eMedicine Specialties > Infectious Diseases > CNS Infections

Meningitis: Treatment & Medication

Author: Raymund R Razonable, MD, Consultant, Division of Infectious Diseases, Mayo Clinic of Rochester; Associate Professor of Medicine, Mayo Clinic College of Medicine
Coauthor(s): Michael R Keating, MD, Consultant, Assistant Professor of Medicine, Division of Infectious Diseases, Department of Medicine, Mayo Clinic College of Medicine
Contributor Information and Disclosures

Updated: Aug 26, 2009

Treatment

Medical Care

General guidelines

Lumbar puncture for CSF examination is urgently warranted in individuals in whom meningitis is clinically suspected.

In the absence of focal neurologic deficit, radiographic imaging of the head should not preclude performing a lumbar puncture. In addition, the performance of radiographic imaging should not defer the institution of empiric antimicrobial therapy.

Bacterial meningitis is a neurological emergency that is associated with significant morbidity and mortality. The initiation of empiric antibacterial therapy is therefore essential for better outcome.

Institute empiric antimicrobial therapy (ie, antibacterial treatment, or antivirals and antifungal therapy in selected cases) as soon as possible (see Table 6 and Table 7). This is usually based on the known predisposing factors and/or initial CSF Gram-stain results.

Significant delays in instituting antimicrobial treatment in individuals with bacterial meningitis could lead to significant morbidity and mortality.

The chosen antibiotic should attain adequate levels in the CSF. Achieving this usually depends on the drug's lipid solubility, its molecular size, its protein-binding capability, and the state of inflammation at the meninges. The penicillins, certain cephalosporins (ie, third- and fourth-generation cephalosporins), the carbapenems, fluoroquinolones, and rifampin provide high CSF levels.

Monitor for possible drug toxicity during treatment (eg, with blood counts and renal and liver function monitoring).

The dose of the chosen antimicrobial agent should always be adjusted based on the renal and hepatic function of the patient. At times, obtaining serum drug concentrations may be necessary to ensure adequate levels and to avoid toxicity in drugs with a narrow therapeutic index (eg, vancomycin, aminoglycosides).

Once the pathogen has been identified and antimicrobial susceptibilities determined, the antibiotics may be modified for optimal targetted treatment (see Table 8).

One of the major contributors to the morbidity associated with bacterial meningitis is the severity of inflammation. Therefore, pharmacologic interventions to reduce the degree of inflammation may improve outcome. Strongly consider the use of steroids as adjunctive treatment of bacterial meningitis. If steroids are given, they should be administered prior to or during the administration of antimicrobial therapy. The use of steroids has been shown to improve the overall outcome of patients with certain types of bacterial meninigitis, such as H influenzae, tuberculous, and pneumococcal meningitis.

Monitor for the occurrence of complications from the disease (eg, hydrocephalus, seizures, hearing defects) and its treatment (eg, drug toxicity, hypersensitivity).

Table 6. Recommended Empiric Antibiotics According to Predisposing Factors for Patients With Suspected Bacterial Meningitis

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Table
Predisposing FeatureAntibiotic(s)
Age 0-4 weeksAmpicillin plus cefotaxime or an aminoglycoside
Age 1-3 monthsAmpicillin plus cefotaxime plus vancomycin*
Age 3 months to 50 yearsCeftriaxone or cefotaxime plus vancomycin*
Older than 50 yearsAmpicillin plus ceftriaxone or cefotaxime plus vancomycin*
Impaired cellular immunityAmpicillin plus ceftazidime plus vancomycin*
Neurosurgery, head trauma, or CSF shuntVancomycin plus ceftazidime
Predisposing FeatureAntibiotic(s)
Age 0-4 weeksAmpicillin plus cefotaxime or an aminoglycoside
Age 1-3 monthsAmpicillin plus cefotaxime plus vancomycin*
Age 3 months to 50 yearsCeftriaxone or cefotaxime plus vancomycin*
Older than 50 yearsAmpicillin plus ceftriaxone or cefotaxime plus vancomycin*
Impaired cellular immunityAmpicillin plus ceftazidime plus vancomycin*
Neurosurgery, head trauma, or CSF shuntVancomycin plus ceftazidime

*Vancomycin is added empirically to the initial regimen if the presence of penicillin-resistant S pneumoniae is suspected or if a high incidence of resistance is reported in the community.

Table 7. Recommended Empiric Antibiotics for Patients With Suspected Bacterial Meningitis and Known CSF Gram Stain Results

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Table
Gram Stain MorphologyAntibiotic(s)
Gram-positive cocciVancomycin plus ceftriaxone or cefotaxime
Gram-negative cocciPenicillin G*
Gram-positive bacilliAmpicillin plus an aminoglycoside
Gram-negative bacilliBroad-spectrum cephalosporin† plus an aminoglycoside
Gram Stain MorphologyAntibiotic(s)
Gram-positive cocciVancomycin plus ceftriaxone or cefotaxime
Gram-negative cocciPenicillin G*
Gram-positive bacilliAmpicillin plus an aminoglycoside
Gram-negative bacilliBroad-spectrum cephalosporin† plus an aminoglycoside

*Use ceftriaxone if penicillin-resistant N meningitidis occurs in the community.

