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Meningitis Medication

  • Author: Rodrigo Hasbun, MD, MPH; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Feb 16, 2016
 

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.

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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)

 

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.

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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)

 

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.

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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]

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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]

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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.

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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.

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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.

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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

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Penicillins, Natural

Class Summary

Penicillins are highly active against gram-positive organisms.

Penicillin G (Pfizerpen-G)

 

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).

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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.

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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.

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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.

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Antifungals, Systemic

Class Summary

Antifungal agents are used in the management of infectious diseases caused by fungi.

Amphotericin B, conventional

 

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.

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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.

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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.

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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-α], 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.

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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.

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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.

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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.

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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.

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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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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 Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Suur Biliciler, MD Neuromuscular Fellow, Department of Neurology, Baylor College of Medicine

Disclosure: Nothing to disclose.

Timothy S Brannan, MD Director, Department of Neurology, Jersey City Medical Center; Professor, Department of Neurology, Seton Hall School of Graduate Medical Education

Disclosure: Nothing to disclose.

Robert Cavaliere, MD Assistant Professor of Neurology, Neurosurgery and Medicine, Ohio State University College of Medicine

Disclosure: Nothing to disclose.

Sidney E Croul, MD Director of Neuropathology, Professor, Department of Pathology and Laboratory Medicine, Medical College of Pennsylvania Hahnemann University

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

Uma Iyer, MD Resident Physician, Department of Neurology, State University of New York Upstate Medical Center

Disclosure: Nothing to disclose.

Pieter R Kark, MD, MA, FAAN, FACP Instructor in Palliative Care, The Lifetime Healthcare Companies

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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

Robert Stanley Rust Jr, MD, MA is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, American Headache Society, American Neurological Association, Child Neurology Society, International Child Neurology Association, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Prem C Shukla, MD Associate Chairman, Associate Professor, Department of Emergency Medicine, University of Arkansas for Medical Sciences

Disclosure: Nothing to disclose.

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

Manish K Singh, MD is a member of the following medical societies: American Academy of 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

Disclosure: Nothing to disclose.

Niranjan N Singh, MD, DNB Assistant Professor of Neurology, University of Missouri-Columbia School of Medicine

Niranjan N Singh, MD, DNB is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Mark S Slabinski, MD, FACEP, FAAEM Vice President, EMP Medical Group

Mark S Slabinski, MD, FACEP, FAAEM is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Ohio State Medical Association

Disclosure: Nothing to disclose.

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

James G Smirniotopoulos, MD is a member of the following medical societies: American College of 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

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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

Disclosure: Nothing to disclose.

Frederick M Vincent Sr, MD Clinical Professor, Department of Neurology and Ophthalmology, Michigan State University Colleges of Human and Osteopathic Medicine

Frederick M Vincent Sr, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Forensic Examiners, American College of Legal Medicine, American College of Physicians, and Michigan State Medical Society

Disclosure: Nothing to disclose.

Amir Vokshoor, MD Staff Neurosurgeon, Department of Neurosurgery, Spine Surgeon, Diagnostic and Interventional Spinal Care, St John's Health Center

Amir Vokshoor, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, American Medical Association, and North American Spine Society

Disclosure: Nothing to disclose.

Cordia Wan, MD Adult Neurologist, Kaiser Permanente Hawaii, Kaiser Permanente Southern California

Cordia Wan, MD is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Eric L Weiss, MD, DTM&H Medical Director, Office of Service Continuity and Disaster Planning, Fellowship Director, Stanford University Medical Center Disaster Medicine Fellowship, Chairman, SUMC and LPCH Bioterrorism and Emergency Preparedness Task Force, Clinical Associate Progressor, Department of Surgery (Emergency Medicine), Stanford University Medical Center

Eric L Weiss, MD, DTM&H is a member of the following medical societies: American College of Emergency Physicians, American College of Occupational and Environmental Medicine, American Medical Association, American Society of Tropical Medicine and Hygiene, Physicians for Social Responsibility, Southeastern Surgical Congress, Southern Association for Oncology, Southern Clinical Neurological Society, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Lawrence A Zumo, MD Neurologist, Private Practice

Lawrence A Zumo, MD is a member of the following medical societies: American Academy of Neurology, American College of Physicians, American Medical Association, and Southern Medical Association

Disclosure: Nothing to disclose.

