Meningitis is an infection of the meninges in the brain or spinal cord. Common causes include viruses and bacteria, although fungal, parasitic, and noninfectious causes of meningitis are possible. The most common bacterial pathogens (N. meningitidis, S. pneumoniae, H. influenzae, Group B streptococcus, and L. monocytogenes) vary depending on age and underlying medical conditions. Enteroviruses and herpes simplex virus (HSV) are the leading causes of viral meningitis. The (fever, meningismus, altered mental state) occurs in less than half of adult patients and frequently presents with nonspecific symptoms. Advanced infection includes signs of increased intracranial pressure (ICP), neurological deficits, altered mental status, and seizures. Diagnosis is confirmed with CSF analysis and microbiological studies (e.g., PCR, culture). If increased ICP is suspected, a CT of the head is recommended prior to lumbar puncture (LP). Antibiotic therapy should not be delayed for diagnostic testing. Bacterial meningitis requires rapid initiation of empiric antimicrobials and sometimes glucocorticoids to prevent complications, which include neurological deficits (e.g., hearing loss) and end-organ damage (e.g., Waterhouse-Friderichsen syndrome in patients with meningococcal meningitis). While most cases of viral meningitis are self-limiting, herpesvirus infections (e.g., HSV, VZV) must be promptly recognized and treated with IV acyclovir to prevent serious complications and death. Prevention is through vaccination against common causes of meningitis, and chemoprophylaxis for exposed contacts.
- In the pediatric population, meningitis most often occurs in children < 1 year of age. 
- The median age for meningitis in the adult population is 43 years. 
- Sub-Saharan Africa has the worldwide highest incidence of meningitis caused by N. meningitidis. 
Epidemiological data refers to the US, unless otherwise specified.
- CSF leak after head trauma or neurosurgery
- Maternal group B streptococcal infection during birth
- Immunocompromise (e.g., due to AIDS, asplenia, heavy alcohol use disorder, chronic illness, cancer, sickle cell anemia, old age, pregnancy)
- Crowded occupational or living conditions (e.g., college dormitories, military barracks, retirement homes, kindergartens)
- Close contact with an infected person
Most common causative agents of bacterial meningitis by age group and underlying condition 
|< 1 month |
|1 month–2 years  |
|2–50 years |
|> 50 years |
|By underlying condition|
|Basilar skull fracture |
|Penetrating trauma |
|Health care-associated |
Less common bacterial pathogens
- Borrelia spp. ( )
- Treponema pallidum ()
- Mycobacterium tuberculosis ( )
- Actinomyces israelii
- Leptospira ()
Viral meningitis: often associated with encephalitis (meningoencephalitis)
- Enteroviruses (especially coxsackieviruses and echoviruses): the most common cause of all types of meningitis in all patient groups 
- Herpesviruses: HSV (meningitis is more commonly caused by HSV2 than HSV1) , CMV, EBV, VZV
- Lymphocytic choriomeningitis virus (LCMV)
- Mumps virus
- Measles virus
- Some arboviruses (e.g., West Nile virus, TBEV in Eurasia)
- Poliovirus (nonparalytic poliomyelitis: aseptic meningitic form)
- St. Louis encephalitis virus
- California encephalitis virus
- Western equine encephalitis virus
- Influenza virus
- JC virus 
- Fungal meningitis
- Parasitic meningitis
- Noninfectious meningitis
Causes of meningitis in immunocompromised individuals
- Certain immune deficiencies can predispose to certain types of meningitis. 
- Immunocompromised individuals are at increased risk of recurrent bacterial meningitis compared to those with intact immunity. 
- Viral: Risk is higher in individuals with cell-mediated immune deficiencies (e.g., in HIV infection). 
- Fungal: Risk is higher in individuals with cell-mediated immune deficiencies (e.g., HIV infection). 
- Protozoal: Toxoplasma gondii (rare) 
Pathways of infection
- Most pathogens that cause meningitis colonize the nasopharynx or the upper airways before entering the CNS via:
- Direct infection (e.g., due to trauma or head surgery) 
- Bacterial meningitis: usually 3–7 days 
- Viral meningitis: usually 2–14 days, depending on the type of virus
Clinical features of bacterial and viral meningitis are similar, although viral meningitis is less acute and usually self-limiting within 5–14 days. 
