Meningitis

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Resident
Survival
Guide

Template:DiseaseDisorder infobox

Meningitis Main Page

Patient Information

Overview

Causes

Classification

Viral Meningitis
Bacterial Meningitis
Fungal Meningitis

Differential Diagnosis

Diagnosis

Treatment

For patient information click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Muhammad Saad, M.B.B.S.[2] Niloofarsadaat Eshaghhosseiny, MD[3] Alara Ece Dagsali, M.D. Seyedmahdi Pahlavani, M.D. [4]
Synonyms and keywords: Leptomeningitis, Inflammation of meninges, Pyogenic meningitis, Purulent meningitis, Aseptic meningitis, Spinal meningitis, Cerebrospinal fever

Overview

The meninges (singular meninx) is the system of membranes which envelop the central nervous system, consisting of the dura mater, the arachnoid mater and the pia mater. Meningitis is the inflammation of these protective membranes and of the subarachnoid space, and may extend to involve the brain parenchyma (meningoencephalitis). It is classified by tempo (acute, subacute, chronic, recurrent), by cerebrospinal fluid profile (purulent versus lymphocytic), by aetiology (bacterial, viral, mycobacterial, fungal, spirochetal, parasitic and non-infectious), and by mode of acquisition (community-acquired versus healthcare-associated).

While some forms of meningitis are mild and resolve spontaneously (e.g. viral meningitis), acute bacterial meningitis is a medical emergency in which delays in antibiotic administration translate directly into excess mortality. The common presenting features are fever, headache, neck stiffness and altered mental status, although the classic triad is present in fewer than half of adults and infants more often present with poor feeding, a bulging fontanelle and convulsions. Diagnosis rests on clinical assessment combined with prompt lumbar puncture and CSF analysis; computed tomography of the head before lumbar puncture is required only in defined circumstances and must never delay therapy.

Treatment consists of immediate empiric intravenous antibiotics selected by age and predisposing condition, adjunctive dexamethasone given before or with the first antibiotic dose in appropriate populations, supportive neurocritical care, and subsequent pathogen-directed therapy. Procedural and surgical management is reserved for hydrocephalus, refractory intracranial hypertension, infected neurosurgical devices, a parameningeal focus and cerebrospinal fluid fistula. Non-bacterial disease ranges from supportive care alone to prolonged antimycobacterial or antifungal therapy, or chemotherapy and irradiation for neoplastic meningitis. Conjugate vaccination is the single most effective preventive measure, and antimicrobial chemoprophylaxis is indicated for close contacts of patients with invasive meningococcal disease.

Historical Perspective

Meningitis may have been described in the Middle Ages, but it was first accurately identified by the Swiss Vieusseux (a scientific-literary association) during an outbreak in Geneva, Switzerland in 1805. In 1661, Thomas Willis first described inflammation of the meninges and an epidemic of meningitis. In the 17th century, Robert Whytt provided a detailed explanation of tuberculous meningitis and its stages, which was further elaborated by John Cheyne. Meningococcal meningitis was subsequently described by Gaspard Vieusseux and Andre Matthey in Geneva and by Elisha North in Massachusetts.[1]

Bacterial meningitis was almost uniformly fatal before the introduction of antisera and, subsequently, sulfonamides and penicillin. A systematic review of the world literature from 1 January 1935 to 31 December 2019, including 371 studies performed in 108 countries and describing 157 656 episodes, documented an overall case fatality ratio of 18% (95% CI, 16%-19%), decreasing from 32% (95% CI, 24%-40%) before 1961 to 15% (95% CI, 12%-19%) after 2010.[2] The second major inflection followed the introduction of conjugate vaccines against Haemophilus influenzae type b, Neisseria meningitidis and Streptococcus pneumoniae.[3][4] In 2021 the World Health Organization published the Defeating meningitis by 2030 global road map, and in April 2025 issued the first global clinical guidelines on meningitis diagnosis, treatment and care.[5]

Classification

Meningitis may be classified into two main groups based on etiology:

  • Infectious
  • Non-infectious

Infectious meningitis

Infectious meningitis may be classified according to the following algorithm based on chronicity of symptoms.