†Ceftriaxone is preferred. Ceftazidime is used when Pseudomonas infection is likely (eg, neurosurgical procedures).

Table 8. Specific Antibiotics and Duration of Therapy for Patients With Acute Bacterial Meningitis

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Table
BacteriaSusceptibilityAntibiotic(s)Duration
(Days)
S pneumoniaePenicillin MIC <0.1 mg/LPenicillin G10-14
MIC 0.1-1 mg/LCeftriaxone or cefotaxime
MIC >2 mg/LCeftriaxone or cefotaxime
Ceftriaxone MIC >0.5 mg/LCeftriaxone or cefotaxime plus vancomycin or rifampin
H influenzaeBeta-lactamase-negativeAmpicillin7
Beta-lactamase-positiveCeftriaxone or cefotaxime
N meningitidis...Penicillin G or ampicillin7
L monocytogenes...Ampicillin or penicillin G plus an aminoglycoside14-21
S agalactiae...Penicillin G plus an aminoglycoside, if warranted14-21
Enterobacteriaceae...Ceftriaxone or cefotaxime plus an aminoglycoside21
P aeruginosa...Ceftazidime plus an aminoglycoside21
BacteriaSusceptibilityAntibiotic(s)Duration
(Days)
S pneumoniaePenicillin MIC <0.1 mg/LPenicillin G10-14
MIC 0.1-1 mg/LCeftriaxone or cefotaxime
MIC >2 mg/LCeftriaxone or cefotaxime
Ceftriaxone MIC >0.5 mg/LCeftriaxone or cefotaxime plus vancomycin or rifampin
H influenzaeBeta-lactamase-negativeAmpicillin7
Beta-lactamase-positiveCeftriaxone or cefotaxime
N meningitidis...Penicillin G or ampicillin7
L monocytogenes...Ampicillin or penicillin G plus an aminoglycoside14-21
S agalactiae...Penicillin G plus an aminoglycoside, if warranted14-21
Enterobacteriaceae...Ceftriaxone or cefotaxime plus an aminoglycoside21
P aeruginosa...Ceftazidime plus an aminoglycoside21


