
resistant S pneumoniae strains. [17]
Antibiotics, Miscellaneous
Class Summary
Chloramphenicol inhibits bacterial protein synthesis by binding to the 50S ribosomal subunit.
Chloramphenicol
Chloramphenicol is effective against gram-negative and gram-positive bacteria. It can be used as a

substitute in the treatment of a meningococcal infection in penicillin-allergic patients. Worldwide,
however, meningococcal strains have shown increasing resistance to chloramphenicol, and
patients with pneumococcal meningitis have poor outcomes with chloramphenicol.
Glycopeptides
Class Summary
Vancomycin inhibits bacterial cell wall synthesis by blocking glycopeptide polymerization. It is

indicated for many infections caused by gram-positive bacteria.
Vancomycin
Vancomycin is a glycopeptide antibiotic that is active against staphylococci, streptococci, and other
gram-positive bacteria. It exerts antibacterial activity by inhibiting biosynthesis of peptidoglycan and
is the drug of choice for highly penicillin-resistant and ceftriaxone-resistant S pneumoniae and
methicillin-resistant Staphylococcus aureus (MRSA). It is a component of empiric first-line therapy
for meningitis associated with central nervous system (CNS) shunts.
Because of poor CSF penetration, a higher dose of vancomycin is required for meningitis than for
other infections. In patients with renal impairment, the dose is adjusted on the basis of the
creatinine clearance.
Aminoglycosides
Class Summary
Aminoglycosides primarily act by binding to 16S ribosomal RNA within the 30S ribosomal subunit.
They have mainly bactericidal activity against susceptible aerobic gram-negative bacilli.
Gentamicin
Although newer antibiotics are available, aminoglycosides such as gentamicin remain significant in
treating severe infections. Aminoglycosides inhibit protein synthesis by irreversibly binding to the
30S ribosomal subunit. In meningitis or gram-negative meningitides, it must be administered
intrathecally because of its poor CNS penetration. Dosing regimens are numerous; the dose is
adjusted on the basis of the creatinine clearance and changes in the volume of distribution.
Streptomycin
Streptomycin has bactericidal action and inhibits bacterial protein synthesis. Susceptible organisms
include Mycobacterium tuberculosis, Pasteurella pestis, Francisella tularensis, Haemophilus
influenzae, Haemophilus ducreyi, donovanosis (granuloma inguinale), Brucella species, Klebsiella
pneumoniae, Escherichia coli, Proteus species, Aerobacter species, Enterococcus faecalis, and
Streptococcus viridans (in endocarditis, with penicillin). Streptomycin is always given as part of a
total antituberculosis regimen.
Penicillins, Amino
Class Summary
Ampicillin is a second-generation penicillin that is active against many strains of E coli, Proteus
mirabilis, Salmonella, Shigella, and H influenzae.
Ampicillin
A bactericidal beta-lactam antibiotic, ampicillin inhibits cell wall synthesis by interfering with
peptidoglycan formation. The drug is indicated for L monocytogenes and Streptococcus agalactiae
(group B streptococcus [GBS]) meningitis, usually in combination with gentamicin
Penicillins, Natural
Class Summary
Penicillins are highly active against gram-positive organisms.
Penicillin G aqueous (Crystapen, Penicillin G potassium, Penicillin G sodium)
A beta-lactam antibiotic, penicillin G inhibits bacterial cell wall synthesis, resulting in bactericidal
activity against susceptible microorganisms. It is active against many gram-positive organisms and
is the drug of choice for syphilitic meningitis and susceptible organisms (eg, N meningitidis and
penicillin-susceptible S pneumoniae).
Cephalosporins, 3rd Generation

Class Summary
Third-generation cephalosporins are less active against gram-positive organisms than first-
generation cephalosporins are. They are highly active against Enterobacteriaceae, Neisseria, and
H influenzae.
Ceftriaxone (Rocephin)
Ceftriaxone is a third-generation cephalosporin with broad-spectrum gram-negative activity. It has

lower efficacy against gram-positive organisms but excellent activity against susceptible
pneumococcal organisms. It exerts an antimicrobial effect by interfering with the synthesis of
peptidoglycan, a major structural component of the bacterial cell wall. It is an excellent antibiotic for
the empiric treatment of bacterial meningitis.
Ceftazidime (Fortaz, Tazicef)
Ceftazidime is a third-generation cephalosporin with broad-spectrum activity against gram-negative

organisms, lower efficacy against gram-positive organisms, and higher efficacy against resistant
organisms. By binding to 1 or more of the penicillin-binding proteins, it arrests bacterial cell wall
synthesis and inhibits bacterial replication.
Cefotaxime (Claforan)
Cefotaxime is a third-generation cephalosporin that is used to treat suspected or documented

