Meningitis Treatment & Management

The performance of radiographic imaging should not defer the institution of empiric antimicrobial therapy.

The emergence of bacterial resistance, especially penicillin-resistant S pneumoniae, has been increasing worldwide, and the reported rates are 41-56% in Southeast Asia and the Far East. In the United States in 1998, the CDC conducted a study on 3335 isolates from 8 states and found 10.2% intermediate penicillin resistant (minimum inhibitory concentration [MIC] of 0.1-1 mcg/mL) and 13.6% highly resistant (MIC >2 mcg/mL) strains.

The geographic distribution of this resistance is variable, and knowledge of this is important when deciding on local empiric antibiotic therapy (see Medication).

Evaluate and treat the patient for shock or hypotension, and infuse crystalloid until he or she is euvolemic. Consider seizure precautions, treat seizures according to the usual protocol, and consider airway protection in patients with altered mental status. For alert patients in stable condition who have normal vital signs, administer oxygen, establish IV access, and transport them rapidly to the ED.

In acute meningitis, regardless of presentation, perform CSF examination to identify the causative organism and susceptibilities. Institute treatment as early as possible in the disease course, since delay in instituting treatment may contribute significantly to morbidity and mortality.

The patient's condition and ED organization may warrant a watchful wait for 8-12 hours and then a reexamination of the CSF (sooner if patient's condition deteriorates). If initial granulocytosis changes to mononuclear predominance, CSF glucose remains normal, and the patient continues to look well, the infection is most likely nonbacterial.

In acutely ill patients, perform an LP (if appropriate) and administer the first dose(s) of antibiotics with or without steroids within 30 minutes of presentation to the ED. Consider instituting ED triage protocol to identify patients at risk. Initiate empiric therapy if LP cannot be performed within 30 minutes. Begin empiric therapy prior to a head CT scan if a focal neurologic deficit is present. If no mass effect is present, perform LP to obtain microbiology studies.

Treat systemic complications of acute bacterial meningitis, including the following:

• Hypotension and/or shock
• Hypoxemia
• Hyponatremia (SIADH)
• Cardiac arrhythmias and ischemia
• Cerebrovascular accident (CVA)
• Exacerbation of chronic diseases

Look for signs of hydrocephalus and increasing ICP. Manage fever and pain, control straining and coughing, avoid seizures, and avoid systemic hypotension. In otherwise stable patients, sufficient care includes elevating the head and monitoring neurologic status. When more aggressive maneuvers are indicated, some authorities favor early use of diuresis (ie, furosemide 20 mg IV, mannitol 1 g/kg IV), provided circulatory volume is protected.

Hyperventilation in intubated patients, with a goal of PaCO₂ of 25-30 mm Hg, may briefly lower ICP; hyperventilation with PaCO₂ of less than 25 mm Hg may decrease CBF disproportionately and lead to CNS ischemia. Consider placing an ICP monitor in comatose patients or in those with signs of increased ICP. With elevated ICP, remove CSF until pressure decreases by 50% and maintain at less than 300 mm water.

Aggressively control seizures if present, since seizure activity increases ICP (ie, lorazepam 0.1 mg/kg IV and IV load with phenytoin 15 mg/kg or phenobarbital 5-10 mg/kg).

Most patients with subacute bacterial meningitis present more of a diagnostic challenge than do individuals with acute illness. In patients with subacute bacterial meningitis, CSF examination constitutes the critical step in documenting the presence or absence of a CNS infection and the type of infecting organism. If the patient's condition is serious and antibiotics have been given (arguably masking symptoms and hindering growth of organisms on culture), assume that a bacterial infection is present, provide adequate antibiotic coverage, and admit the patient.

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

Ideal ED antibiotic therapy is based on a clearly identified organism on CSF Gram stain. Age and underlying conditions dictate empiric treatment in an ED patient without trauma or CNS instrumentation. Information presented in this article is taken from the 2003 edition of The Sanford Guide to Antimicrobial Therapy.^[12] (See Table 7, Table 8, and Table 9, below.)