  • Antimicrobial therapy for bacterial meningitis
    • S pneumoniae
      • The increasing incidence of penicillin-resistant strains has changed the management of pneumococcal meningitis.
      • The third-generation cephalosporins (ceftriaxone 2-4 g/d or cefotaxime 8-12 g/d) with vancomycin (2-3 g/d, adjusted to therapeutic serum levels) are first-line empiric therapy, depending on the resistance patterns in the community.
      • The use of corticosteroids such as dexamethasone as adjunctive treatment for pneumococcal meningitis is now supported by recent studies demonstrating significant benefit with regards to reduction in case-fatality rate and neurologic sequelae.2
      • Vancomycin has poor CSF penetration. The addition of dexamethasone could further decrease CSF penetration (see Use of steroids).
      • The efficacy of fluoroquinolones and newer agents, such as linezolid, has not been investigated in detail, and their use as first-line agents is not recommended.
      • Penicillin G (24 million U/d) remains the drug of choice for penicillin-susceptible strains.
    • N meningitidis
      • The antimicrobial therapy of choice is penicillin G (24 million U/d) or ampicillin (12 g/d).
      • Ceftriaxone (2-4 g/d) is used in the presence of resistant strains (MIC of 0.1-1 mcg/mL).
      • Data on the use of corticosteroids as adjunctive treatment of meningococcal meningitis are not as strong as those for pneumococcal meningitis. The systematic review on this topic indicates that the reduction in mortality and neurologic sequelae did not reach statistical significance.
    • H influenzae
      • Third-generation cephalosporins (ceftriaxone 4 g/d or cefotaxime 8-12 g/d) are first-line empiric therapy. Resistance to chloramphenicol and ampicillin is common.
      • The efficacy of dexamethasone (0.15 mg/kg q6h) in decreasing the incidence of hearing loss and neurologic sequelae has been clearly demonstrated in children.
    • L monocytogenes
      • Ampicillin (12 g/d) or penicillin G (24 million U/d) is the drug of choice.
      • The addition of gentamicin (3-5 mg/kg/d, divided tid) may add synergy.
      • The third-generation cephalosporins are inactive against L monocytogenes.
      • In patients who are allergic to penicillin, use trimethoprim-sulfamethoxazole (TMP-SMX) at 10 mg/kg/d of the TMP component.
    • Aerobic gram-negative bacilli
      • Third-generation cephalosporins are the drugs of choice. Cefepime is also commonly used. An aminoglycoside may be added for synergy.
      • In cases of P aeruginosa meningitis, the agent of choice among the third-generation cephalosporins is ceftazidime (2 g IV q8h). Ceftriaxone and cefotaxime are not effective against P aeruginosa.
      • The use of imipenem is limited because of seizure potential.
      • Quinolones are under investigation but are not currently recommended as first-line agents.
    • S agalactiae
      • Treat meningitis caused by S agalactiae with ampicillin (12 g/d) and an aminoglycoside.
      • Alternatives include third-generation cephalosporins and vancomycin.
    • Staphylococcus species
      • Treat meningitis caused by S aureus with nafcillin (9-12 g/d) or oxacillin (9-12 g/d).
      • Vancomycin (2-3 g/d, adjusted to serum levels) is the alternative in patients who are allergic to penicillin and is the first-line therapy for methicillin-resistant S aureus (MRSA) strains.
      • Vancomycin is the first-line therapy for coagulase-negative staphylococci. Adding rifampin (600 mg/d) may have a synergistic effect.
      • The use of newer agents such as linezolid and daptomycin for the treatment of staphylococcal meningitis remains investigational.
    • [#UseOfSteroids]Use of steroids
      • The present understanding of the pathogenesis of bacterial meningitis has led to multiple therapeutic trials that involve means to attenuate the detrimental effects of the host defenses (eg, inflammatory response to the bacterial products and the products of neutrophil activation) while eradicating bacteria with antibiotics.
      • Foremost among these measures is the use of steroids. However, in the experimental meningitis model, the use of steroids has been associated with decreased antimicrobial penetration into the CSF and decreased bactericidal activity of some antimicrobials, such as vancomycin. Recent clinical data, however, indicate that steroid use may offer benefit in certain cases of acute bacterial meningitis.
      • The use of adjunctive dexamethasone (0.15 mg/kg per dose q6h for 2-4 d) decreases hearing loss and neurologic sequelae in children and infants with meningitis caused by HIB. The studies that support this largely have been carried out during the era when HIB was the most common meningeal pathogen.
      • More recent studies indicate that adjunctive steroids are also beneficial in the treatment of meningitis caused by bacterial pathogens other than HIB. In a large cohort of patients with acute meningitis due to pneumococcus, meningococcus, and other bacteria, the administration of adjunctive dexamethasone was significantly associated with a reduction in mortality and other unfavorable outcomes. The benefit was most apparent in cases due to pneumococcus.
      • The recent accumulation of scientific evidence about the benefits of steroid use suggests that it should be considered as adjunctive treatment in most adult patients in whom acute bacterial meningitis is suspected.
      • The timing of dexamethasone administration is crucial. If used, it should be administered before or with the first dose of antibacterial therapy. This is to counteract the initial inflammatory burst consequent to antibiotic-mediated bacterial killing. A more intense inflammatory reaction has been documented following the massive bacterial killing induced by antibiotics.
  • Viral meningitis
    • Most viral meningitides are benign and self-limited. Often, they require only supportive care and do not require specific therapy. In certain instances, specific antiviral therapy may be indicated, if available.
    • In patients with immune deficiency (eg, agammaglobulinemia), immunoglobulin replacement has been used to treat chronic enterovirus infections.
    • The antiviral management of herpes meningitis is controversial. Acyclovir (10 mg/kg IV q8h) has been administered for HSV-1 and HSV-2 meningitis. Some experts do not advocate antiviral therapy unless associated encephalitis is present because the condition is usually benign and self-limited. This is exemplified by Mollaret syndrome, a recurrent but benign syndrome of lymphocytic pleocytosis that is now attributed to HSV.
    • Ganciclovir (induction dose of 5 mg/kg IV q12h, maintenance dose of 5 mg/kg q24h) and foscarnet (induction dose of 60 mg/kg IV q8h, maintenance dose of 90-120 mg/kg IV q24h) are used for CMV meningitis in immunocompromised hosts.
    • Instituting highly active antiretroviral therapy (HAART) may be necessary for patients with HIV meningitis that occurs during an acute seroconversion syndrome.
  • Fungal meningitis
    • A number of different regimens have been demonstrated to be effective in the treatment of fungal meningitis. The following treatment options have been shown to be effective in many cases.
    • Treatment of AIDS-related cryptococcal meningitis (ie, C neoformans)
      • Induction therapy: Administer amphotericin B (0.7-1 mg/kg/d IV) for at least 2 weeks, with or without flucytosine (100 mg/kg PO) in 4 divided doses. Liposomal preparations of amphotericin B may be beneficial, but optimal doses have not been determined.