bacterial meningitis caused by susceptible organisms, such as H influenzae or N meningitidis. Like
other beta-lactam antibiotics, cefotaxime inhibits bacterial growth by arresting bacterial cell wall
synthesis.
Antivirals, CMV
Class Summary
Ganciclovir can be used to treat cytomegalovirus (CMV) meningitis in immunocompromised hosts.
Ganciclovir (Cytovene)
Ganciclovir is a synthetic guanine derivative that is active against CMV. An acyclic nucleoside
analog of 2-deoxyguanosine, it inhibits the replication of herpesviruses in vitro and in vivo. Levels
of ganciclovir-triphosphate are as much as 100-fold greater in CMV-infected cells than in
uninfected cells, possibly because of preferential phosphorylation of ganciclovir in virus-infected
cells.
Antivirals, Other
Class Summary
Antiviral agents interfere with viral replication; they weaken or abolish viral activity. They can be
used in viral meningitis.
Acyclovir (Zovirax)
A prodrug activated by cellular enzymes, acyclovir inhibits the activity of herpes simplex virus 1
(HSV-1), HSV-2, and varicella-zoster virus (VZV) by competing for viral DNA polymerase and
incorporation into viral DNA. Acyclovir is used in HSV meningitis.
Foscarnet (Foscavir)
Foscarnet is an organic analogue of inorganic pyrophosphate that inhibits the replication of known
herpesviruses, including CMV, HSV-1, and HSV-2. It inhibits viral replication at the pyrophosphate-
binding site on virus-specific DNA polymerases. Foscarnet is used to treat CMV meningitis in
immunocompromised hosts at induction dosages of 60 mg/kg IV every 8 hours and maintenance
dosages of 90-120 mg/kg IV every 24 hours.
Antifungals, Systemic
Class Summary
Antifungal agents are used in the management of infectious diseases caused by fungi.
Amphotericin B deoxycholate (Amphotericin B (conventional), Fungizone)
A polyene antibiotic produced by a strain of Streptomyces nodosus, amphotericin B can be

fungistatic or fungicidal. It binds to sterols, such as ergosterol, in the fungal cell membrane,
causing intracellular components to leak with subsequent fungal cell death. The drug is used to
treat severe systemic infection and meningitis caused by susceptible fungi (ie, Candida albicans,
Histoplasma capsulatum, and Cryptococcus neoformans).
Amphotericin B does not penetrate the CSF well. Intrathecal amphotericin may be needed in
addition.
Amphotericin B lipid complex (Abelcet)

This agent is amphotericin B in phospholipid complexed form; it is a polyene antibiotic with poor
oral availability. Amphotericin B is produced by a strain of S nodosus; it can be fungistatic or
fungicidal. The drug binds to sterols (eg, ergosterol) in the fungal cell membrane, causing leakage
of intracellular components and fungal cell death. Toxicity to human cells may occur via this same
mechanism.
Fluconazole (Diflucan)
Fluconazole has fungistatic activity. It is a synthetic oral antifungal (broad-spectrum bistriazole) that
selectively inhibits fungal cytochrome P450 and sterol C-14 alpha-demethylation, which prevents
conversion of lanosterol to ergosterol, thereby disrupting cellular membranes.
Flucytosine (Ancobon)
Flucytosine is converted to fluorouracil after penetrating fungal cells and inhibits RNA and protein
synthesis by competing with uracil. It is active against candidal and cryptococcal species and is
used in combination with amphotericin B.
Itraconazole (Sporanox, Onmel)
Itraconazole has fungistatic activity. It is a synthetic triazole antifungal agent that slows fungal cell
growth by inhibiting cytochrome P450-dependent synthesis of ergosterol, a vital component of
fungal cell membranes.
Antituberculous Agents
Class Summary
These agents are used in the management of mycobacterial disease in combination with other
antituberculous agents.
Rifampin (Rifadin)
Rifampin is used in combination with other antituberculous drugs. It inhibits DNA-dependent

bacterial, but not mammalian, RNA polymerase. Cross-resistance may occur.
Isoniazid
Isoniazid is a first-line antituberculous drug that is used in combination with other antituberculous
drugs to treat meningitis. It is usually administered for at least 12-24 months. Addition of pyridoxine
(6-50 mg/day) is recommended if peripheral neuropathies secondary to isoniazid therapy develop.
Pyrazinamide
Pyrazinamide is a pyrazine analogue of nicotinamide; it may be bacteriostatic or bactericidal

against Mycobacterium tuberculosis, depending on the drug concentration attained at the site of
infection. Pyrazinamide's mechanism of action is unknown.
Ethambutol (Myambutol)
Ethambutol diffuses into actively growing mycobacterial cells (eg, tubercle bacilli). It impairs cell
metabolism by inhibiting the synthesis of 1 or more metabolites, which in turn causes cell death.
No cross-resistance has been demonstrated. Mycobacterial resistance is frequent with previous
therapy.
Ethambutol is used in combination with second-line drugs that have not been administered
previously. It is administered every 24 hours until permanent bacteriologic conversion and maximal
clinical improvement are observed. Absorption is not significantly altered by food.
Vaccines, Inactivated, Bacterial

Class Summary
Inactivated bacterial vaccines are used to induce active immunity against pathogens responsible
for meningitis.
Meningococcal (group A C Y and W-135) diphtheria conjugate vaccine