Symptoms of meningitis 
- Classic triad of meningitis ; 
- Nausea, vomiting
- Neonates and young children often present with nonspecific symptoms; see also “Meningitis in infants and children.”
- Patients with N. meningitidis: signs of meningococcemia
- Patients with viral meningitis
Less than half of adult patients have all three features of the classic triad of meningitis; the percentage is even lower in neonates and young infants, who typically present with nonspecific symptoms
Physical examination 
Signs of meningeal irritation
- Systemic signs of inflammation
- Signs of increased intracranial pressure: (< 5% of cases), e.g., cranial nerve palsies, papilledema 
Signs of underlying infections
- Bulging and redness of tympanic membrane: acute otitis media
- Skin manifestations 
Features suggestive of meningoencephalitis 
- Focal neurological signs (e.g., paresis, extrapyramidal symptoms, aphasia)
- Seizures (focal-onset or generalized)
- Behavioral changes, psychosis
- Altered consciousness
- Bacterial meningitis is a medical emergency and requires immediate treatment.
- Diagnostic and treatment steps should be initiated simultaneously and empiric treatment should not be delayed for diagnostic steps.
- If the patient is stable and has no LP contraindications: Perform LP as soon as possible before starting empiric antibiotics.
- If the patient is unstable, requires neuroimaging (see criteria for imaging prior to LP in suspected meningitis), or has relative contraindications to LP (e.g., coagulopathy): Defer LP and start empiric antibiotic treatment (see empiric antibiotic therapy for bacterial meningitis). 
Do not delay empiric antibiotic therapy in patients suspected of having bacterial meningitis.
- Bacterial meningitis can be rapidly progressive and life-threatening.
- Patients may present as critically ill and with complications (e.g., sepsis, multiorgan failure) requiring early aggressive supportive care.
- Empiric antibiotic treatment must be initiated as soon as possible (i.e., often prior to diagnosis).
- Obtain samples immediately for blood cultures, routine laboratory tests, and screening for organ dysfunction.
- Confirm the diagnosis with LP and CSF analysis (if no are present).
- See also “Meningitis in infants and children.”
Start empiric antibiotics immediately after obtaining blood cultures and CSF samples. If LP is delayed for any reason (e.g., the need for a CT or hemodynamic stabilization), obtain blood cultures and administer antibiotics until it can be performed.
Laboratory studies 
- Blood cultures (two sets): obtain before starting antibiotic therapy
- BMP: Blood glucose is needed to analyze CSF glucose.
- CRP: elevated 
- Additional tests
- Recommended criteria for imaging prior to LP in suspected meningitis 
- Supportive findings
To remember the indications for imaging before LP, think of LP FAILS: Focal neurological deficits, Altered mental status, Immunocompromised or ↑ ICP, Lesions (space-occupying lesions in the brain), Seizures.
Interpretation of CSF analysis
- Confirmatory findings: pathogen identification on CSF OR positive blood cultures in a patient with highly suggestive CSF findings
- Highly suggestive findings: pleocytosis (granulocytic or lymphocytic), low glucose, high protein
- Nonspecific findings: high opening pressure
Routine testing 
|Cerebrospinal fluid analysis in meningitis |
|Normal||Bacterial meningitis||Viral meningitis|
|Appearance|| || || |
|Cell count and differential|| |
|Opening pressure || || || |
|Lactate || || || |
|Protein|| || || |
|Glucose|| || || |
|Gram stain and culture || || |
Atypical pathogen testing
Atypical pathogen testing is not necessary for all patients and should be performed as directed by clinical suspicion.
|Cerebrospinal fluid analysis in meningitis due to atypical pathogens |
|Tuberculous meningitis ||Lyme meningitis ||Cryptococcal meningitis |
|Appearance|| || || |
|Cell count and differential|
|Opening pressure|| || || |
|Lactate || || || |
|Protein|| || || |
|Glucose|| || || |
Additional microbiological testing
- Special microbiological stains
Special cultures 
- Viral culture
- M. tuberculosis cultures: Results can take up to 6 weeks. 
- Fungal cultures: for the identification of Candida spp., Cryptococcus spp. 