      • Consolidation therapy: Administer fluconazole (400 mg/d for 8 wk). Itraconazole is an alternative if fluconazole is not tolerated.
      • Maintenance therapy: Long-term antifungal therapy with fluconazole (200 mg/d) is most effective (superior to itraconazole and amphotericin B at 1 mg/kg/wk) to prevent relapse. The risk of relapse is high in patients with AIDS.
      • In many cases, cryptococcal meningitis is complicated by increased ICP. Measuring the opening pressure during the lumbar puncture is strongly advised. Make an effort to reduce such pressure by repeated lumbar puncture, a lumbar drain, or a shunt. Medical maneuvers, such as administration of mannitol, have also been used.
      • Role of newer agents such as voriconazole and posaconazole has not been investigated. Echinocandins do not have activity against cryptococcus.
      • For the optimal treatment for HIV-related acute cryptococcal meningitis in resource-limited areas, the agents that are used are amphotericin B and fluconazole. Hence, the treatment would consist of amphotericin and flucytosine and that policy makers and national departments of heath in such countries should consider adding drugs that are typically unavailable in such settings (eg, flucytosine) for HIV treatment programs.3
    • Treatment of cryptococcal meningitis (ie, C neoformans) in patients without AIDS
      • Induction/consolidation: Administer amphotericin B (0.7-1 mg/kg/d) plus flucytosine (100 mg/kg/d) for 2 weeks. Then, administer fluconazole (400 mg/d) for a minimum of 10 weeks.
      • A lumbar puncture is recommended after 2 weeks to document sterilization of the CSF. If the infection persists, longer therapy is recommended. Solid organ transplant recipients require prolonged therapy.
    • C immitis
      • The preferred treatment for meningitis caused by C immitis is oral fluconazole (400 mg/d). Some physicians initiate therapy with a higher dose of fluconazole (as high as 1000 mg/d) or in combination with intrathecal amphotericin B.
      • Itraconazole (400-600 mg/d) has been reported to be comparably effective.
      • Duration of treatment usually is life long.
    • H capsulatum
      • The optimal treatment of H capsulatum meningitis is unclear.
      • Amphotericin B at 0.7-1 mg/kg/d to complete a total dose of 35 mg/kg has been used.
      • Fluconazole (800 mg/d) for an additional 9-12 months may be used to prevent relapse.
      • Long-term fluconazole maintenance therapy at 800 mg/d may be used for those who relapse despite having received a full course of treatment. Patients with further relapse despite long-term suppression are candidates for intraventricular amphotericin B.
      • Itraconazole, although it has better anti-Histoplasma activity, is not encouraged because of poor CSF penetration.
      • This infection is associated with a poor outcome; 20-40% of patients with meningitis succumb to the infection despite amphotericin B therapy, and 50% of responders relapse following discontinuation of treatment.
    • Candida species
      • The preferred initial therapy for candidal meningitis is amphotericin B (0.7mg/kg/d). Flucytosine (25 mg/kg qid) is usually added and adjusted to maintain serum levels of 40-60 mcg/mL.
      • Azole therapy may be used for follow-up therapy or suppressive treatment.
      • The risk of relapse is high, and the duration of treatment is arbitrary. Some recommend continuing treatment for a minimum of 4 weeks following the complete resolution of symptoms. The removal of prosthetic materials (eg, ventriculoperitoneal shunts) is a significant component of therapy in candidal meningitis associated with neurosurgical procedures.
    • S schenckii
      • Amphotericin B is the treatment of choice.
      • Using itraconazole to achieve lifelong suppression may be attempted after initial therapy with amphotericin B.
      • Fluconazole has less anti-Sporothrix activity compared to itraconazole.
      • The duration of treatment in AIDS-related cases is life long.
  • Tuberculous meningitis
    • Depending on the resistance pattern in the community and the results of susceptibility testing (once available), always treat tuberculous meningitis with a combination of drugs.
    • Isoniazid (INH) and pyrazinamide (PZA) attain good CSF levels (approximate blood levels). Rifampin (RIF) penetrates the BBB less efficiently but still attains adequate CSF levels.
    • The use of a combination of the first-line drugs (ie, INH, RIF, PZA, ethambutol, streptomycin) is advocated. The dosage is similar to what is used for pulmonary tuberculosis (ie, INH 300 mg qd, RIF 600 mg qd, PZA 15-30 mg/kg qd, ethambutol 15-25 mg/kg qd, streptomycin 7.5 mg/kg q12h).
    • Evidence regarding the appropriate duration of treatment is conflicting. A treatment duration of 12 months is the minimum, and some experts suggest a duration of at least 2 years.
    • The use of corticosteroids is indicated for individuals with stage 2 or stage 3 disease (ie, patients with evidence of neurologic deficits or changes in their mental function). The recommended dose is 60-80 mg/d, which may be tapered gradually during a span of 6 weeks. The rationale lies in the reduction of inflammatory effects associated with mycobacterial killing by the antimicrobial agents.
  • Spirochetal meningitis
    • Syphilitic meningitis
      • The treatment of choice for neurosyphilis requires the parenteral administration of aqueous crystalline penicillin G (2-4 million U/d IV q4h) for 10-14 days, often followed with intramuscular (IM) benzathine penicillin G (2.4 million U).
      • Alternatively, administer procaine penicillin G (2.4 million U/d IM) plus probenecid (500 mg PO qid) for 14 days, followed by IM benzathine penicillin G (2.4 million U).
      • Patients with HIV who have neurosyphilis are treated similarly.
      • Repeat CSF examination is performed regularly (eg, every 6 mo) following treatment to document the success of therapy. Failure of the cell count to normalize or the serologic titers to fall may warrant re-treatment.
      • Because penicillin G is considered the medical treatment of choice, patients who are allergic to penicillin should undergo penicillin desensitization in order to receive optimal treatment.
    • Lyme meningitis
      • Neurologic complications of Lyme disease (other than Bell palsy) ideally require parenteral antibiotic administration.
      • The drug of choice is ceftriaxone (2 g/d) for 14-28 days. The alternative therapy is penicillin G (20 million U/d) for 14-28 days.
      • Doxycycline (100 mg PO/IV bid) for 14-28 days or chloramphenicol (1 g qid) for 14-28 days has also been used.
  • Parasitic meningitis
    • Primary amebic meningoencephalitis caused by N fowleri is usually fatal. The few survivors reported in the scientific literature have benefited from early diagnosis and treatment with high-dose intravenous and intrathecal amphotericin B or miconazole and rifampin.
    • The treatment for helminthic (ie, A cantonensis, G spinigerum) eosinophilic meningitis has largely been supportive in nature. This includes adequate analgesia, therapeutic CSF aspiration, and the use of anti-inflammatory agents such as corticosteroids. The use of antihelminthic therapy may be contraindicated because clinical deterioration and death may occur following severe inflammatory reactions to the dying worms.