(Menactra, Menveo)
This vaccine is composed of capsular polysaccharide antigens (groups A, C, Y, and W-135) of N

meningitidis. Meningococcal vaccine may be used to prevent and control outbreaks of serogroup C
meningococcal disease, according to Centers for Disease Control and Prevention (CDC)
guidelines. It induces formation of bactericidal antibodies to meningococcal antigens.
The vaccine is used for active immunization against invasive meningococcal disease caused by
inclusive serogroups. Although the vaccine induces antibody response for serogroup A in
individuals as young as age 3 months, it is poorly immunogenic for serogroup C in recipients who
are younger than age 18-24 months.
Meningococcal group B vaccine (Trumenba, Bexsero)
The vaccine is administered as a 3-dose series at months 0, 2, and 6 (Trumenba) or a 2-dose

series given at least 1 month apart (Bexsero). It induces production of bactericidal antibodies
directed against the capsular polysaccharides of serogroup B. It is indicated for active
immunization to prevent invasive meningococcal disease caused by Neisseria meningitidis
serogroup B in individuals aged 10 through 25 years.
Pneumococcal polysaccharide vaccine polyvalent (Pneumovax 23)
This vaccine contains capsular polysaccharides of 23 pneumococcal types, which constitute 98%
of pneumococcal disease isolates.
Pneumococcal vaccine 13-valent (Prevnar 13)
Capsular polysaccharide vaccine against 13 strains of S pneumoniae conjugated to nontoxic

diphtheria protein. Includes serotypes 1, 3, 4, 5, 6A, 6B, 7F, 9V, 14, 18C, 19A, 19F, and 23F.
Corticosteroids
Class Summary
The use of steroids has been shown to improve overall outcome for patients with certain types of
bacterial meningitis, such as H influenzae, tuberculous, and pneumococcal meningitis. If steroids
are given, they should be administered before or during the administration of antimicrobial therapy.
Dexamethasone (Baycadron)
Dexamethasone has many pharmacologic benefits, such as stabilizing cell and lysosomal
membranes. It increases surfactant synthesis, increases serum vitamin A concentrations, and
inhibits prostaglandin and proinflammatory cytokines (eg, tumor necrosis factor alpha [TNF-],
interleukin [IL]-6, IL-2, and interferon gamma).
The timing of dexamethasone administration is crucial. If this agent is used, it should be

administered before or with the first dose of antibacterial therapy, so as to counteract the initial
inflammatory burst consequent to antibiotic-mediated bacterial killing. A more intense inflammatory
reaction has been documented after the massive bacterial killing induced by antibiotics.
Diuretics, Osmotic Agents

Class Summary
Mannitol produces osmotic diuresis and reduces intracranial pressure (ICP).
Mannitol (Osmitrol)
Mannitol may reduce subarachnoid-space pressure by creating an osmotic gradient between CSF
in the arachnoid space and plasma. Doses of 1 g/kg IV have been used.
Diuretics, Loop
Class Summary
Loop diuretics are used to reduce ICP and treat cerebral edema.
Furosemide (Lasix)
Furosemide is a loop diuretic that increases the excretion of water by interfering with the chloride-
binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the
ascending loop of Henle and distal renal tubule. The proposed mechanisms for furosemide in
lowering ICP include (1) lowering cerebral sodium uptake, (2) affecting water transport into
astroglial cells by inhibiting the cellular membrane cation-chloride pump, and (3) decreasing CSF
production by inhibiting carbonic anhydrase.
Anticonvulsants, Hydantoins
Class Summary
Anticonvulsants are used to help aggressively control seizures (if present) in acute meningitis,
because seizure activity increases ICP.
Phenytoin (Dilantin, Phenytek)
Phenytoin works on the motor cortex, where it may inhibit the spread of seizure activity. The
activity of brainstem centers responsible for the tonic phase of grand mal seizures may also be
inhibited. Dosing should be individualized. Doses of 15 mg/kg have been used.
Anticonvulsants, Barbiturates
Class Summary
Phenobarbital elevates the seizure threshold, limits the spread of seizure activity, and is a sedative.
Doses of 5-10 mg/kg have been recommended.
Phenobarbital
Phenobarbital elevates the seizure threshold, limits the spread of seizure activity, and is a sedative.
Doses of 5-10 mg/kg have been recommended.
Anticonvulsants, Other
Class Summary
Anticonvulsants are used to help aggressively control seizures (if present) in acute meningitis,
because seizure activity increases ICP.
Lorazepam (Ativan)
Lorazepam is a sedative hypnotic with a short onset of effect and a relatively long half-life. By
increasing the action of gamma-aminobutyric acid (GABA), which is a major inhibitory
neurotransmitter in the brain, it may depress all levels of the CNS, including the limbic system and
the reticular formation. Doses of 0.1 mg/kg IV have been used to control seizures.
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compared to HIV negative patients in an internal medicine ward of Librevile, Gabon. Int Conf
AIDS: International Conference on AIDS. Jul 7-12 2002;abstract no. ThPeB7368.
48. Scheld WM, Koedel U, Nathan B, Pfister HW. Pathophysiology of bacterial meningitis:
mechanism(s) of neuronal injury. J Infect Dis. 2002 Dec 1. 186 Suppl 2:S225-33. [Medline].
49. van de Beek D, de Gans J, Tunkel AR, Wijdicks EF. Community-acquired bacterial meningitis
in adults. N Engl J Med. 2006 Jan 5. 354(1):44-53. [Medline].
50. [Guideline] Tunkel AR, Hasbun R, Bhimraj A, Byers K, Kaplan SL, Michael Scheld W, et al.
2017 Infectious Diseases Society of America's Clinical Practice Guidelines for Healthcare-
Associated Ventriculitis and Meningitis. Clin Infect Dis. 2017 Feb 14. [Medline].
Media Gallery
Pneumococcal meningitis in a patient with alcoholism. Courtesy of the CDC/Dr. Edwin P.