- For patients with CSF shunts or drains: Extend CSF cultures for at least 10 days.
- PCR for viral meningitis and specific bacterial subtypes 
Latex agglutination test 
- Bacterial antigen detection
- Fungal latex agglutinations: especially relevant for cryptococcal antigen testing (see cryptococcal meningitis)
- Apply appropriate isolation precautions.
- Stabilize the patient as needed.
Administer empiric antibiotics as soon as possible, preferably within 1 hour (see empiric antibiotic therapy for bacterial meningitis).
- If LP can be performed rapidly, administer antibiotics and adjuvant therapy (e.g., dexamethasone) after obtaining CSF.
- If LP is delayed (e.g., because neuroimaging is required), administer antibiotics and adjuvant therapy (e.g., dexamethasone) immediately.
- Add other antimicrobial therapy (e.g., antivirals, antifungals) as needed (see “Subtypes and variants” for details).
- Consult the infectious disease team.
- Tailor antimicrobial therapy once the pathogen is identified.
- Provide postexposure prophylaxis for close contacts if indicated (see postexposure chemoprophylaxis for bacterial meningitis).
- See also “Meningitis in infants and children.”
Immediate stabilization for meningitis
- Airway management: Secure the airway (e.g., intubate) if GCS < 8, the patient has intractable seizures, or there are signs of cerebral herniation (see intubation of patients with high ICP).
- Provide hemodynamic support with fluids and/or vasopressors (see “Fluid resuscitation” and “Sepsis”).
- Identify and reverse any coagulopathy (see “Anticoagulant reversal”).
- Identify and treat elevated ICP (see “ICP management”).
- The choice of initial empiric therapy depends primarily on the prevalence of organisms in certain age groups and individual patient risk factors for resistant organisms.
- Factors to consider:
|Empiric antibiotic therapy for bacterial meningitis |
|Patient characteristics||Recommended regimen|
|Age <18 years|
|Age 18–50 years|
|Age > 50 years|
|Healthcare-associated infections |
Suspected rickettsial (e.g., RMSF) or ehrlichial infection 
|Basilar skull fracture|
|Penetrating head trauma|
Ampicillin is added if patients are at risk of Listeria spp. infection (e.g., newborns, pregnant women, adults > 50 years of age, or immunocompromised patients) because cephalosporins are ineffective against Listeria spp.
Empiric therapy for viral meningitis 
Most cases of viral meningitis (e.g., caused by enteroviruses) can be treated supportively. Specific antiviral therapy is only warranted if viral encephalitis is also suspected (see HSV encephalitis for further details).
- Concern for HSV encephalitis, for example:
- Concern for other herpesviruses, e.g., VZV, EBV
- Recommended empiric antiviral agent: acyclovir
Treatment with acyclovir should be started in all patients who present with typical clinical signs of viral meningoencephalitis and only discontinued after PCR and antibody tests are negative for HSV and VZV, even if CSF is initially normal.
The decision to narrow therapy should be guided by final culture and sensitivity results, as well as local resistance patterns. We list a few examples of antimicrobial agents that may be used against specific pathogens.
|Pathogen-specific therapy in meningitis |
|Pathogen||Examples of antimicrobial agents|
S. pneumoniae (penicillin-resistant strains)
|R. rickettsii|| |
|Herpes viruses|| |
|Less frequent pathogens, e.g., M. tuberculosis, C. neoformans, B. burgdorferi|| |
- Indication: suspected or proven meningitis due to S. pneumoniae or H. influenzae
- Mechanism: reduces the local and systemic inflammation seen in bacterial meningitis and improves outcomes
- Recommended agent: dexamethasone for 2–4 days 
- Disadvantages: side effects, e.g., hyperglycemia, GI bleeding 
- For pediatric use, see “Meningitis in infants and children.”
- Electrolyte repletion
- Analgesics as needed (see pain management)
- Antipyretics as needed
- IV fluids as needed
- IV antiemetics as needed
Monitoring and disposition
- Stabilize the patient and obtain IV access
- Identify and treat sepsis, if present.
- Obtain blood cultures (two sets) and routine laboratory studies (e.g., CBC, coagulation studies, CRP).