Table 7. Recommended Empiric Antibiotics According to Predisposing Factors for Patients With Suspected Bacterial Meningitis (Open Table in a new window)

Table 8. Recommended Empiric Antibiotics for Patients With Suspected Bacterial Meningitis and Known CSF Gram Stain Results (Open Table in a new window)

Table 9. Specific Antibiotics and Duration of Therapy for Patients With Acute Bacterial Meningitis (Open Table in a new window)

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

Appropriate antibiotic treatment for the most common types of bacterial meningitis should reduce the risk of death to less than 15%, although the risk is higher among elderly patients. 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 targeted treatment.

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

Antibiotic therapy - Neonate to age 1 month

In neonates to age 1 month, the most common microorganisms are group B or D streptococci, Enterobacteriaceae (eg, E coli), and L monocytogenes. Primary treatment is a combination of ampicillin (age 0-7 d: 50 mg/kg IV q8h; age 8-30 d: 50-100 mg/kg IV q6h) plus cefotaxime 50 mg/kg IV q6h (up to 12 g/d). Alternative treatment is ampicillin (age 0-7 d: 50 mg/kg IV q8h; age 8-30 d: 50-100 mg/kg IV q6h) plus gentamicin (age 0-7 d: 2.5 mg/kg IV or IM q12h; age 8-30 d: 2.5 mg/kg IV or IM q8h). Most authorities recommend adding acyclovir 10 mg/kg IV q8h for herpes simplex encephalitis.

Antibiotic therapy - Age 1-3 months

In infants (1-3 mo), primary treatment is cefotaxime (50 mg/kg IV q6h, up to 12 g/d) or ceftriaxone (initial dose: 75 mg/kg, 50 mg/kg q12h up to 4 g/day) plus ampicillin (50-100 mg/kg IV q6h). Alternative treatment is chloramphenicol (25 mg/kg PO or IV q12h) plus gentamicin (2.5 mg/kg IV or IM q8h). If prevalence of cephalosporin-resistant S pneumoniae (DRSP) is greater than 2%, add vancomycin (15 mg/kg IV q8h). Strongly consider dexamethasone (0.4 mg/kg IV q12h for 2 d or 0.15 mg/kg IV q6h for 4 d) starting 15-20 minutes before first dose of antibiotics.

Antibiotic therapy - Age 3 months to 7 years

In older infants or young children (3 mo - 7 y), the most common microorganisms are S pneumoniae, N meningitidis, and H influenzae. Primary treatment is either cefotaxime (50 mg/kg IV q6h up to 12 g/d) or ceftriaxone (initial dose: 75 mg/kg, then 50 mg/kg q12h up to 4 g/d). If prevalence of DRSP is greater than 2%, add vancomycin (15 mg/kg IV q8h). In countries with low prevalence of DRSP, consider penicillin G (250,000 U/kg/d IM/IV in 3-4 divided doses). Due to DRSP, penicillin G is no longer recommended in the US.

Alternative treatment (or if severely penicillin allergic) is chloramphenicol (25 mg/kg PO/IV q12h) plus vancomycin (15 mg/kg IV q8h). Strongly consider dexamethasone (0.4 mg/kg IV q12h for 2 d or 0.15 mg/kg IV q6h for 4 d) starting 15-20 minutes before the first dose of antibiotics.

Antibiotic therapy - Age 7-50 years

In an older child or an otherwise healthy adult (7-50 y), the most common microorganisms are S pneumoniae, N meningitidis, and L monocytogenes.

In areas where prevalence of DRSP is greater than 2%, primary treatment is either cefotaxime (pediatric dose: 50 mg/kg IV q6h up to 12 g/d; adult dose: 2 g IV q4h) or ceftriaxone (pediatric dose: initial dose: 75 mg/kg, then 50 mg/kg q12h up to 4 g/day; adult dose: 2 g IV q12h) plus vancomycin (pediatric dose: 15 mg/kg IV q8h; adult dose: 750-1000 mg IV q12h or 10-15 mg/kg IV q12h). Some add rifampin (pediatric dose: 20 mg/kg/d IV; adult dose: 600 mg PO qd). If Listeria species is suspected, add ampicillin (50 mg/kg IV q6h).

Alternative treatment (or if severely penicillin allergic) is chloramphenicol (12.5 mg/kg IV q6h: not bactericidal) or clindamycin (pediatric dose: 40 mg/kg/day IV in 3-4 doses; adult dose: 900 mg IV q8h: active in vitro but no clinical data) or meropenem (pediatric dose: 20-40 mg/kg IV q8h; adult dose: 1 g IV q8h: active in vitro but few clinical data; avoid imipenem, as it is proconvulsant).