Ewing, Jr.
Acute bacterial meningitis. This axial nonenhanced computed tomography scan shows mild
ventriculomegaly and sulcal effacement.
Acute bacterial meningitis. This axial T2-weighted magnetic resonance image shows only
mild ventriculomegaly.
Acute bacterial meningitis. This contrast-enhanced, axial T1-weighted magnetic resonance
image shows leptomeningeal enhancement (arrows).
Chronic mastoiditis and epidural empyema in a patient with bacterial meningitis. This axial
computed tomography scan shows sclerosis of the temporal bone (chronic mastoiditis), an
adjacent epidural empyema with marked dural enhancement (arrow), and the absence of left
mastoid air.
Subdural empyema and arterial infarct in a patient with bacterial meningitis. This contrast-
enhanced axial computed tomography scan shows left-sided parenchymal hypoattenuation in
the middle cerebral artery territory, with marked herniation and a prominent subdural
empyema.
of 6
Tables
Table 1. Infectious Agents Causing Aseptic Meningitis

Table 2. Causes of Chronic Meningitis
Table 3. Changing Epidemiology of Acute Bacterial Meningitis in United States*
Table 4. Most Common Bacterial Pathogens on Basis of Age and Predisposing Risks
Table 5. CSF Findings in Meningitis by Etiologic Agent
Table 6. Comparison of CSF Findings by Type of Organism
Table 7. Recommended Empiric Antibiotics for Suspected Bacterial Meningitis, According to
Age or Predisposing Factors [25]
Table 8. Specific Antibiotics and Duration of Therapy for Acute Bacterial Meningitis
Table 1. Infectious Agents Causing Aseptic Meningitis
Category Agent
Bacteria Partially treated

bacterial meningitis
Listeria
monocytogenes
Brucella spp
Rickettsia rickettsii
Ehrlichia spp
Mycoplasma
pneumoniae
Borrelia burgdorferi
Treponema
pallidum
Leptospira spp
Mycobacterium
tuberculosis
Nocardia spp
Naegleria fowleri
Acanthamoeba spp
Balamuthia spp
Angiostrongylus
cantonensis
Gnathostoma
Parasites spinigerum
Baylisascaris
procyonis
Strongyloides
stercoralis
Taenia solium
(cysticercosis)
Fungi Cryptococcus
neoformans
Coccidioides
immitis
Blastomyces
dermatitidis
Histoplasma
capsulatum
Candida spp
Aspergillus spp
Poliovirus
Echovirus
Coxsackievirus
A
Viruses Enterovirus
Coxsackievirus
B
Enterovirus
68-71
Herpesvirus (HSV) HSV-1 and HSV-2
Varicella-zoster
virus
Epstein-Barr virus
Cytomegalovirus
HHV-6 and HHV-7
Mumps virus
Paramyxovirus
Measles virus
Togavirus Rubella virus
West Nile virus
Japanese
encephalitis virus
Flavivirus
St Louis
encephalitis virus
California
encephalitis virus
Bunyavirus
La Crosse
encephalitis virus
Alphavirus Eastern equine

encephalitis virus
Western equine
encephalitis virus
Venezuelan
encephalitis virus
Colorado tick fever

Reovirus
virus
Arenavirus LCM virus
Rhabdovirus Rabies virus
Retrovirus HIV
HHV = human herpesvirus; HSV = herpes

simplex virus; LCM = lymphocytic
choriomeningitis.
Table 2. Causes of Chronic Meningitis
Category Agent
Bacteria Mycobacterium tuberculosis
Borrelia burgdorferi
Treponema pallidum
Brucella spp
Francisella tularensis
Nocardia spp
Actinomyces spp
Cryptococcus neoformans
Coccidioides immitis
Blastomyces dermatitidis
Histoplasma capsulatum
Fungi
Candida albicans
Aspergillus spp
Sporothrix schenckii
Parasites Acanthamoeba spp
Naegleria fowleri
Angiostrongylus cantonensis
Gnathostoma spinigerum
Baylisascarisprocyonis
Schistosoma spp
Strongyloides stercoralis
Echinococcus granulosus
Table 3. Changing Epidemiology of Acute Bacterial Meningitis in United States*
1978- 1998-
Bacteria 1986 1995
1981 2007
Haemophilus influenzae 48% 45% 7% 6.7%
Listeria monocytogenes 2% 3% 8% 3.4%
Neisseria meningitidis 20% 14% 25% 13.9%
Streptococcus agalactiae (group B streptococcus) 3% 6% 12% 18.1%
Streptococcus pneumoniae 13% 18% 47% 58%
*Nosocomial meningitis is not included; these data

include only the 5 major meningeal pathogens.
Table 4. Most Common Bacterial Pathogens on Basis of Age and Predisposing Risks
Risk or Predisposing Factor Bacterial Pathogen
Streptococcus agalactiae (GBS)
Escherichia coli K1
Age 0-4 weeks
Listeria monocytogenes
Age 4-12 weeks S agalactiae
E coli
Haemophilus influenzae
Streptococcus pneumoniae
Neisseria meningitidis
N meningitidis
S pneumoniae
Age 3 months to 18 years
H influenzae
S pneumoniae
N meningitidis
Age 18-50 years
H influenzae
S pneumoniae
N meningitidis
Age >50 years