 
 
 
 
 
 
 
 
 
 
 
 
 
 
Infectious Meningitis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Viral
 
 
 
 
 
 
 
Bacterial
 
 
 
 
 
 
 
 
 
 
 
 
Fungal
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Acute
 
Chronic
 
Recurrent
 
 
Acute
 
Subacute
 
Chronic
 
 
Recurrent


Bacterial meningitis is additionally classified by mode of acquisition into community-acquired disease and healthcare-associated meningitis and ventriculitis, because the causative organisms, the empiric antimicrobial regimens and the role of device management differ substantially between the two.[6]

Non-infectious meningitis

Systemic illnesses, such as malignancies and connective tissue diseases (e.g. sarcoidosis, SLE, and granulomatosis with polyangiitis) may involve the meninges in their course and present as chronic meningitis.

Certain drugs may cause meningeal irritation and mimic infectious meningitis, including:

Pathophysiology

Most bacterial meningitis begins with nasopharyngeal colonisation, mucosal invasion, bacteraemia, and subsequent traversal of the blood-brain barrier at the choroid plexus and cerebral microvascular endothelium. Alternative routes include contiguous spread from otitis media, mastoiditis or sinusitis, and direct inoculation after head trauma, neurosurgery, or through a cerebrospinal fluid fistula.[7]

Within the subarachnoid space, bacterial cell-wall components trigger pattern-recognition receptor signalling, release of TNF-α, IL-1β and IL-6, neutrophil recruitment, and complement activation. The resulting inflammatory cascade produces cerebral oedema (vasogenic, cytotoxic and interstitial), raised intracranial pressure, impaired cerebral autoregulation, cerebral vasculitis with arterial and venous thrombosis leading to stroke, hydrocephalus, and cochlear injury causing sensorineural hearing loss. Antibiotic-induced bacteriolysis transiently amplifies this inflammatory burst, which is the rationale for administering dexamethasone before or together with the first antibiotic dose.[7][8]

Causes


Etiology Common causes Less common causes
Bacterial
Viral
Fungal
Mycobacterial
  • Non-tuberculous mycobacteria (largely in advanced immunosuppression)
Spirochetal
  • Leptospira species
Protozoal and Helminthic
Noninfectious conditions


The distribution of causative organisms varies by age and host status. In United States active laboratory-based surveillance covering 2008-2023, S. pneumoniae was the dominant pathogen overall, accounting for 59% (2922/5032) of cases, whereas group B Streptococcus predominated among infants aged 0-2 months at 85% (660/775).[25]

Epidemiology and Demographics

Bacterial meningitis can be community acquired or health care associated.

Reported incidence of bacterial meningitis ranges from approximately 0.9 per 100 000 individuals per year in high-income countries to 80 per 100 000 individuals per year in low-income countries; in low-income countries bacterial meningitis has a mortality rate of up to 54%, and up to 24% of survivors develop chronic neurological sequelae such as hearing loss or focal neurological deficits.[27]

In 2023 there were an estimated 259 000 (95% uncertainty interval 202 000-335 000) deaths and 2·54 million (2·20-2·93) incident cases of meningitis worldwide; children younger than 5 years accounted for more than a third of deaths (86 600 [53 300-149 000]), and the four WHO-defined vaccine-preventable pathogens of interest contributed 98 700 deaths (77 000-127 000) and 594 000 cases (514 000-686 000).[28][29]