Surgical Care

  • In certain cases of increased ICP, repeated lumbar puncture or the insertion of a ventricular drain may be necessary to relieve the effects of increased ICP.
  • Consultations with neurosurgical service may be needed when a skull fracture is suspected or an abscess formation is demonstrated.

Consultations

  • Consultation with an infectious diseases specialist
  • Consultation with a neurosurgeon in cases of severe intracranial hypertension, suspicion of basilar skull fracture, and abscess formation

Diet

No strict dietary restriction is necessary. To diminish the risks of aspiration, nothing by mouth is recommended for patients with altered levels of consciousness.

Medication

This section discusses antimicrobials commonly used to treat meningitis. Antimicrobials recommended for specific pathogens are discussed in Medical Care.

Antimicrobial agents

These agents are used to treat or prevent infection caused by the most likely pathogen suspected or identified.


Ceftriaxone (Rocephin)

Third-generation cephalosporin with broad-spectrum gram-negative activity. Lower efficacy against gram-positive organisms but excellent activity against susceptible pneumococcal organisms. Exerts antimicrobial effect by interfering with synthesis of peptidoglycan, a major structural component of bacterial cell wall. Excellent antibiotic for empiric treatment of bacterial meningitis.

Adult

2 g IV q24h

Pediatric

75 mg/kg IV followed by 100 mg/kg/d IV divided bid; not to exceed 4 g/d

Probenecid may increase levels by decreasing its elimination half-life; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Documented hypersensitivity; neonates with hyperbilirubinemia caused by increased risk of kernicterus

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in renal impairment; caution in breastfeeding women and people with penicillin allergy; caution in gallbladder, biliary tract, liver, or pancreatic disease


Cefotaxime (Claforan)

Third-generation cephalosporin used to treat suspected or documented bacterial meningitis caused by susceptible organisms such as H influenzae or N meningitides. Like other beta-lactam antibiotics, inhibits bacterial growth by arresting bacterial cell wall synthesis.

Adult

2-3 g IV q4-6h; not to exceed 12 g/d

Pediatric

<12 years: 200 mg/kg/d IV divided q6h; not to exceed 12 g/d
>12 years: Administer as in adults

Probenecid may increase levels by prolonging its half-life; coadministration with furosemide and aminoglycosides may increase nephrotoxicity

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe renal impairment; has been associated with severe antibiotic-associated pseudomembranous colitis; may cause transient neutropenia and thrombocytopenia; may cause transient elevation in liver enzymes; caution in penicillin allergy


Penicillin G (Pfizerpen)

Beta-lactam antibiotic. Inhibits bacterial cell wall synthesis, resulting in bactericidal activity against susceptible microorganisms. Active against many gram-positive organisms. DOC for syphilitic meningitis and susceptible organisms (eg, N meningitides, penicillin-susceptible S pneumoniae).