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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.
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



Parasites Naegleria fowleri



Acanthamoeba spp



Balamuthia spp



Angiostrongylus cantonensis



Gnathostoma spinigerum



Baylisascaris procyonis



Strongyloides stercoralis



Taenia solium (cysticercosis)



Fungi Cryptococcus neoformans



Coccidioides immitis



Blastomyces dermatitidis



Histoplasma capsulatum



Candida spp



Aspergillus spp



Viruses Enterovirus Poliovirus



Echovirus



Coxsackievirus A



Coxsackievirus B



Enterovirus 68-71



Herpesvirus (HSV) HSV-1 and HSV-2



Varicella-zoster virus



Epstein-Barr virus



Cytomegalovirus



HHV-6 and HHV-7



Paramyxovirus Mumps virus



Measles virus



Togavirus Rubella virus
Flavivirus West Nile virus



Japanese encephalitis virus



St Louis encephalitis virus



Bunyavirus California encephalitis virus



La Crosse encephalitis virus



Alphavirus Eastern equine encephalitis virus



Western equine encephalitis virus



Venezuelan encephalitis virus



Reovirus Colorado tick fever 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



Fungi Cryptococcus neoformans



Coccidioides immitis



Blastomyces dermatitidis



Histoplasma capsulatum



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*
Bacteria 1978-1981 1986 1995 1998-2007
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
Age 0-4 weeks Streptococcus agalactiae (GBS)



Escherichia coli K1



Listeria monocytogenes



Age 4-12 weeks S agalactiae



E coli



Haemophilus influenzae



Streptococcus pneumoniae



Neisseria meningitidis



Age 3 months to 18 years N meningitidis



S pneumoniae



H influenzae



Age 18-50 years S pneumoniae



N meningitidis



H influenzae



Age >50 years S pneumoniae



N meningitidis



L monocytogenes



Aerobic gram-negative bacilli



Immunocompromised state S pneumoniae



N meningitidis



L monocytogenes



Aerobic gram-negative bacilli



Intracranial manipulation, including neurosurgery Staphylococcus aureus



Coagulase-negative staphylococci



Aerobic gram-negative bacilli, including Pseudomonas aeruginosa



Basilar skull fracture S pneumoniae



H influenzae



Group A streptococci



CSF shunts Coagulase-negative staphylococci



S aureus



Aerobic gram-negative bacilli



Propionibacterium acnes



CSF = cerebrospinal fluid; GBS = group B streptococcus.
Table 5. CSF Findings in Meningitis by Etiologic Agent
Agent Opening Pressure (mm H2 O) WBC count (cells/µL) Glucose (mg/dL) Protein (mg/dL) Microbiology
Bacterial meningitis 200-300 100-5000; >80% PMNs < 40 >100 Specific pathogen demonstrated in 60% of Gram stains and 80% of cultures
Viral meningitis 90-200 10-300; lymphocytes Normal, reduced in LCM and mumps Normal but may be slightly elevated Viral isolation, PCR assays
Tuberculous meningitis 180-300 100-500; lymphocytes Reduced, < 40 Elevated, >100 Acid-fast bacillus stain, culture, PCR
Cryptococcal meningitis 180-300 10-200; lymphocytes Reduced 50-200 India ink, cryptococcal antigen, culture
Aseptic meningitis 90-200 10-300; lymphocytes Normal Normal but may be slightly elevated Negative findings on workup
Normal values 80-200 0-5; lymphocytes 50-75 15-40 Negative findings on 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**
Pressure (mm H2 O)



50-150



Increased Normal or mildly increased Normal or mildly increased in tuberculous meningitis; may be increased in fungal; AIDS patients with cryptococcal meningitis have increased risk of blindness and death unless kept below 300 mm H2 O
Cell count (mononuclear cells/µL)