Population / study Period Key findings
United States, Active Bacterial Core surveillance[25] 2008-2023 5032 cases identified; 11% (573/5028) of those with outcome data died. Overall incidence fell from 1.3 to 1.1 per 100 000 between 2008-2009 and 2010-2019, with a nadir during 2020-2021 and resurgence during 2022-2023. Of 2606 pneumococcal isolates tested, 1099 (42.2%) were non-susceptible to at least one agent
United States, Emerging Infections Programs[4] 1998-2007 3188 patients; 466 of 3155 (14.8%) with outcome data died. Incidence fell from 2.00 per 100 000 (95% CI, 1.85 to 2.15) to 1.38 per 100 000 (95% CI, 1.27 to 1.50)
Netherlands, MeninGene nationwide cohort[26] 2006-2014 1412 episodes; case fatality 244 (17%); unfavourable outcome 531 (38%)
Netherlands, adult meningococcal meningitis[30] 2006-2021 442 episodes; in the clinical cohort of 274 episodes, case fatality was 4% (10 of 274) and unfavourable outcome 16% (43 of 274). Serogroup W was associated with unfavourable outcome in 6 of 16 (38%) versus 37 of 251 (15%), P = 0.03, and death in 4 of 16 (25%) versus 6 of 251 (2%), P = 0.001
Global meta-analysis, 371 studies, 108 countries[2] 1935-2019 157 656 episodes. Overall case fatality ratio 18% (95% CI, 16%-19%), decreasing from 32% (95% CI, 24%-40%) before 1961 to 15% (95% CI, 12%-19%) after 2010. Highest for Listeria monocytogenes at 27% (95% CI, 24%-31%) and pneumococci at 24% (95% CI, 22%-26%)

Risk Factors

Differential Diagnosis

Condition Distinguishing clinical features Neuroimaging CSF findings Confirmatory test
Acute bacterial meningitis Onset over hours; fever, headache, neck stiffness, depressed consciousness; petechial rash or purpura fulminans suggests meningococcaemia Usually normal; may show cerebral oedema, hydrocephalus, infarction, or a parameningeal focus Neutrophilic pleocytosis, low glucose, elevated protein, elevated lactate CSF analysis with Gram stain and culture[32]
Viral meningitis Prodromal illness, preserved alertness, headache and photophobia without focal deficit Normal Lymphocytic pleocytosis, normal glucose, normal or mildly elevated protein CSF PCR for enterovirus, parechovirus, herpes simplex virus
Encephalitis Fever with altered behaviour, aphasia, seizures, focal neurological abnormalities Temporal or limbic abnormality on MRI in herpes simplex encephalitis Lymphocytic pleocytosis, sometimes red cells; glucose usually normal CSF PCR; EEG
Subarachnoid haemorrhage Thunderclap headache maximal at onset, often afebrile, neck stiffness Blood on non-contrast computed tomography Uniformly blood-stained fluid that does not clear between tubes; xanthochromia Non-contrast CT followed by lumbar puncture for xanthochromia if CT negative
Subdural haemorrhage History of trauma or fall; confusion, dizziness, nausea, vomiting, fluctuating consciousness Extra-axial crescentic collection on CT Xanthochromia may be present; lumbar puncture generally avoided[33] CT scan without contrast
Haemorrhagic stroke Sudden focal deficit, hypertension, reduced consciousness Intraparenchymal haemorrhage on CT Lumbar puncture not indicated CT scan without contrast[34]
CNS abscess or subdural empyema Progressive headache, focal deficit, papilledema; history of drug abuse, endocarditis or immunosuppression Ring-enhancing lesion or extra-axial collection on contrast-enhanced MRI Variable pleocytosis; lumbar puncture often contraindicated because of mass effect Contrast-enhanced MRI
Brain tumour and neoplastic meningitis Subacute headache, cranial neuropathies, radicular pain, weight loss, cachexia Parenchymal mass or leptomeningeal enhancement Lymphocytic pleocytosis, very low glucose, high protein, malignant cells on cytology MRI with contrast and CSF cytology[35]
Tuberculous meningitis Subacute onset over 1-3 weeks, cranial nerve palsy, hyponatraemia, exposure or endemic residence Basal meningeal enhancement, hydrocephalus, tuberculomas, basal ganglia infarcts Lymphocytic pleocytosis, markedly elevated protein, low glucose Xpert MTB/RIF Ultra, mycobacterial culture, CSF PCR[36]
Cryptococcal meningitis Insidious headache, advanced HIV, visual loss, often minimal meningism Often normal; may show dilated Virchow-Robin spaces or cryptococcomas Markedly raised opening pressure, mild lymphocytic pleocytosis, low glucose CSF and serum cryptococcal antigen, India ink, fungal culture
Neurosyphilis Chronic course, cranial nerve palsy, uveitis, blindness, confusion, abnormal gait, history of STI Variable; may show infarcts or meningeal enhancement Elevated leukocytes and protein Reactive serum treponemal test with CSF VDRL[37]
Drug-induced aseptic meningitis Recurrent episodes temporally linked to NSAIDs, trimethoprim-sulfamethoxazole, intravenous immunoglobulin or monoclonal antibodies Normal Neutrophilic or lymphocytic pleocytosis with sterile cultures Resolution after withdrawal of the implicated agent
Complex or atypical migraine Recurrent headache with aura, nausea, vomiting, family history of migraine; afebrile Normal Normal Clinical assessment
Hypertensive encephalopathy Severe hypertension, delirium, cortical blindness, seizure Posterior white matter oedema Normal or mildly elevated protein Clinical assessment with blood pressure response
Wernicke's encephalopathy Ophthalmoplegia, ataxia, confusion; history of alcohol use disorder or malnutrition Mammillary body and periaqueductal signal change on MRI Normal Clinical assessment and thiamine response
Drug toxicity Altered consciousness, ataxia, nystagmus; lithium, sedatives, phenytoin, carbamazepine Normal Normal Drug levels and toxicology screen
Metabolic disturbances (electrolyte imbalance, hypoglycemia) Confusion, seizure, palpitations, sweating, dizziness Normal Normal Serum glucose, sodium, potassium, calcium
Multiple sclerosis exacerbation Relapsing-remitting focal deficits, blurred vision, urinary incontinence, fatigue Periventricular and juxtacortical demyelinating lesions Mild lymphocytic pleocytosis with oligoclonal bands Clinical assessment and MRI[38]
Seizure and postictal state Previous history of seizures, abrupt onset, postictal confusion and apathy May show an underlying structural lesion Transient mild pleocytosis may occur; sterile cultures Clinical assessment and EEG[39]
Conversion disorder Non-anatomical deficits, tremors, blindness, difficulty swallowing; history of emotional stress Normal Normal Diagnosis of exclusion

