How to Cite This Chapter: Chagla Z, Przyjałkowski W. Meningitis. McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. Accessed July 18, 2024.
Last Updated: September 29, 2018
Last Reviewed: May 1, 2019
Chapter Information

Definition, Etiology, PathogenesisTop

Meningitis is an inflammatory disease involving the arachnoid mater, pia mater, and subarachnoid space. It is caused by penetration of pathogens to the cerebrospinal fluid (CSF). Untreated infection spreads to the cerebral parenchyma (meningoencephalitis).

The most common source of infection is hematogenous spread from other locations. Bacterial and fungal infections may also spread by continuity from a fractured skull or injured meninges or as a complication of acute otitis media or sinusitis. Although meningitis is typically community acquired, nosocomial meningitis may occur through neurosurgical manipulation.

1. Etiology:

1) Viral (aseptic) meningitis: The most commonly involved pathogens are enteroviruses, herpes simplex virus (HSV), and varicella-zoster virus (VZV). Less common pathogens include Epstein-Barr virus, cytomegalovirus, human herpesvirus 6, adenoviruses (in individuals with impaired cell-mediated immunity), and HIV. A number of other flaviviruses, such as West Nile virus, may cause seasonal transmission of aseptic meningitis. Tick-borne encephalitis virus (TBEV), also a flavivirus, is endemic in some areas, mostly outside North America.

2) Bacterial meningitis: The most common pathogens in adults are Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae type b (Hib) (rare in adults, becoming less common in children thanks to vaccination), Listeria monocytogenes (particularly in adults with impaired innate immune systems), and occasionally Staphylococcus aureus. In newborns, the predominant pathogens are Escherichia coli, Streptococcus agalactiae, L monocytogenes, and other gram-negative intestinal bacilli; in infants and children aged <5 years, N meningitidis, H influenzae, and S pneumoniae; and in children >5 years, N meningitidis and S pneumoniae.

In patients with meningitis associated with neurosurgery, the common pathogens include organisms such as S aureus, coagulase-negative staphylococci, Candida spp, and gram-negative bacilli, particularly Pseudomonas aeruginosa.

3) Bacterial aseptic meningitis: Acid-fast mycobacteria, particularly Mycobacterium tuberculosis (tuberculous meningitis); spirochetes Borrelia spp (neuroborreliosis [see Lyme Borreliosis]) or Leptospira spp (leptospirosis), L monocytogenes (more commonly causing purulent meningitis), Treponema pallidum (neurosyphilis), Francisella tularensis (tularemia), and coccobacilli Brucella spp (brucellosis).

4) Fungal meningitis (aseptic or purulent): Predominantly Cryptococcus neoformans (among patients with impaired cell-mediated defenses and HIV), Cryptococcus gattii, rarely dimorphic fungi such as Histoplasma and Blastomyces, and occasionally Aspergillus spp among severely immunocompromised individuals.

2. Reservoir and transmission vary with etiologic factors. The reservoir is predominantly humans (sick individuals or carriers) and rarely wild or domestic animals (eg, L monocytogenes, Borrelia spp), including birds (Cryptococcus spp), or the environment (molds). Depending on the pathogen, transmission occurs through respiratory droplets, direct contact, vectors such as mosquitoes and ticks, fecal-oral route, and rarely via other routes (eg, L monocytogenes is transmitted by consumption of infected dairy products, undercooked meat, salads, or seafood).

3. Epidemiology: Viral meningitis: 3 to 5 cases per 100,000 persons per year; bacterial purulent meningitis: ~3 cases per 100,000 persons per year. Tuberculous meningitis is rare. Other types are very rare. Risk factors: Table 1.

4. Incubation and contagious period: In meningococcal infection, the incubation period is from 2 to 10 days; in Hib infection, it is 2 to 4 days; and in viral infections, it differs depending on the species from a few days up to 3 weeks. Incubation periods for other pathogens are not well established and may vary from 2 to 14 days. Infectivity and contagious periods are specific for individual pathogens; infectivity is highest in viral meningitis, such as enteroviral meningitis, and lower or low in bacterial meningitis (eg, transmission of meningococcal infection requires prolonged close contact with an infected individual) and fungal meningitis.