In areas with low prevalence of DRSP, use cefotaxime (pediatric dose: 50 mg/kg IV q6h up to 12 g/d; adult: 2 g IV q4h) or ceftriaxone (pediatric dose: 75 mg/kg initial dose then 50 mg/kg q12h up to 4 g/d; adult: 2 g IV q12h) plus ampicillin (50 mg/kg IV q6h).

Alternative treatment (or if severely penicillin allergic) is chloramphenicol (12.5 mg/kg IV q6h) plus trimethoprim/sulfamethoxazole (TMP/SMX; TMP 5 mg/kg IV q6h) or meropenem (pediatric dose: 20-40 mg/kg IV q8h; adult dose: 1 g IV q8h).

Data are limited on the need for dexamethasone in adults, although there is support for its use in developed countries when S. pneumoniae is the suspected organism. Administer the first dose of dexamethasone (0.4 mg/kg q12h IV for 2 d or 0.15 mg/kg q6h for 4 d) 15-20 minutes before first dose of antibiotics.

Antibiotic therapy - Age 50 years and older

In adults older than 50 years or adults with disabling disease or alcoholism, the most common microorganisms are S pneumoniae, coliforms, H influenzae, Listeria species, Pseudomonas aeruginosa, and N meningitidis.

Primary treatment if the prevalence of DRSP is greater than 2% is either cefotaxime (2 g IV q4h) or ceftriaxone (2 g IV q12h) plus vancomycin (750-1000 mg IV q12h or 10-15 mg/kg IV q12h). If CSF Gram stain shows gram-negative bacilli, use ceftazidime (2 g IV q8h). In areas of low prevalence of DRSP, use cefotaxime (2 g IV q4h) or ceftriaxone (2 g IV q12h) plus ampicillin (50 mg/kg IV q6h). Other options for treatment include meropenem, TMP/SMX, and doxycycline.

Data are limited on the need for dexamethasone in adults, although there is support for its use in developed countries when S pneumoniae is the suspected organism and suspicion for TB or fungal etiologies is low. Administer the first dose of dexamethasone (0.4 mg/kg q12h IV for 2 d or 0.15 mg/kg q6h for 4 d) 15-20 minutes before the first dose of antibiotics.

Go to the following articles for complete information on these topics:

• Meningococcal Meningitis
• Staphylococcal Meningitis
• Haemophilus Meningitis

The present understanding of the pathogenesis of bacterial meningitis has led to multiple therapeutic trials that involve the means to attenuate the detrimental effects of the host’s 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. Clinical data, however, indicate that steroid use may offer benefit in certain cases of acute bacterial meningitis.

Therefore, pharmacologic interventions to reduce the degree of inflammation may improve outcome. Strongly consider the use of steroids as adjunctive treatment for 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.

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. Controversy surrounds the administration of dexamethasone, which is given with or just before antibiotics.^[13] Dexamethasone may interrupt the cytokine-mediated neurotoxic effects of bacteriolysis, which are at maximum in the first days of antibiotic use.

A meta-analysis of 10 years of clinical trials confirmed that dexamethasone decreases morbidity, especially incidence and severity of neurosensory hearing loss, for H influenzae meningitis and suggested comparable benefit for S pneumoniae meningitis in childhood. No adequate adult studies exist, although the pathophysiology is presumably similar. Meta-analysis suggests that limiting dexamethasone therapy to 2 days may be optimal. Studies conducted in Europe have continued to support the use of dexamethasone in developed (as opposed to developing) countries, perhaps related to the relative incidence of TB meningitis.

Theoretically, anti-inflammatory effects of steroids decrease blood-brain barrier permeability and impede penetration of antibiotics into CSF. Decreased CSF levels of vancomycin have been confirmed in steroid-treated animals but not in human studies. Many authorities believe that all other antibiotics achieve minimal inhibitory concentrations (MICs) in CSF regardless of steroid use. Dexamethasone may not clinically impede even vancomycin.

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.