L monocytogenes
Aerobic gram-negative bacilli
Immunocompromised state S pneumoniae
N meningitidis
L monocytogenes
Staphylococcus aureus
Coagulase-negative staphylococci
Intracranial manipulation, including
neurosurgery
Aerobic gram-negative bacilli, including
Pseudomonas aeruginosa
S pneumoniae
H influenzae
Basilar skull fracture
Group A streptococci
CSF shunts Coagulase-negative staphylococci
S aureus
Propionibacterium acnes
CSF = cerebrospinal fluid; GBS = group B

streptococcus.
Table 5. CSF Findings in Meningitis by Etiologic Agent
Opening
Pressure WBC count Glucose Protein
Agent Microbiology
(mm H2 (cells/L) (mg/dL) (mg/dL)
O)
Specific
pathogen
100-5000; demonstrated
Bacterial meningitis 200-300 >80% < 40 >100 in 60% of
PMNs Gram stains
and 80% of
cultures
Normal, Normal
reduced but may
10-300; Viral isolation,
Viral meningitis 90-200 in LCM be
lymphocytes PCR assays
and slightly
mumps elevated
Acid-fast
Tuberculous 100-500; Reduced, Elevated,
180-300 bacillus stain,
meningitis lymphocytes < 40 >100
culture, PCR
India ink,
Cryptococcal 10-200; cryptococcal
180-300 Reduced 50-200
meningitis lymphocytes antigen,
culture
Normal
but may Negative
10-300;
Aseptic meningitis 90-200 Normal be findings on
lymphocytes
slightly workup
elevated
Negative
0-5;
Normal values 80-200 50-75 15-40 findings on
lymphocytes
workup
LCM = lymphocytic
choriomeningitis; PCR
= polymerase chain
reaction; PMN =
polymorphonuclear
leukocyte; WBC =
white blood cell.
Table 6. Comparison of CSF Findings by Type of Organism
Normal Finding Bacterial Meningitis Viral Meningitis* Fungal Meningitis**
Normal or mildly
increased in
Pressure (mm H2
tuberculous
O) meningitis; may be
increased in fungal;
Normal or mildly AIDS patients with
Increased
increased cryptococcal
50-150 meningitis have
increased risk of
blindness and death
unless kept below
300 mm H2 O
No cell count result

can exclude bacterial
meningitis; PMN
count typically in
1000s but may be
less dramatic or even
normal (classically, in
Cell count Cell count usually <
very early
(mononuclear cells/ 500, nearly 100%
meningococcal
L) mononuclear; up to
meningitis and in
48 hours, significant
extremely ill
PMN pleocytosis
neonates);
may be
lymphocytosis with
Preterm: 0-25 indistinguishable
normal CSF
from early bacterial
chemistries seen in
meningitis; this is Hundreds of
15-25%, especially
particularly true with mononuclear cells
when cell counts <
Term: 0-22 eastern equine
1000 or with partial
encephalitis;
treatment; ~90% of
presence of
patients with
nontraumatic RBCs
ventriculoperitoneal
>6 months: 0-5 in 80% of HSV
shunts who have CSF
meningoencephalitis,
WBC count >100 are
though 10% have
infected; CSF glucose
normal CSF results
is usually normal, and
organisms are less
pathogenic; cell count
and chemistries
normalize slowly
(over days) with
antibiotics
Microscopy Gram stain 80% No organism India ink is 50%

sensitive; inadequate sensitive for fungi;
decolorization may cryptococcal antigen
mistake Haemophilus is 95% sensitive;
No organisms influenzae for gram- AFB stain is 40%
positive cocci; sensitive for
pretreatment with tuberculosis
antibiotics may affect (increase yield by

stain uptake, causing staining supernatant
gram-positive from at least 5 mL
organisms to appear CSF)
gram-negative and
decrease culture yield
by average of 20%
Glucose
Sometimes
Euglycemia: >50%
decreased; aside
serum
from fulminant
bacterial meningitis,
lowest levels of CSF
glucose are seen in
Hyperglycemia: Decreased Normal
tuberculous
>30% serum
meningitis, primary
amebic
meningoencephalitis,
and
Wait 4 hr after
neurocysticercosis
glucose load
Protein (mg/dL)
Preterm: 65-150
Increased; >1000
with relatively benign
Usually >150, may be
Mildly increased clinical presentation
Term: 20-170 >1000
suggestive of fungal
disease
>6 months: 15-45
AFB = acid-fast
bacillus; CSF =
cerebrospinal fluid;
HSV = herpes
simplex virus; RBC
= red blood cell;
PMN =
polymorphonuclear
leukocyte.
*Some bacteria (eg,

Mycoplasma,
Listeria, Leptospira
spp, Borrelia
burgdorferi [Lyme],
and spirochetes)
produce spinal fluid
alterations that
resemble the viral
profile. An aseptic
profile also is
typical of partially
treated bacterial
infections (>33% of
patients have
received
antimicrobial
treatment,
especially children)
and the 2 most
common causes of
encephalitisthe
potentially curable
HSV and
arboviruses.
**In contrast,
tuberculous
meningitis and
parasites resemble
the fungal profile
more closely.
Table 7. Recommended Empiric Antibiotics for Suspected Bacterial Meningitis, According to Age or
Predisposing Factors [25]
Age or Predisposing Feature Antibiotics
Ampicillin plus either cefotaxime or an