Adult

Up to 24 million U/d IV divided q4h or as continuous IV infusion

Pediatric

100,000-400,000 U/kg/d IV divided q4h; not to exceed 24 million U/d

Probenecid can increase effects; coadministration of tetracyclines can decrease effects

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in impaired renal function, seizure disorder, and hypersensitivity to cephalosporins


Vancomycin (Vancocin)

Glycopeptide antibiotic active against staphylococci, streptococci, and other gram-positive bacteria. Exerts antibacterial activity by inhibiting biosynthesis of peptidoglycan. DOC for highly penicillin-resistant and ceftriaxone-resistant S pneumoniae and methicillin-resistant S aureus. Component of empiric DOC for CNS-shunt–associated meningitis. Because of poor CSF penetration, higher dose is required for meningitis than for other infections. Use CrCl to adjust dose in renal impairment.

Adult

Meningitis: 1 g IV q8h; adjust dose based on measured peak and trough levels, which are dependent on body weight and renal clearance
Nonmeningitis infections: 15-30 mg/kg/d IV in divided doses

Pediatric

40 mg/kg/d IV divided qid

Erythema, histaminelike flushing, and anaphylactic reactions may occur when administered with anesthetic agents; when taken concurrently with aminoglycosides, risk of nephrotoxicity may increase above that with aminoglycoside monotherapy; effects in neuromuscular blockade may be enhanced when coadministered with nondepolarizing muscle relaxants

Documented hypersensitivity; history of severe hearing loss

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal failure and neutropenia; red man syndrome is caused by IV infusion that is too rapid (dose administered over a few min) but rarely occurs when dose is administered as a 2-h administration or as PO or IP administration; red man syndrome is not an allergic reaction


Ampicillin (Omnipen, Polycillin)

Bactericidal beta-lactam antibiotic that inhibits cell wall synthesis by interfering with peptidoglycan formation. Indicated for L monocytogenes and S agalactiae meningitis, usually in combination with gentamicin.

Adult

12 g/d IV divided q3-4h

Pediatric

200 mg/kg/d IV divided q4-6h; not to exceed 12 g/d

Probenecid and disulfiram elevate levels; allopurinol decreases effects and has additive effects on ampicillin rash; may decrease effects of PO contraceptives

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in renal failure; evaluate rash and differentiate from hypersensitivity reaction


Gentamicin (Garamycin)

Newer antibiotics are available, but aminoglycosides remain significant in treating severe infections. Aminoglycosides inhibit protein synthesis by irreversibly binding to 30s ribosome. In meningitis or gram-negative meningitides, administer intrathecally because of poor CNS penetration. Dosing regimens are numerous; adjust dose based on CrCl and changes in volume of distribution.

Adult

Serious infections and normal renal function: 3 mg/kg/d IV q8h
Loading dose: 1-2.5 mg/kg IV
Maintenance: 1-1.5 mg/kg IV q8h
Extended dosing regimen for life-threatening infections: 5 mg/kg/d IV/IM q6-8h
Follow each regimen by at least a trough level drawn on the third or fourth dose (0.5 h before dosing); may draw a peak level 0.5 h after 30-min infusion

Pediatric

<5 years: 2.5 mg/kg/dose IV/IM q8h
>5 years: 1.5-2.5 mg/kg/dose IV/IM q8h or 6-7.5 mg/kg/d divided q8h; not to exceed 300 mg/d; monitor as in adults

Coadministration with other aminoglycosides, cephalosporins, penicillins, and amphotericin B may increase nephrotoxicity; aminoglycosides enhance effects of neuromuscular blocking agents, thus, prolonged respiratory depression may occur; coadministration with loop diuretics may increase auditory toxicity of aminoglycosides; possible irreversible hearing loss of varying degrees may occur (monitor regularly)

Documented hypersensitivity; non–dialysis-dependent renal insufficiency

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Narrow therapeutic index (not intended for long-term therapy); caution in renal failure (not on dialysis), myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission; adjust dose in renal impairment

Antiviral agents

These agents interfere with viral replication; they weaken or abolish viral activity.


Acyclovir (Zovirax)

Prodrug activated by cellular enzymes. Inhibits activity of HSV-1, HSV-2, and varicella zoster virus by competing for viral DNA polymerase and incorporation into viral DNA. Used in HSV meningitis.

Adult

1500 mg/m2/d or 10 mg/kg IV q8h for 14-28 d (encephalitis caused by HSV)

Pediatric

Administer as in adults

Concomitant use of probenecid or zidovudine prolongs half-life and increases CNS toxicity

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal failure or when using nephrotoxic drugs, can precipitate in renal tubules; may cause delirium, lethargy, and seizures


Ganciclovir (Cytovene)

Synthetic guanine derivative active against CMV. An acyclic nucleoside analog of 2'-deoxyguanosine that inhibits replication of herpes viruses both 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.