In a meta-analysis, dexamethasone had no effect in any of the prespecified subgroups, including specific causative organisms, predexamethasone antibiotic treatment, HIV status, or age. The meta-analysis was also unable to show a significant reduction in death or neurologic disability.^[14]

In developing countries, the use of oral glycerol (rather than dexamethasone) has been studied as adjunctive therapy in the treatment of bacterial meningitis in children. In limited studies, it appears to reduce the incidence of neurologic sequelae with few side effects.^[15]

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.

Go to Viral Meningitis for complete information on this topic.

Herpes simplex meningitis

The antiviral management of HSV 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.

CMV meningitis

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.

HIV meningitis

Instituting highly active antiretroviral therapy (HAART) may be necessary for patients with HIV meningitis that occurs during an acute seroconversion syndrome.

Go to HIV-1 Associated CNS Conditions - Meningitis for complete information on this topic.

For initial 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 used in patients with or who are predisposed to develop renal dysfunction (amphotericin B liposome 3-4 mg/kg/d or amphotericin B lipid complex 5 mg/kg/d).

For consolidation therapy, administer fluconazole (400 mg/d for 8 wk). Itraconazole is an alternative if fluconazole is not tolerated.

For 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.

The 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 policy makers and national departments of health in such countries should consider adding drugs that are typically unavailable in such settings (eg, flucytosine) for HIV treatment programs.^[16]

Go to HIV-1 Associated CNS Conditions - Meningitis for complete information on this topic.

For induction and consolidation therapy, administer amphotericin B (0.7-1 mg/kg/d) plus flucytosine (100 mg/kg/d) for at least 4 weeks. This may be extended to 6 weeks in neurological complications. Then, administer fluconazole (400 mg/d) for a minimum of 8 weeks.

A lumbar puncture is recommended after 2 weeks to document sterilization of the CSF. If the infection persists, longer induction therapy is recommended (6 weeks).

Solid organ transplant recipients with cryptococcal meningitis should be treated with liposomal amphotericin B (3-4 mg/kg/d IV) or amphotericin B lipid complex (5 mg/kg/d IV) plus flucytosine (100 mg/kg/d in 4 divided doses) for at least 2 weeks of induction therapy. This is followed by consolidation treatment using fluconazole at 400-800 mg/d orally for 8 weeks, and then maintenance treatment with fluconazole at 200 mg/d orally for 6-12 months.

Coccidioides immitis

The preferred treatment for meningitis caused by C immitis is oral fluconazole (400 mg/d). Some physicians initiate therapy with a larger dose of fluconazole (as high as 1000 mg/d) or with a combination of fluconazole and intrathecal amphotericin B. Itraconazole (400-600 mg/d) has been reported to be comparably effective. The duration of treatment usually is lifelong.

Histoplasma capsulatum

The recommended treatment of H capsulatum meningitis is liposomal amphotericin B at 5-mg/kg/d IV for a total of 175 mg/kg given over 4-6 weeks, followed by oral itraconazole 200-300 mg twice to thrice daily for at least 1 year or until the resolution of CSF abnormalities and Histoplasma antigen levels. Blood levels of itraconazole should be measured to ensure good absorption of the oral drug.

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 (0.7 mg/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.

Sporothrix 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 than itraconazole. The duration of treatment in AIDS-related cases is lifelong.

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 blood-brain barrier 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.

Go to Tuberculous Meningitis for complete information on this topic.

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.

Following treatment, repeat CSF examination is performed regularly (eg, every 6 mo) to document the success of therapy. Failure of the cell count to normalize or the serologic titers to fall may warrant retreatment.

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.

Primary amebic meningoencephalitis (PAM), caused by N fowleri, is usually fatal. The few survivors reported in the scientific literature benefitted 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.

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.

Vaccination and chemoprophylaxis are 2 means of preventing meningitis.

Vaccination

The use of H influenzae type B (HIB) vaccination is strongly recommended in susceptible individuals (although there is no standard recommendation for H influenzae vaccination in adults).

Vaccination against S pneumoniae is also strongly encouraged for susceptible individuals, including people older than 65 years and individuals with chronic cardiopulmonary illnesses. It is not known whether the adult use of conjugate pneumococcal vaccine decreases the incidence of S pneumoniae meningitis.