Clinical Features and Natural HistoryTop

1. Clinical features:

1) Signs of meningeal irritation are the key signs of meningitis; they may be absent in elderly patients. Manifestations include neck stiffness, photophobia, and phonophobia.

2) Signs and symptoms of increased intracranial pressure: Headache (severe, throbbing or dull, not responding to analgesics and nonsteroidal anti-inflammatory drugs [NSAIDs]), nausea and vomiting, bradycardia, respiratory failure.

3) Fever >39 degrees Celsius.

4) Other signs and symptoms of encephalitis: Agitation, altered mental status (this may progress to coma), focal or generalized seizures, spastic paresis or other manifestations of pyramidal tract involvement, paresis or paralysis of the cranial nerves (particularly in tuberculous meningitis, which most commonly affects nerves VI, III, IV, and VII), clinical features of brainstem or cerebellar involvement (particularly in advanced L monocytogenes meningitis).

5) Other signs and symptoms: Labial or facial herpes; petechiae and purpura, predominantly on extremities (these suggest meningococcal meningitis); symptoms of systemic inflammatory response syndrome, disseminated intravascular coagulation, shock, and multiple organ dysfunction syndrome.

2. Natural history: Although the dynamics of the disease and intensity of signs and symptoms vary with etiology, the causative factor cannot be established on the basis of clinical features alone. Results of routine CSF analysis confirm meningitis and help narrow down the diagnosis to a particular group of pathogens. Bacterial purulent meningitis is associated with a sudden onset and rapid progression; patients are usually severely ill and within <24 hours the disease becomes life-threatening. Viral meningitis usually has a milder course. In bacterial aseptic meningitis (eg, tuberculous) and fungal meningitis, the onset is nonspecific and the course is usually subacute or chronic. In untreated or inadequately treated patients, the inflammation spreads to the brain, leading to altered mental status and focal neurologic deficits (encephalitis).


Management Algorithm

If you suspect meningitis, stabilize the patient, collect blood specimens for cultures, and determine if there are any contraindications to lumbar puncture. If it is not contraindicated, promptly perform lumbar puncture, collect CSF for a routine analysis (eg, glucose, protein, and cell count) and for microbiologic studies, including culture, sensitivity, and viral polymerase chain reaction (PCR)/culture if available, and start empiric treatment. If there is a significant delay to lumbar puncture owing to contraindications and the clinical suspicion is sufficient, our pattern is to do blood cultures and initiate antimicrobial therapy immediately afterwards, followed by lumbar puncture as soon as feasible. Adjust treatment after receiving the results of microbiologic studies (including cultures) of CSF, blood, or both and of drug susceptibility analysis.

Diagnostic Tests

1. Routine CSF analysis (see Laboratory Tests): CSF opening pressure is usually elevated (>200 mm H2O), particularly in patients with bacterial or cryptococcal meningitis. Alteration in the CSF cell count is a distinguishing feature, with a predominantly neutrophilic pleocytosis characteristic for bacterial meningitis and lymphocytic predominance typical for viral, tuberculous, and cryptococcal meningitis. Protein levels may be elevated in all conditions; a significant protein elevation in CSF may be suggestive of tuberculous meningitis. Low glucose levels are often seen with bacterial meningitis and should be correlated with serum glucose levels. In patients with significant immunosuppression, such as in advanced HIV disease, there may be fairly minimal changes to the CSF cell count and chemistry results because of the lack of inflammatory response.