Diagnosis

Diagnosis of meningitis is based on clinical presentation in combination with CSF analysis. CSF analysis has a central role in establishing the diagnosis and in excluding other possibilities.

Diagnostic Approach

The dominant principle is that neither computed tomography nor lumbar puncture should delay antimicrobial therapy. In a cohort of 123 episodes of adult acute bacterial meningitis with a case fatality rate of 13% (16/123), the adjusted odds ratio for death was 8.4 (95% CI 1.7-40.9) for a door-to-antibiotic time greater than 6 hours, 39.4 (95% CI 4.3-358.1) for afebrility at presentation, and 12.6 (95% CI 2.2-72.0) for severely impaired mental status at presentation; the diagnostic-treatment sequence of head CT, then lumbar puncture, then antibiotics was itself a predictor of delay (OR 5.6).[40] A Swedish national guideline revision that removed moderate to severe impairment of mental status and new-onset seizures as contraindications to immediate lumbar puncture was followed by earlier treatment and improved outcome.[41][5]

 
 
 
 
 
 
 
Suspected acute meningitis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Assess airway, breathing, circulation; draw blood cultures immediately
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
No indication for cranial computed tomography
 
 
 
 
 
Indication present: immunocompromise, history of CNS disease, new-onset seizure, papilloedema, focal deficit, GCS below 10
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Immediate lumbar puncture, then dexamethasone plus antibiotics without delay
 
 
 
 
 
Give dexamethasone plus antibiotics FIRST, then CT, then lumbar puncture if safe
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
CSF analysis: opening pressure, cell count and differential, protein, glucose with paired serum glucose, lactate, Gram stain, culture, targeted PCR
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Purulent profile: continue antibacterial therapy and dexamethasone
 
 
 