Age 0-4 wk
aminoglycoside
Age 1 mo-50 y Vancomycin plus cefotaxime or ceftriaxone*
Vancomycin plus ampicillin plus ceftriaxone or

Age >50 y
cefotaxime plus vancomycin*
Vancomycin plus ampicillin plus either cefepime

Impaired cellular immunity
or meropenem
Recurrent meningitis Vancomycin plus cefotaxime or ceftriaxone

Basilar skull fracture Vancomycin plus cefotaxime or ceftriaxone
Vancomycin plus ceftazidime, cefepime, or

Head trauma, neurosurgery, or CSF shunt
meropenem
CSF = cerebrospinal fluid.
*Add ampicillin if Listeria monocytogenes

is a suspected pathogen.
Table 8. Specific Antibiotics and Duration of Therapy for Acute Bacterial Meningitis
Duration
Bacteria Susceptibility Antibiotic(s)
(days)
Recommended: Penicillin
G or ampicillin
Streptococcus Penicillin MIC 0.06

Alternatives: Cefotaxime, 10-14
pneumoniae g/mL
ceftriaxone,
chloramphenicol
Recommended:
Penicillin MIC 0.12
Cefotaxime or
g/mL
ceftriaxone
Cefotaxime or
Alternatives:
ceftriaxone MIC 0.12
Cefepime,
g/mL
meropenem
Cefotaxime or Recommended:
ceftriaxone MIC 1.0 Vancomycin plus
g/mL cefotaxime or
ceftriaxone
Alternatives:
Vancomycin plus
moxifloxacin
Recommended: Ampicillin
Alternatives: Cefotaxime,
Beta- ceftriaxone, cefepime,
Haemophilus influenzae 7
lactamasenegative chloramphenicol,
aztreonam, a
fluoroquinolone
Recommended:
Cefotaxime or
ceftriaxone
Alternatives:
Beta-lactamasepositive
Cefepime,
chloramphenicol,
aztreonam, a
fluoroquinolone
Recommended:
Meropenem
Beta- Alternatives:
lactamasenegative, Cefepime,
ampicillin-resistant chloramphenicol,
aztreonam, a
fluoroquinolone
Neisseria meningitidis Penicillin MIC < 0.1 Recommended: Penicillin 7

g/mL G or ampicillin
ceftriaxone,
chloramphenicol
Recommended:
Cefotaxime or
ceftriaxone
Penicillin MIC 0.1 Alternatives:

g/mL Cefepime,
chloramphenicol, a
fluoroquinolone,
meropenem
or penicillin G
Listeria monocytogenes ... 14-21

Alternative: TMP-SMX
or penicillin G
Streptococcus agalactiae ... 14-21

ceftriaxone, vancomycin
Recommended:
Cefotaxime or ceftriaxone
Enterobacteriaceae ... Alternatives: Aztreonam, a 21

fluoroquinolone, TMP-SMX,
meropenem, ampicillin
Pseudomonas ... Recommended: 21

aeruginosa Ceftazidime or cefepime
Alternatives: Aztreonam,
meropenem, ciprofloxacin
Recommended:
Vancomycin
Alternative: Linezolid
Staphylococcus
epidermidis
Consider addition of
rifampin
MIC= minimal inhibitory

concentration; TMP-SMX
= trimethoprim-
sulfamethoxazole.
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Contributor Information and Disclosures
Author
Rodrigo Hasbun, MD, MPH Associate Professor of Medicine, Section of Infectious Diseases,
University of Texas Medical School at Houston
Disclosure: Received honoraria from Medicine''''''''s Company for speaking and teaching; Received
honoraria from Cubicin for speaking and teaching; Received honoraria from Theravance for
speaking and teaching; Received honoraria from Pfizer for speaking and teaching.
Chief Editor
Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine,
Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of
Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious
Diseases Society of America
Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha,
American College of Physicians, American Medical Association, Association of Professors of
Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, Southern
Society for Clinical Investigation
Disclosure: Nothing to disclose.

Acknowledgements
Suur Biliciler, MD Neuromuscular Fellow, Department of Neurology, Baylor College of Medicine
Timothy S Brannan, MD Director, Department of Neurology, Jersey City Medical Center;

Professor, Department of Neurology, Seton Hall School of Graduate Medical Education
Robert Cavaliere, MD Assistant Professor of Neurology, Neurosurgery and Medicine, Ohio State
University College of Medicine
Sidney E Croul, MD Director of Neuropathology, Professor, Department of Pathology and

Laboratory Medicine, Medical College of Pennsylvania Hahnemann University
Francisco de Assis Aquino Gondim, MD, MSc, PhD Associate Professor of Neurology,
Department of Neurology and Psychiatry, St Louis University School of Medicine
Francisco de Assis Aquino Gondim, MD, MSc, PhD is a member of the following medical societies:
American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic
Medicine, and Movement Disorders Society
Alan Greenberg, MD Director, Associate Professor, Department of Internal Medicine, Jersey City
Medical Center, Seton Hall University
Alan Greenberg, MD is a member of the following medical societies: Alpha Omega Alpha and
American College of Physicians
Ronald A Greenfield, MD Professor, Department of Internal Medicine, University of Oklahoma