2. Microbiology:

1) CSF: Microscopic examination of a Gram-stained centrifuged sediment serves as the preliminary identification of bacteria and fungi; India ink staining is used in the preliminary identification of Cryptococcus spp, and acid-fast staining is used for the identification of M tuberculosis. The latex agglutination test, where available, can help with detecting antigens of Hib, S pneumoniae, N meningitidis, and C neoformans; results can be obtained within 15 minutes. This test is particularly useful in patients who have already been treated with antibiotics or in those with negative results of the Gram stain or cultures. Bacterial and fungal cultures allow for a definitive diagnosis of the causative factor of meningitis and determination of drug sensitivity of the isolated pathogen. In bacterial infections, the results are usually obtained within 48 hours (except for tuberculosis). In fungal infections, repeated cultures may be necessary until fungal growth is obtained. PCR (bacteria, viruses, fungi) is used to establish etiology when cultures are negative (eg, in patients treated with antibiotics prior to lumbar puncture); this is the key diagnostic method in viral meningitis. Serologic studies: Detection of specific IgM (in some cases also IgG) using the enzyme-linked immunosorbent assay (ELISA) is helpful in diagnosing certain cases of viral meningitis and neuroborreliosis.

2) Blood cultures (bacteria, fungi) should be performed prior to antibiotic treatment in all patients with suspected meningitis (sensitivity is 60%-90%).

3) Throat and rectal swabs: Viral culture is recommended if enteroviral etiology is suspected.

3. Computed tomography (CT) or magnetic resonance imaging (MRI) of the head are not essential for the diagnosis of isolated meningitis (although the results may suggest tuberculous meningitis). The studies are helpful in excluding cerebral edema or a brain tumor prior to lumbar puncture and in detecting early and late complications of meningitis in patients with persisting neurologic signs and symptoms (eg, focal deficits, altered mental status), with positive follow-up CSF cultures, or with recurrent meningitis. Imaging should be performed both with and without contrast enhancement. MRI is able to diagnose sagittal sinus thrombosis, a rare complication of purulent meningitis.

4. In case of suspected tuberculous etiology, search for the primary source, such as in the lungs, and perform microbiologic studies from that site. This may yield a higher positivity rate than staining and culture of CSF. The tuberculin skin test is not useful in this setting.

Differential Diagnosis

Differential diagnosis includes:

1) Subarachnoid hemorrhage.

2) Focal central nervous system (CNS) infections (abscess or empyema) and brain tumor.

3) Meningeal irritation in the course of an infection located outside the CNS or of noninfectious etiology (signs and symptoms of increased intracranial pressure may be present but CSF is always normal).

4) Carcinomatous meningitis resulting from metastases or lymphoproliferative infiltrates in the meninges (CSF features are usually similar to bacterial aseptic meningitis; detection of tumor cells in CSF cytology and identification of the primary tumor are essential for diagnosis).

5) Drugs: NSAIDs (particularly in patients with rheumatoid arthritis and other systemic connective tissue diseases), sulfamethoxazole/trimethoprim, carbamazepine, cytarabine, IV immunoglobulin. Clinical features are similar to aseptic meningitis.

6) Systemic connective tissue diseases (including systemic vasculitis). Clinical features are similar to aseptic meningitis.


Patients with acute meningitis should be treated in a monitored setting with intensity of care depending on the acuity and severity of presentation. Management may require admission to an intensive care unit (ICU) or a center with expertise in the diagnosis and treatment of CNS infections.

Treatment of Bacterial Meningitis

Start antibacterial treatment immediately after obtaining specimens for microbiologic studies. Results of microscopic evaluation of CSF and of the latex agglutination test may be helpful in the immediate initiation of targeted antimicrobial treatment. If necessary, modify empiric treatment after obtaining culture results. If clinical features and CSF analysis results indicate tuberculous meningitis, start empiric treatment of tuberculosis before confirming the diagnosis with microbiologic tests.

Treatment of Viral Meningitis

Treatment of viral meningitis is typically not indicated unless there are signs and symptoms of concomitant encephalitis. In such patients acyclovir (INN aciclovir) at a dose of 30 mg/kg/d administered in 3 divided doses should be considered while pending definitive cause identification.

1. Empiric antimicrobial therapy:

1) Adults aged <50 years: IV ceftriaxone 2 g every 12 hours + vancomycin 15 mg/kg every 8 hours for 10 to 14 days; this is the basic panel covering the most common pathogens. Alternatively use IV meropenem 2 g every 8 hours if the patient has a known significant allergy to ceftriaxone.