Lymphocytic profile: test for herpes simplex, enterovirus, M. tuberculosis, Cryptococcus, syphilis, Borrelia
 
 
 
Non-inflammatory CSF: reconsider subarachnoid haemorrhage, encephalitis, metabolic and toxic causes
 


History and Symptoms

Cardinal symptoms are headache, fever, neck stiffness and altered mental status. In a nationwide prospective series of 696 episodes of community-acquired acute bacterial meningitis in adults, headache occurred in 87 percent, neck stiffness in 83 percent, fever in 77 percent, and a change in mental status (Glasgow Coma Scale score below 14) in 69 percent. The classic triad of fever, neck stiffness and a change in mental status was present in only 44 percent of episodes; however, 95 percent had at least two of the four symptoms of headache, fever, neck stiffness and altered mental status. On admission, 14 percent of patients were comatose and 33 percent had focal neurologic abnormalities.[42][43]

Additional symptoms include photophobia, phonophobia, nausea, vomiting, myalgia, irritability and seizure. Elderly patients and those with diabetes mellitus, chronic kidney disease or cirrhosis may present with lethargy or confusion and minimal meningeal features.[44] Neonates and young infants present with poor feeding, temperature instability, lethargy, bulging fontanelle and convulsions rather than neck stiffness.

Physical Examination

Laboratory Findings

  • Two sets of blood cultures before antibiotics; these remain positive in a substantial proportion of patients even after CSF sterilisation
  • Full blood count, coagulation screen, C-reactive protein, procalcitonin, serum electrolytes, renal and hepatic function, and serum glucose drawn at the time of lumbar puncture
  • HIV testing in all adults with meningitis
  • Blood and CSF PCR for Neisseria meningitidis and Streptococcus pneumoniae where available, particularly when antibiotics have already been given
  • Serum and CSF cryptococcal antigen in immunocompromised patients
  • Throat swab for meningococcal culture in suspected meningococcal disease

Cerebrospinal Fluid Analysis

The following table summarizes the CSF findings in different types of meningitis.[1][47][48][49][50][35][36]

Cerebrospinal fluid level Normal level Bacterial meningitis Viral meningitis (except SARS-CoV-2 meningitis) SARS-CoV-2 associated meningitis Fungal meningitis Tuberculous meningitis Neoplastic meningitis
Cells/µL < 5 Typically > 1000 (range 100 to > 10 000) 10-1000 10-1000 10-500 50-500 > 4
Predominant cell Lymphocyte and monocyte Neutrophil > lymphocyte Lymphocyte > neutrophil Lymphocyte > neutrophil Lymphocyte > neutrophil Lymphocyte > neutrophil Lymphocyte with malignant cells
Total protein (mg/dL) 15-45 Typically 100-500 Normal or slightly high Normal or slightly high High Typically 100-500 > 50
Glucose ratio (CSF/plasma) > 0.6 < 0.4, often < 0.3 > 0.6 > 0.6 < 0.3 < 0.5 < 0.5
Lactate (mmol/L) < 2.1 ≥ 3.5 < 2.1 Not established > 3.2 > 2.1 > 2.1
Opening pressure and other tests Opening pressure 6-20 cm H2O Elevated opening pressure; CSF gram stain, culture, bacterial PCR Normal or mildly elevated; PCR for enterovirus, HSV, VZV RT-PCR for viral RNA in CSF (not FDA approved for this indication) Markedly elevated in cryptococcal meningitis; India ink, cryptococcal antigen, fungal culture Xpert MTB/RIF Ultra, mycobacterial culture, TB PCR Cytology and CSF tumour markers such as alpha-fetoprotein and CEA

A CSF white-cell count lower than 1000 cells per µL in culture-proven bacterial meningitis is a predictor of unfavourable outcome and reflects an inadequate inflammatory response rather than mild disease.[26] Prior antibiotic exposure lowers the yield of Gram stain and culture but does not normalise the cell count, protein or glucose in the first hours.