College of Medicine
Ronald A Greenfield, MD is a member of the following medical societies: American College of

Physicians, American Federation for Medical Research, American Society for Microbiology, Central
Society for Clinical Research, Infectious Diseases Society of America, Medical Mycology Society of
the Americas, Phi Beta Kappa, Southern Society for Clinical Investigation, and Southwestern
Association of Clinical Microbiology
Disclosure: Pfizer Honoraria Speaking and teaching; Gilead Honoraria Speaking and teaching;
Ortho McNeil Honoraria Speaking and teaching; Abbott Honoraria Speaking and teaching; Astellas
Honoraria Speaking and teaching; Cubist Honoraria Speaking and teaching; Forest
Pharmaceuticals Speaking and teaching
J Stephen Huff, MD Associate Professor of Emergency Medicine and Neurology, Department of

Emergency Medicine, University of Virginia School of Medicine
J Stephen Huff, MD is a member of the following medical societies: American Academy of

Emergency Medicine, American Academy of Neurology, American College of Emergency
Physicians, and Society for Academic Emergency Medicine

Lutfi Incesu, MD Professor, Department of Radiology, Ondokuz Mayis University School of

Medicine; Chief, Neuroradiology and MR Unit, Department of Radiology, Ondokuz Mayis University
Hospital, Turkey
Lutfi Incesu, MD is a member of the following medical societies: American Society of

Neuroradiology and Radiological Society of North America
Uma Iyer, MD Resident Physician, Department of Neurology, State University of New York Upstate
Medical Center
Pieter R Kark, MD, MA, FAAN, FACP Instructor in Palliative Care, The Lifetime Healthcare
Companies
Michael R Keating, MD Associate Professor of Medicine, Chair, Division of Infectious Diseases,

Department of Medicine, Mayo Clinic College of Medicine
Michael R Keating, MD is a member of the following medical societies: American College of

Physicians, American Medical Association, American Society for Microbiology, American Society of
Transplantation, Infectious Diseases Society of America, and International Immunocompromised
Host Society
Anil Khosla, MBBS, MD Assistant Professor, Department of Radiology, St Louis University School
of Medicine, Veterans Affairs Medical Center of St Louis
Anil Khosla, MBBS, MD is a member of the following medical societies: American College of
Radiology, American Roentgen Ray Society, American Society of Neuroradiology, North American
Spine Society, and Radiological Society of North America
John W King, MD Professor of Medicine, Chief, Section of Infectious Diseases, Director, Viral
Therapeutics Clinics for Hepatitis, Louisiana State University Health Sciences Center; Consultant
in Infectious Diseases, Overton Brooks Veterans Affairs Medical Center
John W King, MD is a member of the following medical societies: American Association for the
Advancement of Science, American College of Physicians, American Federation for Medical
Research, American Society for Microbiology, Association of Subspecialty Professors, Infectious
Diseases Society of America, and Sigma Xi
Disclosure: MERCK None Other
Marjorie Lazoff, MD Editor-in-Chief, Medical Computing Review
Marjorie Lazoff, MD is a member of the following medical societies: Alpha Omega Alpha, American
College of Emergency Physicians, American Medical Informatics Association, and Society for
Academic Emergency Medicine
Glenn Lopate, MD Associate Professor, Department of Neurology, Division of Neuromuscular

Diseases, Washington University School of Medicine; Director of Neurology Clinic, St Louis
ConnectCare; Consulting Staff, Department of Neurology, Barnes-Jewish Hospital
Glenn Lopate, MD is a member of the following medical societies: American Academy of

Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, and Phi Beta
Kappa
Disclosure: Baxter Grant/research funds Other; Amgen Grant/research funds None
Joseph Richard Masci, MD Professor of Medicine, Professor of Preventive Medicine, Mount Sinai
School of Medicine; Director of Medicine, Elmhurst Hospital Center
Joseph Richard Masci, MD is a member of the following medical societies: Alpha Omega Alpha,
American College of Physicians, Association of Professors of Medicine, and Royal Society of
Medicine
C Douglas Phillips, MD Director of Head and Neck Imaging, Division of Neuroradiology, New York
Presbyterian Hospital, Weill Cornell Medical College
C Douglas Phillips, MD is a member of the following medical societies: American College of

Radiology, American Medical Association, American Society of Head and Neck Radiology,
American Society of Neuroradiology, Association of University Radiologists, and Radiological
Society of North America
Tarakad S Ramachandran, MBBS, FRCP(C), FACP Professor of Neurology, Clinical Professor of

Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State
University of New York Upstate Medical University; Chair, Department of Neurology, Crouse Irving
Memorial Hospital
Tarakad S Ramachandran, MBBS, FRCP(C), FACP is a member of the following medical societies:
American Academy of Neurology, American Academy of Pain Medicine, American College of
Forensic Examiners, American College of International Physicians, American College of Managed
Care Medicine, American College of Physicians, American Heart Association, American Stroke
Association, Royal College of Physicians, RoyalCollegeofPhysicians and Surgeons of Canada,
Royal College of Surgeons of England, and Royal Society of Medicine
Disclosure: Abbott Labs None None; Teva Marion None None; Boeringer-Ingelheim Honoraria
Speaking and teaching
Raymund R Razonable, MD Consultant, Division of Infectious Diseases, Mayo Clinic of