2) Adults aged ≥50 years or with other risk factors for L monocytogenes infection (Table 1): As in adults aged <50 years + IV ampicillin 2 g every 4 hours. If the patients has a significant allergy to ampicillin, use IV sulfamethoxazole/trimethoprim at a dose of 20 mg/kg/d of the trimethoprim component divided every 6 to 12 hours.

3) Patients with basal skull fracture: Treat as adult patients <50 years.

4) Patients after penetrating head trauma, after neurosurgical procedures, or with CSF shunts: IV vancomycin 15 mg/kg every 8 hours for 10 to 14 days; IV ceftazidime or IV meropenem, both at a dose of 2 g every 8 hours, may be added to vancomycin. Serum levels of vancomycin should be monitored during treatment and the trough level should be maintained at 15 to 20 microg/mL.

2. Targeted antimicrobial therapy:

1) S pneumoniae: For penicillin-sensitive strains (minimum inhibitory concentration [MIC] ≤0.064 mg/L), use IV penicillin G (INN benzylpenicillin) at a dose of 4 million IU every 4 hours for 10 to 14 days. For strains with decreased sensitivity to penicillin (MIC >0.064 mg/L), use ceftriaxone (see above) or meropenem (see above). For cephalosporin-resistant strains (MIC ≥2 microg/mL), use vancomycin 15 mg/kg every 8 hours + oral rifampin (INN rifampicin) 600 mg every 24 hours.

2) N meningitidis: For penicillin-sensitive strains (MIC <0.1 mg/mL), use penicillin G or ampicillin, as in treatment against S pneumoniae; alternatively use ceftriaxone. For strains with decreased sensitivity to penicillin, use ceftriaxone, or alternatively meropenem as second-line therapy (see above).

3) L monocytogenes: Use IV ampicillin 2 g every 4 hours in combination with IV amikacin 5 mg/kg every 8 hours (or another aminoglycoside) for ≥21 days. Alternatively use IV penicillin G, meropenem, or sulfamethoxazole/trimethoprim for 21 days.

4) S aureus: For methicillin-sensitive strains, use IV cloxacillin 2 g every 4 hours for 14 days; alternatively use vancomycin or ceftriaxone (see above). For methicillin-resistant strains, use vancomycin (see above); alternatively use IV linezolid 600 mg every 12 hours or IV ceftaroline 600 mg every 12 hours for 10 to 14 days.

5) S epidermidis: Vancomycin + rifampin (see above); alternatively IV or oral linezolid 600 mg every 12 hours for 10 to 14 days.

6) Enterococcus spp: For ampicillin-sensitive strains, use IV ampicillin + gentamicin 5 mg/kg/d in divided doses every 8 hours. For ampicillin-resistant strains, use vancomycin + gentamicin. For ampicillin-resistant and vancomycin-resistant strains, use linezolid.

7) Gram-negative bacilli, antibiotic-resistant strains (hospital-acquired purulent meningitis): Use IV meropenem 2 g every 8 hours (if there is no response, consider intrathecal amikacin 20-25 mg/d). For carbapenem-resistant strains, use colistin 100,000 IU via the intrathecal and/or intraventricular route every 24 hours for 14 to 21 days, IV aztreonam 2 g every 6 to 8 hours for 21 days (intrathecal and intraventricular routes of administration are off-label).

8) Gram-negative bacilli, antibiotic-sensitive strains (community-acquired purulent meningitis): Use IV ceftazidime 2 g every 8 hours combined with IV amikacin 5 mg/kg in a slow infusion every 8 hours for 14 days, or IV cefepime 2 g every 8 hours; alternatively use IV meropenem 2 g every 8 hours or IV ceftriaxone 2 g every 12 hours.

Treatment of Fungal Meningitis

Administer IV antifungal drugs for the first 6 weeks of treatment followed by oral fluconazole or voriconazole until the resolution of all CNS signs and symptoms (including neuroimaging features). Removal or replacement of a CSF shunt, if present, is recommended. In patients with severe disease not responding to treatment, consider intrathecal drug administration (except for aspergillosis). Because itraconazole, caspofungin, and anidulafungin penetrate poorly to the CSF and brain parenchyma, these agents should not be used in fungal CNS infections, and particularly not as monotherapy.