Molecular and Rapid Diagnostics

Multiplex CSF panels shorten the time to aetiological diagnosis but do not replace Gram stain and culture. In a systematic review and meta-analysis, the summary sensitivity and specificity of the BioFire FilmArray meningitis/encephalitis panel were 90% (95% CI 86-93%) and 97% (95% CI 94-99%) respectively, with both false-positive and false-negative results described.[51][52] Culture remains essential for antimicrobial susceptibility testing, particularly given that 1099 of 2606 (42.2%) United States pneumococcal meningitis isolates tested were non-susceptible to at least one agent.[25]

Clinical Decision Rules

The Bacterial Meningitis Score identifies children with CSF pleocytosis at very low risk of bacterial meningitis: none of a positive CSF Gram stain, CSF absolute neutrophil count of at least 1000 cells per µL, CSF protein of at least 80 mg/dL, peripheral blood absolute neutrophil count of at least 10 000 cells per µL, or seizure at or before presentation. In the multicentre validation of 3295 patients with CSF pleocytosis, 121 (3.7%; 95% CI, 3.1%-4.4%) had bacterial meningitis; of the 1714 patients categorised as very low risk, only 2 had bacterial meningitis, giving a sensitivity of 98.3% (95% CI, 94.2%-99.8%) and a negative predictive value of 99.9% (95% CI, 99.6%-100%), and both missed cases were younger than 2 months old.[53] In a meta-analysis of eight validation studies including 4896 evaluable children, the combined sensitivity was 99.3% (1224/1233; 95% CI 98.7% to 99.7%), specificity 62.1% (2274/3663; 95% CI 60.5% to 63.7%), negative predictive value 99.7% (2274/2283; 95% CI 99.3% to 99.9%), positive likelihood ratio 2.6 (95% CI 2.5 to 2.7) and negative likelihood ratio 0.01 (95% CI 0.01 to 0.02).[54] The score should not be applied to infants younger than 2 months, to pretreated patients, or to those who are critically ill.

Neuroimaging

Cranial computed tomography before lumbar puncture is indicated only for defined clinical features. In a prospective study of 301 adults with suspected meningitis, 235 (78 percent) underwent CT of the head before lumbar puncture; in 56 of the 235 patients (24 percent) the results of CT were abnormal, and 11 patients (5 percent) had evidence of a mass effect. Clinical features at baseline associated with abnormal CT were an age of at least 60 years, immunocompromise, a history of central nervous system disease, a history of seizure within one week before presentation, and abnormal neurological findings including reduced level of consciousness, inability to answer two questions or follow two commands, gaze palsy, abnormal visual fields, facial palsy, arm or leg drift, and abnormal language.[55]

Magnetic resonance imaging with contrast and diffusion-weighted sequences is superior for detecting cerebral infarction, hydrocephalus, subdural empyema, brain abscess, cerebral venous sinus thrombosis, labyrinthitis and leptomeningeal enhancement, and should be performed in patients who fail to improve, who develop new focal deficits or seizures, or in whom tuberculous meningitis or neoplastic meningitis is suspected. Dedicated imaging of the temporal bones and paranasal sinuses, and high-resolution CT or MR cisternography, is indicated in recurrent meningitis to identify a cerebrospinal fluid fistula.[50][56]

Treatment

Initial Management

Acute bacterial meningitis is a medical emergency. The following steps are performed in parallel rather than in sequence.[50][57][5][56]

  • Assess and support airway, breathing and circulation; manage septic shock with fluid resuscitation and vasopressors as required
  • Obtain two sets of blood cultures immediately
  • Perform lumbar puncture without delay unless a contraindication is present. Contraindications include clinical signs of raised intracranial pressure with a risk of herniation, cardiorespiratory compromise, extensive or spreading purpura, uncorrected coagulopathy or thrombocytopenia, and infection at the puncture site
  • Administer dexamethasone and the first dose of antibiotics as soon as possible and, where lumbar puncture is deferred, before imaging. Antimicrobial therapy must not be withheld pending CSF acquisition
  • Target initiation of therapy within one hour of presentation
  • Monitor conscious level, pupillary responses, blood glucose, sodium and coagulation; admit to a critical care environment if there is reduced consciousness, seizures, shock or a rapidly evolving rash
  • Notify public health authorities for suspected invasive meningococcal disease and initiate contact tracing