Rochester; Associate Professor of Medicine, Mayo Clinic College of Medicine
Raymund R Razonable, MD is a member of the following medical societies: American Medical

Association, American Society for Microbiology, Infectious Diseases Society of America, and
International Immunocompromised Host Society
Norman C Reynolds Jr, MD Neurologist, Veterans Affairs Medical Center of Milwaukee; Clinical
Professor, Medical College of Wisconsin
Norman C Reynolds Jr, MD is a member of the following medical societies: American Academy of
Neurology, Association of Military Surgeons of the US, Movement Disorders Society, Sigma Xi,
and Society for Neuroscience
Robert Stanley Rust Jr, MD, MA Thomas E Worrell Jr Professor of Epileptology and Neurology,
Co-Director of FE Dreifuss Child Neurology and Epilepsy Clinics, Director, Child Neurology,
University of Virginia School of Medicine; Chair-Elect, Child Neurology Section, American

Academy of Neurology
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Academy of Neurology, American Epilepsy Society, American Headache Society, American
Neurological Association, Child Neurology Society, International Child Neurology Association, and
Society for Pediatric Research
Prem C Shukla, MD Associate Chairman, Associate Professor, Department of Emergency

Medicine, University of Arkansas for Medical Sciences
Manish K Singh, MD Assistant Professor, Department of Neurology, Teaching Faculty for Pain
Management and Neurology Residency Program, Hahnemann University Hospital, Drexel College
of Medicine; Medical Director, Neurology and Pain Management, Jersey Institute of Neuroscience
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Neurology, American Academy of Pain Medicine, American Association of Physicians of Indian
Origin, American Headache Society, American Medical Association, and American Society of
Regional Anesthesia and Pain Medicine
Niranjan N Singh, MD, DNB Assistant Professor of Neurology, University of Missouri-Columbia

School of Medicine
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Neurology
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Omega Alpha, American Academy of Emergency Medicine, American College of Emergency
Physicians, American Medical Association, and Ohio State Medical Association
James G Smirniotopoulos, MD Professor of Radiology, Neurology, and Biomedical Informatics,

Program Director, Diagnostic Imaging Program, Center for Neuroscience and Regenerative
Medicine (CNRM), Uniformed Services University of the Health Sciences
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Radiology, American Roentgen Ray Society, American Society of Head and Neck Radiology,
American Society of Neuroradiology, American Society of Pediatric Neuroradiology, Association of
University Radiologists, and Radiological Society of North America
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Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
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Florian P Thomas, MD, MA, PhD, Drmed Director, Spinal Cord Injury Unit, St Louis Veterans
Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Director,
Neuropathy Association Center of Excellence, Professor, Department of Neurology and Psychiatry,

Associate Professor, Institute for Molecular Virology, and Department of Molecular Microbiology
and Immunology, St Louis University School of Medicine
Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American
Academy of Neurology, American Neurological Association, American Paraplegia Society,
Consortium of Multiple Sclerosis Centers, and National Multiple Sclerosis Society
Frederick M Vincent Sr, MD Clinical Professor, Department of Neurology and Ophthalmology,

Michigan State University Colleges of Human and Osteopathic Medicine
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American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic
Medicine, American College of Forensic Examiners, American College of Legal Medicine,
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Amir Vokshoor, MD Staff Neurosurgeon, Department of Neurosurgery, Spine Surgeon, Diagnostic

and Interventional Spinal Care, St John's Health Center
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Fellowship Director, Stanford University Medical Center Disaster Medicine Fellowship, Chairman,
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Progressor, Department of Surgery (Emergency Medicine), Stanford University Medical Center
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Cefotaxime is a third-generation cephalosporin that is used to treat suspected or documented

Ganciclovir can be used to treat cytomegalovirus (CMV) meningitis in immunocompromised hosts.

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Amphotericin B deoxycholate (Amphotericin B (conventional), Fungizone)

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A polyene antibiotic produced by a strain of Streptomyces nodosus, amphotericin B can be

Amphotericin B lipid complex (Abelcet)

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Itraconazole (Sporanox, Onmel)

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Rifampin is used in combination with other antituberculous drugs. It inhibits DNA-dependent

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Pyrazinamide is a pyrazine analogue of nicotinamide; it may be bacteriostatic or bactericidal

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Vaccines, Inactivated, Bacterial

Meningococcal (group A C Y and W-135) diphtheria conjugate vaccine

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This vaccine is composed of capsular polysaccharide antigens (groups A, C, Y, and W-135) of N

Meningococcal group B vaccine (Trumenba, Bexsero)

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The vaccine is administered as a 3-dose series at months 0, 2, and 6 (Trumenba) or a 2-dose

Pneumococcal polysaccharide vaccine polyvalent (Pneumovax 23)

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Pneumococcal vaccine 13-valent (Prevnar 13)

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Capsular polysaccharide vaccine against 13 strains of S pneumoniae conjugated to nontoxic

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The timing of dexamethasone administration is crucial. If this agent is used, it should be

Diuretics, Osmotic Agents

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Phenytoin (Dilantin, Phenytek)

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