Vaccinations against encapsulated bacterial organisms (eg, S pneumoniae, N meningitidis) are encouraged for people with functional or structural asplenia. Always administer vaccinations expediently to individuals who undergo splenectomy.

Offer vaccination with quadrivalent meningococcal polysaccharide vaccine to all high-risk populations, including those with underlying immune deficiencies, those who travel to hyperendemic areas and epidemic areas, and those involved with laboratory work that deals with routine exposure to N meningitidis. College students who live in dormitories or residence halls are at modest risk; inform them about the risk and offer vaccination.

One vaccine protects against 4 strains of N meningitidis. As of February 2008, the Advisory Committee on Immunization Practices no longer recommends routine immunization of children, but they continue to recommend routine immunization of teenagers and all children/adults at increased risk.^[17]

The Centers for Disease Control and Prevention (CDC) Advisory Committee on Immunization Practices (ACIP) issued updated recommendations in 2010 for use of meningococcal conjugate vaccines. Two new recommendations focus on the routine vaccination of adolescents and on a primary series of vaccinations of persons aged 2-55 years with certain risk factors for meningococcal infection.^[18]

Regarding the routine use of vaccines in adolescents, the 2010 CDC-ACIP guidelines specifically recommend 1 dose of meningococcal conjugate vaccine, preferably starting at 11 or 12 years. A booster dose should be given at age 16 years. If the primary dose was at age 13-15 years, the booster can be given at age 16-18 years. No booster is needed if the primary dose was on or after age 16 years.^[18]

The 2010 CDC-ACIP issued specific recommendations for those with certain risk factors for meningococcal infection. HIV-infected individuals aged 11-18 years should be given a primary series of 2 doses, 2 months apart. This should be followed by a booster dose administered at age 16 years if the primary dose was at age 11 or 12, and at age 16-18 years if the primary dose was at age 13-15 years. No booster is needed if the primary dose was on or after age 16 years.^[18]

Persons aged 2-55 years with persistent complement component deficiency or asplenia (functional or anatomic) should be given a primary series of 2 doses, 2 months apart, followed by a booster dose every 5 years. If a 1-dose primary series was given, the booster dose should be given as soon as possible, then every 5 years thereafter.^[18]

In persons aged 2-55 years with a protracted increased risk for exposure to meningitis, the 2010 CDC-ACIP guidelines recommend a 1-dose primary series. The booster dose should be given after 3 years for children aged 2-6 years, and after 5 years for persons aged 7 years or older, if the person remains at increased risk.^[18]

Vaccination against measles and mumps effectively eliminates aseptic meningitis syndrome caused by these pathogens.

Chemoprophylaxis

Following exposure to an index case, it is typical for an individual to temporarily carry H influenzae, N meningitidis, and S pneumoniae nasopharyngeally. An association between carriage and the risk of disease has been described, especially for N meningitidis and H influenzae. This is the basis for the recommendations on chemoprophylaxis. However, this prophylaxis does not treat incubating invasive disease, and closely monitor individuals at highest risk.

To eliminate nasopharyngeal carriage of H influenzae type b and to decrease invasion of colonized susceptible individuals, use rifampin (20 mg/kg/d) for 4 days. The index patient may need chemoprophylaxis if the administered treatment does not eliminate carriage.

Prophylaxis is suggested for contacts of persons with meningococcal meningitis. These contacts include household contacts, daycare center members who eat and sleep in the same dwelling, close contacts in military barracks or boarding schools, and medical personnel performing mouth-to-mouth resuscitation. Rifampin (600 mg PO q12h) for 2 days has been shown to rapidly eradicate the carrier stage, and the prophylaxis persists for as long as 10 weeks following treatment.

Alternative agents include ceftriaxone (250 mg IM) as a single dose in adults. It also is the safest choice in pregnant patients. It has been shown to eradicate the carrier state for 14 days. Ciprofloxacin (500-750 mg) as a single dose also is efficacious.

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

Vigilant surveillance for the development of complications is required. Seizure precautions are indicated, especially for patients with impaired mental function.

Proper isolation precautions are indicated in cases of invasive meningococcal disease.

Monitor patients for potential adverse effects of medications, such as hypersensitivity reactions, cytopenia, or liver dysfunction.

Drug-level monitoring may be needed for some antibiotics, such as vancomycin and the aminoglycosides.