Medical Therapy

Adjunctive Dexamethasone

In a randomised, double-blind, placebo-controlled trial of adults with acute bacterial meningitis, dexamethasone 10 mg or placebo was administered 15 to 20 minutes before or with the first dose of antibiotic and continued every 6 hours for four days. At eight weeks, 15% of patients in the dexamethasone group and 25% in the placebo group had an unfavourable neurological outcome, defined as a Glasgow Outcome Scale score of 1 to 4 (relative risk 0.59, 95% confidence interval 0.37-0.94; P = 0.03). Among patients with pneumococcal meningitis, unfavourable outcome occurred in 26% versus 52%. Gastrointestinal bleeding occurred in two patients in the dexamethasone group and in five patients in the placebo group.[8]

The Cochrane systematic review of randomised trials found insufficient evidence that corticosteroids reduced mortality overall (17.8% versus 19.9%; risk ratio 0.90, 95% confidence interval 0.80 to 1.01; P = 0.07) or in adults specifically (RR 0.74, 95% CI 0.53 to 1.05; P = 0.09). However, corticosteroids caused lower rates of severe hearing loss (RR 0.67, 95% CI 0.51 to 0.88), any hearing loss (RR 0.74, 95% CI 0.63 to 0.87) and neurological sequelae (RR 0.83, 95% CI 0.69 to 1.00). Corticosteroids reduced mortality in Streptococcus pneumoniae meningitis (RR 0.84, 95% CI 0.72 to 0.98) but not in Haemophilus influenzae or Neisseria meningitidis meningitis, and reduced severe hearing loss in children with H. influenzae meningitis (RR 0.34, 95% CI 0.20 to 0.59). Benefit was greatest in high- and middle-income settings and was not demonstrated in low-income settings.[58]

Population Dexamethasone regimen Comment
Adults with suspected or proven community-acquired bacterial meningitis 10 mg intravenously every 6 hours for 4 days First dose 15 to 20 minutes before, or together with, the first antibiotic dose[8][50]
Children beyond the neonatal period 0.15 mg/kg intravenously every 6 hours for 2 to 4 days Clearest benefit for hearing preservation in H. influenzae type b meningitis[58][57]
Neonates Not recommended No applicable randomised controlled trial data[58]
Already established on antibiotics Do not initiate Benefit depends on administration before or with the first antibiotic dose[8]
Confirmed non-pneumococcal, non-Hib aetiology Discontinue Dexamethasone may be stopped once Listeria, meningococcal or another non-benefiting aetiology is confirmed[50][56]

Empiric Antimicrobial Therapy

  • Empiric therapy is initiated immediately and must not await CSF results.
  • The choice of empiric antibiotic therapy depends on patient age and underlying comorbid disease.
  • Adapted from IDSA, ESCMID and WHO guidelines.[57][50][5]
Predisposing factor Common bacterial pathogen Antimicrobial therapy
Age less than 1 month Streptococcus agalactiae, Escherichia coli, Listeria monocytogenes, Klebsiella species Ampicillin plus cefotaxime, or ampicillin plus an aminoglycoside
Age 1-23 months Streptococcus pneumoniae, Neisseria meningitidis, S. agalactiae, Haemophilus influenzae, E. coli Vancomycin plus a third-generation cephalosporin (cefotaxime or ceftriaxone)
Age 2-50 years N. meningitidis, S. pneumoniae Vancomycin plus a third-generation cephalosporin
Age over 50 years S. pneumoniae, N. meningitidis, L. monocytogenes, aerobic gram-negative bacilli Vancomycin plus ampicillin plus a third-generation cephalosporin
Impaired cell-mediated immunity L. monocytogenes, aerobic gram-negative bacilli including Pseudomonas aeruginosa, S. pneumoniae Vancomycin plus ampicillin plus cefepime or meropenem
Head trauma: basilar skull fracture S. pneumoniae, H. influenzae, group A beta-haemolytic streptococci Vancomycin plus a third-generation cephalosporin
Penetrating trauma Staphylococcus aureus, coagulase-negative staphylococci (especially Staphylococcus epidermidis), aerobic gram-negative bacilli including P. aeruginosa Vancomycin plus cefepime, vancomycin plus ceftazidime, or vancomycin plus meropenem
Post-neurosurgery Aerobic gram-negative bacilli including P. aeruginosa, S. aureus, coagulase-negative staphylococci Vancomycin plus cefepime, vancomycin plus ceftazidime, or vancomycin plus meropenem
CSF shunt or external ventricular drain Coagulase-negative staphylococci (especially S. epidermidis), S. aureus, aerobic gram-negative bacilli including P. aeruginosa, Cutibacterium (Propionibacterium) acnes Vancomycin plus cefepime, vancomycin plus ceftazidime, or vancomycin plus meropenem[6]