- Consider indications for imaging prior to LP (i.e., presence of any criteria for imaging prior to LP in suspected meningitis)
- Perform LP and order CSF analysis if there are no LP contraindications
- Begin empiric antibiotics and steroids as soon as possible (see empiric antibiotic therapy for bacterial meningitis). 
- Consider empiric viral coverage.
- Provide supportive therapy as needed.
- Admit to medicine or neurology service.
- Ensure 24 hours of droplet isolation for all patients suspected of having bacterial meningitis.
- Consider indications for prophylactic treatment (see postexposure chemoprophylaxis for bacterial meningitis).
- Consult infectious diseases.
- Consult ICU, neurology, neurosurgery as needed.
Subtypes and variants
- Pathogen: : Mycobacterium tuberculosis
- Incubation period: approximately 2–8 weeks
- Risk factors: immunocompromise (e.g., HIV infection)
- Subacute course over several weeks or months
- Gradual manifestation with intermittent fever
- Typical symptoms of meningitis, including fever, headache, neck stiffness, and altered mental status (see “Clinical features” section above for details)
- Focal neurological deficits (e.g., hemiparesis) due to hematogenous dissemination of cranial arteritis
- Cranial nerve deficits; are most commonly seen in basal meningitis and predominantly involve the abducens nerve 
- Presence of acid-fast bacilli on CSF Gram stain 
- Culture is the gold standard for diagnosis, but results may take weeks. 
Analysis of adenosine deaminase (ADA) activity
- ↑↑ Activity in CSF of individuals with tuberculous meningitis compared to CSF of individuals with other types of meningitis (e.g., cryptococcal or bacterial meningitis)
- For the differentiation of tuberculous from other types of meningitis, combining serum and CSF ADA activity can increase sensitivity and specificity. 
- However, reported sensitivity and specificity vary greatly in the literature; confounding factors include the CSF ADA cut-offs, assay types, and comorbidities (especially HIV). 
- CT/MRI: possible hydrocephalus, basilar meningeal thickening, tuberculomas, edema, infarcts 
- CSF fluid
- Pathogen: Cryptococcus neoformans (a type of encapsulated yeast)
- Exposure to pigeon droppings
- Clinical course: : subacute onset with (low) fever, fatigue, and headaches
- See section on “Clinical features” above
- Meningeal symptoms are often absent
Cryptococcal antigen testing of CSF and serum
- Highly specific and sensitive 
- Typically performed via latex agglutination or enzyme immunoassay
- CSF culture (Sabouraud agar)
- CSF gram staining: India Ink (clear halo), mucicarmine (red inner capsule)
- MRI: gelatinous pseudocysts (soap bubble appearance)
- Cryptococcal antigen testing of CSF and serum
- Induction: Intravenous amphotericin B PLUS flucytosine for at least 2 weeks
- Consolidation: fluconazole for at least 8 weeks
- Maintenance: fluconazole for at least 1 year
- Manage raised ICP with therapeutic lumbar puncture.
- Important consideration: Delay initiation of cART for 4–6 weeks after starting antifungal therapy to reduce the risk of .
Eurasia: Tick-borne meningoencephalitis
- Pathogen: tick-borne encephalitis virus (TBEV)
Route of infection: tick-borne
- Ixodid tick acts as a vector; therefore, transmission is predominantly in June/July and September/October.
- Occasional transmission via unpasteurized dairy products from infected livestock
- Incubation period: usually 7–14 days
- Clinical features:
- Treatment: symptomatic
- Full recovery is common (particularly in children and adolescents).
- In symptomatic disease, residual symptoms may occur.
Prevention: A vaccine is not available in the US.
- Active immunization with an inactivated TBEV (inactivated vaccination): Large-scale implementation of this vaccination is not generally recommended.
- The CDC's Advisory Committee on Immunization Practices (ACIP) recommends the vaccination only for individuals living, traveling, or working in high-risk areas (laboratory staff exposed to TBEV, foresters, etc.).