1. Candidiasis: Administer IV amphotericin B 0.8 to 1 mg/kg/d in 500 mL of 5% glucose (dextrose) as an infusion over 4 to 5 hours (or as a liposomal formulation 5 mg/kg/d) as monotherapy or in combination with IV flucytosine 25 mg/kg every 6 hours for the first few weeks, followed by oral fluconazole 800 mg/d for 6 days, then 400 mg/d. Alternatively use IV fluconazole 800 mg/d or IV voriconazole 6 mg/kg every 12 hours on the first day followed by 4 mg/kg every 12 hours for a minimum of 2 to 3 weeks, depending on organism clearance and normalization of CSF parameters.

2. Cryptococcosis: Administer amphotericin B (a liposomal formulation may also be used) and flucytosine (see above) for a minimum of 2 weeks, based on organism clearance and clinical response. Consolidation therapy with fluconazole 400 mg/d is continued for 10 weeks and subsequently followed by long-term oral fluconazole 200 mg/d for 6 to 12 months (under supervision of an infectious disease specialist). Therapy may be discontinued in HIV patients on antiretroviral therapy when CD4 counts are >200. Antiretroviral therapy should not be initiated for 6 to 8 weeks as the risk of mortality is higher in this population.

3. Aspergillosis: Use voriconazole 6 mg/kg IV every 12 hours on day 1, followed by 4 mg/kg IV every 12 hours, and subsequently 200 mg orally every 12 hours. Alternatively administer IV amphotericin B up to 1 mg/kg/d (in a liposomal formulation 5-7 mg/kg/d) as an infusion (see above) or combine both agents. Therapy should be continued for a minimum of 6 weeks with reassessment of clinical and radiologic improvement.

Supportive Treatment

1. General recommendations:

1) IV fluid therapy, depending on the patient’s hemodynamic parameters, and restoration of water and electrolyte balance. Routine limitation of fluid intake below daily requirements is not recommended, except for patients with syndrome of inappropriate antidiuretic hormone secretion (SIADH).

2) Enteral or parenteral nutrition.

3) Physical therapy: As soon as cerebral edema has decreased and signs and symptoms of increased intracranial pressure are reduced, start passive physical therapy and move on to active therapy.

2. Treatment reducing cerebral edema and inflammation: In every patient with purulent meningitis use IV dexamethasone 8 to 10 mg every 6 hours (up to 1 mg/kg/d in patients with cerebral edema). Administer the first dose 15 to 20 minutes prior to or at the moment of initiating antimicrobial treatment and continue for 2 to 4 days if pneumococcal meningitis is confirmed.Evidence 1Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). High Quality of Evidence (high confidence that we know true effects of the intervention). de Gans J, van de Beek D; European Dexamethasone in Adulthood Bacterial Meningitis Study Investigators. Dexamethasone in adults with bacterial meningitis. N Engl J Med. 2002 Nov 14;347(20):1549-56. PubMed PMID: 12432041. The benefit of this intervention in other forms of purulent bacterial meningitis is less clear.

3. Treatment and prevention of complications: Increased intracranial pressure or cerebral edema: see Stroke. Seizures: see Stroke. In patients with hypogammaglobulinemia, consider IV immunoglobulin. Antithrombotic prophylaxis: see Primary Prevention of Venous Thromboembolism. Prevention of acute hemorrhagic gastropathy (stress ulcers): see Peptic Ulcer Disease; and combine this with initiation of enteral nutrition as soon as possible. Also see Acute Respiratory Failure; see Septic Shock; see Disseminated Intravascular Coagulation.


1. Bacterial meningitis: Routine follow-up examinations of CSF are not necessary if signs and symptoms resolve and the patient’s general condition is improving. The effectiveness of treatment of causative pathogens is indicated by clinical improvement, a decrease in CSF inflammatory marker levels, and an increase in CSF mononuclear cell counts and glucose levels. Follow-up CSF culture should be negative.