Adult

Induction: 5 mg/kg IV over 1 h q12h for 14-21 d (do not use PO ganciclovir for induction treatment)
Maintenance PO: 500 mg q4h or 1 g tid for life
Maintenance IV: 5 mg/kg qd for 5-7 d/wk

Pediatric

<3 months: Not established
>3 months: Administer as in adults

Concomitant administration with cytotoxic drugs, such as dapsone, vinblastine, Adriamycin, pentamidine, flucytosine, vincristine, amphotericin B, TMP/SMX combinations, or other nucleoside analogs, may result in additive toxicity in bone marrow, spermatogonia, and germinal layers of skin and GI mucosa (coadminister only if potential benefits outweigh risks); coadministration with imipenem and cilastatin may cause generalized seizures (use only if potential benefits outweigh risks); serum creatinine may increase following concurrent use with either cyclosporine or amphotericin B; in the presence of probenecid, ganciclovir renal clearance is reduced; bioavailability may increase when didanosine is administered either 2 h prior to or simultaneously with ganciclovir; bioavailability may decrease in the presence of zidovudine, while bioavailability of zidovudine is increased in the presence of ganciclovir

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Clinical toxicity includes granulocytopenia, anemia, and thrombocytopenia; half-life and plasma/serum concentrations may be increased as a result of reduced renal clearance; dosages >6 mg/kg IV may result in increased toxicity; rapid infusions may result in increased toxicity; initially, reconstituted solutions of IV ganciclovir have a high pH (11); phlebitis or pain may occur at site of IV infusion despite further dilution in IV fluids; should be accompanied by adequate hydration; photosensitization (ie, photoallergy, phototoxicity) may occur

Antifungal agents

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


Amphotericin B, conventional (Amphocin, Fungizone)

Polyene antibiotic produced by a strain of S nodosus; can be fungistatic or fungicidal. Binds to sterols, such as ergosterol, in the fungal cell membrane, causing intracellular components to leak with subsequent fungal cell death. Used to treat severe systemic infection and meningitis caused by susceptible fungi (ie, C albicans, H capsulatum, C neoformans). Also available in liposomal (AmBisome) and lipid-complex (Abelcet) formulations. Amphotericin B does not penetrate the CSF well. Intrathecal amphotericin may be needed in addition.

Adult

Conventional: 0.7-1.0 mg/kg/d IV infusion; not to exceed 1.5 mg/kg/d
Liposomal: 3-5 mg/kg/d IV infusion
Lipid-complex: 5 mg/kg/d IV infusion

Pediatric

Administer as in adults

Antineoplastic agents may enhance the potential of amphotericin B for renal toxicity, bronchospasm, and hypotension; corticosteroids, digitalis, and thiazides may potentiate hypokalemia; the risk of renal toxicity is increased with cyclosporine

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal insufficiency, monitor renal function, serum electrolytes (eg, magnesium, potassium), liver function, CBC count, and hemoglobin concentrations; resume therapy at lowest level (eg, 0.25 mg/kg) when therapy is interrupted for longer than 7 d; hypoxemia, acute dyspnea, and interstitial infiltrates may occur in patients with neutropenia who are receiving leukocyte transfusions (separate time of amphotericin infusion from time of leukocyte transfusion); fever and chills are not uncommon after first few administrations of drug; rare acute reactions may include hypotension, bronchospasm, arrhythmias, and shock


Fluconazole (Diflucan)

Fungistatic activity. Synthetic PO antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation, which prevents conversion of lanosterol to ergosterol, thereby disrupting cellular membranes.

Adult

200-800 mg PO qd; not to exceed 1000 mg/d

Pediatric

3-6 mg/kg PO qd for 14-28 d or 6-12 mg/kg qd depending on severity of infection

Levels may increase with hydrochlorothiazides; fluconazole levels may decrease with long-term coadministration of rifampin; may increase concentrations of theophylline, phenytoin, tolbutamide, cyclosporine, glyburide, and glipizide; effects of anticoagulants may increase with fluconazole coadministration

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adjust dose for renal insufficiency; monitor closely if rashes develop and discontinue drug if lesions progress; may cause clinical hepatitis, cholestasis, and fulminant hepatic failure (including death) with underlying medical conditions (eg, AIDS, malignancy) and while taking multiple concomitant medications; not recommended for breastfeeding women

Antitubercular agents

These agents are used in the management of mycobacterial disease in combination with other antitubercular agents.


Rifampin (Rifadin, Rimactane)

Used in combination with other antituberculous drugs. Inhibits DNA-dependent bacterial but not mammalian RNA polymerase. Cross-resistance may occur.

Adult

600 mg PO/IV qd

Pediatric

10-20 mg/kg PO/IV; not to exceed 600 mg/d

Induces microsomal enzymes, which may decrease effects of acetaminophen, PO anticoagulants, barbiturates, benzodiazepines, beta-blockers, chloramphenicol, PO contraceptives, corticosteroids, mexiletine, cyclosporine, digitoxin, disopyramide, estrogens, hydantoins, methadone, clofibrate, quinidine, dapsone, tazobactam, sulfonylureas, theophyllines, tocainide, and digoxin; blood pressure may increase with coadministration of enalapril; coadministration with isoniazid may result in a higher rate of hepatotoxicity than with either agent alone (discontinue one or both agents if alterations in LFTs occur)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Obtain CBC counts and baseline clinical chemistries prior to and throughout therapy; in liver disease, weigh benefits against risk of further liver damage; interruption of therapy and high-dose intermittent therapy are associated with thrombocytopenia that is reversible if therapy is discontinued as soon as purpura occurs; if treatment is continued or resumed after appearance of purpura, cerebral hemorrhage or death may occur


Isoniazid (Laniazid, Nydrazid)

First-line antituberculous drug used in combination with other antituberculous drugs to treat meningitis. Usually administered for at least 12-24 mo. Prophylactic dose of pyridoxine (6-50 mg/d) is recommended if peripheral neuropathies secondary to isoniazid therapy develop.