Primary amebic meningoencephalitis 
- Pathogen: Naegleria fowleri (colloquially referred to as “brain-eating amoeba”), found in warm freshwater (e.g., ponds, hot springs)
- Route of infection: via contaminated water entering the nose (e.g., while swimming) → invades the CNS directly via the cribriform plate
- Clinical features: causes fulminant meningoencephalitis with rapid onset
- Treatment: amphotericin B, miltefosine
- Prognosis: nearly always fatal 
- Most common: sensorineural hearing loss (transient or permanent)
- Focal neurological deficits 
- Cognitive impairment
- Spasticity or paresis
- Cerebral edema and elevated ICP
- Communicating hydrocephalus
- Cerebrovascular disease
- Rare: brain abscess; , subdural empyema, arteritis (risk of cerebral infarction and cerebral venous sinus thrombosis), ventriculitis, cerebritis
- Epidemiology: : predominantly affects small children and asplenic individuals
- Description: acute primary insufficiency of the adrenal gland most commonly caused by adrenal hemorrhage
- Pathophysiology: coagulopathy triggered by endotoxins; , which often leads to hemorrhagic necrosis of the adrenal glands
- Clinical features
- Treatment of the underlying cause (see and )
- and management of
- Prognosis: fatal without treatment and often fatal even with treatment, particularly if associated with meningococcal infection (> 40% mortality rate) 
We list the most important complications. The selection is not exhaustive.
- Fatal if left untreated
- Prognosis in treated patients depends on age, overall condition, immune status and the pathogen(s) involved.
- Viral meningitis
- Fungal meningitis
Primary prevention 
Follow recommended ACIP immunization schedules, particularly for:
- Manage conditions that increase the risk of developing severe infections.
- Promptly treat infections that can spread to the CNS (e.g., mastoiditis, sepsis).
- Prevent vertical transmission of infections to neonates
Meningococcal vaccine 
- There are three types of meningococcal vaccine.
- Meningococcal ACWY vaccines (protein-conjugate) 
- Meningococcal B vaccines (protein-based) 
- Pentavalent meningococcal vaccine (MenABCWY) 
- The meningococcal vaccination schedule varies widely between countries.
Prevention of onward transmission
- Follow empiric droplet precautions and then adjust based on the identified pathogen. 
- Provide postexposure chemoprophylaxis for close contacts. 
- During community outbreaks of N. meningitidis: Vaccinate against the circulating serotype. 
is a nationally ; other etiologies of meningitis may also be reportable depending on local state law. 
|Postexposure chemoprophylaxis for bacterial meningitis |
|Pathogen||Indications||Recommended regimens |
|N. meningitidis || || |
|H. influenzae  || |
Meningitis in infants and children 
Clinical features 
Children < 2 years old often have nonspecific symptoms without meningismus.
- Poor appetite, vomiting
- Neurological signs
- Changes in vital signs
- For children ≥ 2 years of age, see “Clinical features of meningitis.”
Diagnostics for meningitis in children 
- Diagnostics for meningitis do not differ significantly between adults and children.
- In all neonates and in children with signs of complications , consider neuroimaging. 
- A multiplex PCR meningitis panel, if available, may help guide management. 
- If < 60 days old (especially < 21 days old): Evaluate for and, if indicated, obtain . 
Treatment for meningitis in children 
- does not differ between children and adults.
- For unstable patients, initiate .
- Start empiric antimicrobial therapy as appropriate.
- Consult specialists (infectious disease, intensive care, or neurology) as needed.
- Neonates ≤ 28 days ; 
Infants and children ≥ 29 days of age
- Suspected bacterial meningitis: Start empiric antibiotic therapy with vancomycin PLUS ceftriaxone. 
- Suspected viral meningitis in otherwise healthy children : Consider using a meningitis scoring system, e.g., the bacterial meningitis score. 
- Initiate additional therapies if certain pathogens are suspected.
- Suspected HSV meningitis (i.e., infants with red flag features for HSV in infants) : Add acyclovir. 
- Suspected H. influenza or S. pneumonia: Consider dexamethasone (off-label) if it can be given before or within 1 hour of initial antibiotics. 
- Once the etiology is known, change from empiric to .
- Repeat LP in neonates with gram-negative or HSV meningitis. 
- Monitor BMP to help adjust IV fluids and antimicrobial dosages, and to assess for the development of SIADH. 
Ongoing management 
- Obtain an audiology evaluation prior to discharge from the hospital. 
- In children with residual neurological defects, refer to appropriate services. 
- The primary medical provider should monitor closely for:
- Subsequent hearing loss
- Delays in