Preterm: 0-25



Term: 0-22



>6 months: 0-5



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



No organisms



Gram stain 80% sensitive; inadequate decolorization may mistake Haemophilus influenzae for gram-positive cocci; pretreatment with antibiotics may affect stain uptake, causing gram-positive organisms to appear gram-negative and decrease culture yield by average of 20% No organism India ink is 50% sensitive for fungi; cryptococcal antigen is 95% sensitive; AFB stain is 40% sensitive for tuberculosis (increase yield by staining supernatant from at least 5 mL CSF)
Glucose



Euglycemia: >50% serum



Hyperglycemia: >30% serum



Wait 4 hr after glucose load



Decreased Normal Sometimes decreased; aside from fulminant bacterial meningitis, lowest levels of CSF glucose are seen in tuberculous meningitis, primary amebic meningoencephalitis, and neurocysticercosis
Protein (mg/dL)



Preterm: 65-150



Term: 20-170



>6 months: 15-45



Usually >150, may be >1000 Mildly increased Increased; >1000 with relatively benign clinical presentation suggestive of fungal disease
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 encephalitis—the 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
Age 0-4 wk Ampicillin plus either cefotaxime or an aminoglycoside
Age 1 mo-50 y Vancomycin plus cefotaxime or ceftriaxone*
Age >50 y Vancomycin plus ampicillin plus ceftriaxone or cefotaxime plus vancomycin*
Impaired cellular immunity Vancomycin plus ampicillin plus either cefepime or meropenem
Recurrent meningitis Vancomycin plus cefotaxime or ceftriaxone
Basilar skull fracture Vancomycin plus cefotaxime or ceftriaxone
Head trauma, neurosurgery, or CSF shunt Vancomycin plus ceftazidime, cefepime, or 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
Bacteria Susceptibility Antibiotic(s) Duration (days)
Streptococcus pneumoniae Penicillin MIC ≤0.06 μg/mL Recommended: Penicillin G or ampicillin



Alternatives: Cefotaxime, ceftriaxone, chloramphenicol



10-14
Penicillin MIC ≥0.12 μg/mL



Cefotaxime or ceftriaxone MIC ≥0.12 μg/mL



Recommended: Cefotaxime or ceftriaxone



Alternatives: Cefepime, meropenem



Cefotaxime or ceftriaxone MIC ≥1.0 μg/mL Recommended: Vancomycin plus cefotaxime or ceftriaxone



Alternatives: Vancomycin plus moxifloxacin



Haemophilus influenzae Beta-lactamase−negative Recommended: Ampicillin



Alternatives: Cefotaxime, ceftriaxone, cefepime, chloramphenicol, aztreonam, a fluoroquinolone



7
Beta-lactamase−positive Recommended: Cefotaxime or ceftriaxone



Alternatives: Cefepime, chloramphenicol, aztreonam, a fluoroquinolone



Beta-lactamase−negative, ampicillin-resistant Recommended: Meropenem



Alternatives: Cefepime, chloramphenicol, aztreonam, a fluoroquinolone



Neisseria meningitidis Penicillin MIC < 0.1 μg/mL Recommended: Penicillin G or ampicillin



Alternatives: Cefotaxime, ceftriaxone, chloramphenicol



7
Penicillin MIC ≥0.1 μg/mL Recommended: Cefotaxime or ceftriaxone



Alternatives: Cefepime, chloramphenicol, a fluoroquinolone, meropenem



Listeria monocytogenes ... Recommended: Ampicillin or penicillin G



Alternative: TMP-SMX



14-21
Streptococcus agalactiae ... Recommended: Ampicillin or penicillin G



Alternatives: Cefotaxime, ceftriaxone, vancomycin



14-21
Enterobacteriaceae ... Recommended: Cefotaxime or ceftriaxone



Alternatives: Aztreonam, a fluoroquinolone, TMP-SMX, meropenem, ampicillin



21
Pseudomonas aeruginosa ... Recommended: Ceftazidime or cefepime



Alternatives: Aztreonam, meropenem, ciprofloxacin



21
Staphylococcus epidermidis   Recommended: Vancomycin



Alternative: Linezolid



Consider addition of rifampin



 
MIC= minimal inhibitory concentration; TMP-SMX = trimethoprim-sulfamethoxazole.
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