2. Fungal meningitis: Monitor the patient’s condition, resolution of signs and symptoms (including neuroimaging features), CSF markers of inflammation, and clearance of fungi from CSF and blood. Repeat lumbar puncture for culture is suggested at 2 weeks before switching to consolidation therapy, and earlier if the patient deteriorates or for relief of elevated intracranial pressure. We do not recommend serial antigen testing for monitoring the response to treatment.

3. Tuberculous meningitis: Monitor the resolution of signs and symptoms, CSF markers of inflammation, and structural abnormalities in the brain detected by CT or MRI. The first indicators of effective therapy may be observed as late as after 2 to 4 weeks of treatment.


Purulent and bacterial aseptic meningitis (tuberculosis, listeriosis) as well as fungal meningitis are characterized by a higher risk and severity of complications than viral meningitis. Complications may include status epilepticus (in acute disease) and epilepsy, hydrocephalus, cerebral edema, SIADH, spastic paresis or paralysis (in tuberculous meningitis often affecting the cranial nerves), cognitive impairment and speech impairment, mental retardation, and hearing impairment or loss (particularly in pneumococcal meningitis). Rare complications include brain abscess (particularly in infections with gram–negative bacilli, eg, Enterobacter spp and Citrobacter spp), inflammatory aneurysm, transverse myelitis, and sphincter dysfunction (particularly in tuberculous meningitis with spinal cord involvement).


1. Viral meningitis: Prognosis is good. Usually the disease has a mild course and resolves completely without permanent sequelae. The mortality rate is <1%.

2. Bacterial purulent meningitis: Prognosis is worse in the case of advanced age, immunodeficiency, higher pathogen virulence (pneumococci, gram–negative bacilli, antibiotic-resistant strains), delayed initiation of effective treatment (including treatment of cerebral edema), shock, altered mental status, and seizures in acute disease. Permanent neurologic deficits occur in 9% of patients, or more often in higher-risk populations. Mortality rates depend on etiologic factors and are on average ~20%.

3. Tuberculous meningitis: The mortality rate is ~30%. Permanent neurologic deficits develop in 40% of patients. Delayed diagnosis and initiation of effective treatment increases the risk of death and permanent neurologic sequelae.

4. Fungal meningitis: The disease has a poor prognosis and is associated with high mortality rates.


Specific Prevention

1. Vaccination against pneumococcal, meningococcal, and Hib infections, as well as against tuberculosis (only in children), mumps, VZV, and poliomyelitis. The preferred pneumococcal vaccine is the 13-valent conjugate vaccine in children and high-risk individuals and the polysaccharide 23-valent vaccine in those aged >65 years and high-risk individuals who have received conjugate vaccines. Meningococcal vaccination includes serogroup C meningococcal conjugate vaccine, quadrivalent meningococcal vaccine (targeting serogroups A, C, W, and Y), and serogroup B meningococcal vaccine in high-risk individuals and children.

High-risk individuals include, among others, those with chronic heart, lung, kidney, or liver disease; diabetes mellitus; a history of solid organ or stem cell transplant; immunodeficiency or immunosuppression (including HIV and treatment with steroids); malignancies.

2. Postexposure chemoprophylaxis is indicated in selected persons after close contact with a patient diagnosed with purulent meningococcal or Hib meningitis. All individuals who have had contact with such persons and who develop signs and symptoms suggestive of meningitis or sepsis should seek immediate medical attention.

1) N meningitidis: One dose of oral ciprofloxacin 500 to 750 mg or oral rifampin 600 mg every 12 hours for 2 days, or a single dose of IM ceftriaxone 250 mg (this is the agent of choice in pregnant women). Indications: Individuals who were in close contact with a patient with invasive meningococcal disease (sepsis, purulent meningitis) within 7 days before the onset of signs and symptoms, such as household contacts, persons sleeping in the same room as the infected person (dormitories, shelters), persons who remained in close direct contact with the patient (kissing), persons sharing cooking facilities with the patient (college campuses, dormitories, shelters, hostels, hotels), military, and other personnel living in barracks. Patients with invasive meningococcal disease who were treated with penicillin G (not a third-generation cephalosporin) are at higher risk for recurrent bacterial colonization of the upper respiratory tract and becoming a carrier; chemoprophylaxis is recommended prior to discharge from the hospital.