Adult

5 mg/kg PO qd (usually 300 mg/d) and 10 mg/kg qd or divided bid in patients with disseminated disease; not to exceed 300 mg/d

Pediatric

10-20 mg/kg PO qd; not to exceed 300 mg/d

Higher incidence of isoniazid-related hepatitis can occur with daily alcohol ingestion; aluminum salts may decrease isoniazid serum levels (administer 1-2 h before taking aluminum salts); may increase the effect of anticoagulants with coadministration; may inhibit metabolic clearance of benzodiazepines; carbamazepine toxicity or isoniazid hepatotoxicity may result from concurrent use (monitor carbamazepine concentrations and liver function); coadministration with cycloserine may increase adverse CNS effects (eg, dizziness); acute behavioral and coordination changes may occur with coadministration of disulfiram; coadministration with rifampin after halothane anesthesia may result in hepatotoxicity and hepatic encephalopathy; may inhibit hepatic microsomal enzymes and increase toxicity of hydantoin

Documented hypersensitivity; previous isoniazid-associated hepatic injury or other severe adverse reactions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor patients with active chronic liver disease


Pyrazinamide (PZA)

Pyrazine analog of nicotinamide that may be bacteriostatic or bactericidal against M tuberculosis, depending on the concentration of drug attained at the site of infection; mechanism of action is unknown.

Adult

15-30 mg/kg PO qd; not to exceed 2 g/d

Pediatric

Administer as in adults

Documented hypersensitivity; severe hepatic damage; acute gout

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use only in combination with other effective antituberculous agents; inhibits renal excretion of urates; may result in hyperuricemia (usually asymptomatic); perform baseline serum uric acid determinations; discontinue if signs of hyperuricemia with acute gouty arthritis occur; obtain baseline LFTs (closely monitor in liver disease); discontinue if signs of hepatocellular damage appear; caution in history of diabetes mellitus; pyrazinamide is not usually administered in pregnant patients unless they are HIV-infected or drug resistance to other antitubercular drugs is suspected or known (see pregnancy precaution)


Ethambutol (Myambutol)

Diffuses into actively growing mycobacterial cells (eg, tubercle bacilli). Impairs cell metabolism by inhibiting synthesis of one or more metabolites, which, in turn, causes cell death. No cross-resistance demonstrated. Mycobacterial resistance is frequent with previous therapy. Use in these patients in combination with second-line drugs that have not been administered previously. Administer q24h until permanent bacteriological conversion and maximal clinical improvement is observed. Absorption is not significantly altered by food.

Adult

No previous antituberculous therapy: 15 mg/kg (7 mg/lb) PO qd
Previous antituberculous therapy: 25 mg/kg (11 mg/lb) PO qd

Pediatric

<13 years: Not recommended
>13 years: Administer as in adults

Aluminum salts may delay and reduce absorption (administer several h before or after ethambutol dose)

Documented hypersensitivity; optic neuritis (unless clinically indicated)

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Reduce dose in impaired renal function; may have adverse visual effects that may be reversible if promptly discontinued

More on Meningitis

Overview: Meningitis
Differential Diagnoses & Workup: Meningitis
Treatment & Medication: Meningitis
Follow-up: Meningitis
Multimedia: Meningitis
References
Further Reading
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Keywords

bacterial meningitis, aseptic meningitis, viral meningitis, tuberculous meningitis, syphilitic meningitis, Lyme meningitis, cryptococcal meningitis, fungal meningitis, parasitic meningitis, inflammation of the meninges, headache, nuchal rigidity, photophobia, pleocytosis, acute meningitis, chronic meningitis, Streptococcus pneumoniae meningitis, meningococcal meningitis, Haemophilus influenzae meningitis, Histoplasma meningitis, amebic meningoencephalitis

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Contributor Information and Disclosures

Author

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.

Coauthor(s)

Michael R Keating, MD, Consultant, Assistant Professor of Medicine, 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.

Medical Editor

Joseph Richard Masci, MD, Chief of Infectious Diseases, Associate Director, Associate Professor, Department of Internal Medicine, Division of Infectious Diseases, Elmhurst Hospital Center, Mount Sinai School of Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

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: emedicine $50.00 author of chapter

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

 
 
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