2) Hib: Oral rifampin 20 mg/kg (maximum 600 mg) once daily for 4 days (contraindicated in pregnancy), or a single dose of IM ceftriaxone 250 mg (this is the agent of choice in pregnant women). Indications: Individuals who were in close contact with a patient within 30 days before the onset of signs and symptoms, such as personnel of a daycare facility that supervised an infected child if the facility supervises any other children aged ≤4 years who were not vaccinated or incompletely vaccinated against Hib infection as well as all household contacts of the patient if there is a child ≤4 years who was not vaccinated or incompletely vaccinated against Hib infection or an immunocompromised individual (regardless of age and vaccination status) living in the same household. Patients with Hib meningitis are at higher risk for recurrent bacterial colonization of the upper respiratory tract and becoming a carrier; chemoprophylaxis is recommended prior to discharge from the hospital.

3. Chemoprophylaxis of L monocytogenes infections: The risk of listeriosis in recipients of solid organ or bone marrow transplants is possibly reduced by long-term administration of sulfamethoxazole/trimethoprim used in these patients for Pneumocystis carinii pneumonia prophylaxis.

Nonspecific Prevention

1. Personal protection measures: Use a face mask and gloves while in contact with a patient with meningococcal infection. Maintain good hand hygiene after contact with the patient or their secretions. Precautions should be maintained until 24 hours after the resolution of clinical symptoms in the patient.

2. Nonspecific protection against ticks in endemic areas (not part of Canadian practice): see Infection Prevention: Nonspecific Insect and Tick Bite Precautions.

3. Reportable diseases: In many jurisdictions, including Canada, meningitis cases have to be reported to the public local health authorities.


Table 10.4-1. Risk factors for meningitis

Risk factor

Prevalent pathogens

Crowded residences (school or college dormitories, military barracks)

Neisseria meningitidis, viruses (enteroviruses, measles, mumps)

Public beaches and swimming pools


Age >60 years

Streptococcus pneumoniae and Listeria monocytogenes

Sinusitis, acute or chronic purulent otitis media, mastoiditis

S pneumoniae, Hib

Alcohol abuse

S pneumoniae, L monocytogenes, Mycobacterium tuberculosis

Impaired cell-mediated immune response (HIV and AIDS, immunosuppressive therapy—particularly after transplant—or glucocorticoid treatment, cancer treatment), diabetes, hemodialysis, liver cirrhosis, cachexia in end-stage cancer or other diseases

L monocytogenes, M tuberculosis, fungi

Fractures of the skull base or ethmoidal cells involving the anterior cranial fossa and tears of the dura mater resulting in CSF leakage

S pneumoniae, Hib, group A beta-hemolytic streptococci

Penetrating head injuries

Staphylococcus aureus, Staphylococcus epidermidis, aerobic gram-negative bacilli including Pseudomonas aeruginosa

Neurosurgical procedures

Klebsiella pneumoniae, other Enterobacteriaceae, P aeruginosa, Acinetobacter baumannii, S aureus, S epidermidis (hospital-acquired meningitis)

CSF shunts

S epidermidis, S aureus, P aeruginosa, other aerobic gram-negative bacilli, Propionibacterium acnes, fungi

Complement deficiencies

N meningitidis (frequently familial or recurrent meningitis), Moraxella spp, Acinetobacter spp

Neutropenia <1×109/L

P aeruginosa, other gram-negative bacilli

Impaired humoral immune response

S pneumoniae, Hib, less commonly N meningitidis


S pneumoniae, Hib, N meningitidis

Cranial or vertebral osteomyelitis

S aureus, gram-negative bacilli


M tuberculosis

Burns, severe illness, invasive ICU procedures (intubation, tracheostomy, vascular access procedures, parenteral nutrition), prosthetic heart valves or other prostheses, treatment with broad-spectrum antibiotics


CSF, cerebrospinal fluid; Hib, Haemophilus influenzae type b; ICU, intensive care unit.

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