Ampicillin is added whenever Listeria monocytogenes is a consideration, that is in neonates, adults older than 50 years, pregnant women, and patients with impaired cell-mediated immunity. In patients with severe beta-lactam allergy, meropenem, moxifloxacin, chloramphenicol or trimethoprim-sulfamethoxazole may be used according to the suspected pathogen and local susceptibility data.[56][50]

Pathogen-Directed Therapy

  • Therapy is narrowed once the organism and susceptibility results are available.
  • Adapted from IDSA and ESCMID guidelines.[57][50][1]
Microorganism Recommended therapy Alternative therapies Duration of therapy, days
Streptococcus pneumoniae, penicillin MIC less than 0.1 µg/mL Penicillin G or ampicillin Third-generation cephalosporin, chloramphenicol 10-14
Streptococcus pneumoniae, penicillin MIC 0.1-1.0 µg/mL Third-generation cephalosporin Cefepime, meropenem 10-14
Streptococcus pneumoniae, penicillin MIC at least 2.0 µg/mL or ceftriaxone MIC at least 1.0 µg/mL Vancomycin plus a third-generation cephalosporin, with rifampicin considered Moxifloxacin, meropenem 10-14
Neisseria meningitidis, penicillin MIC less than 0.1 µg/mL Penicillin G or ampicillin Third-generation cephalosporin, chloramphenicol 7
Neisseria meningitidis, penicillin MIC 0.1-1.0 µg/mL Third-generation cephalosporin Chloramphenicol, fluoroquinolone, meropenem 7
Listeria monocytogenes Ampicillin or penicillin G, with gentamicin considered for the first days Trimethoprim-sulfamethoxazole, meropenem At least 21
Streptococcus agalactiae Ampicillin or penicillin G, with gentamicin considered for the first days Third-generation cephalosporin, vancomycin 14-21
Haemophilus influenzae, beta-lactamase negative Ampicillin Third-generation cephalosporin, chloramphenicol, fluoroquinolone 7
Haemophilus influenzae, beta-lactamase positive Third-generation cephalosporin Cefepime, chloramphenicol, meropenem, fluoroquinolone 7
Escherichia coli and other Enterobacterales Third-generation cephalosporin, guided by susceptibility Cefepime, meropenem, aztreonam, fluoroquinolone, trimethoprim-sulfamethoxazole 21
Pseudomonas aeruginosa Cefepime or ceftazidime, with an aminoglycoside considered Meropenem, ciprofloxacin 21
Staphylococcus aureus, methicillin-susceptible Nafcillin or flucloxacillin Vancomycin, linezolid, meropenem At least 14
Staphylococcus aureus, methicillin-resistant Vancomycin, with rifampicin considered Linezolid, trimethoprim-sulfamethoxazole At least 14
Coagulase-negative staphylococci (device-associated) Vancomycin, with rifampicin considered Linezolid, daptomycin At least 10 after device removal, guided by repeat CSF cultures[6]

Routine repeat lumbar puncture is not required when there is clinical improvement. Repeat CSF sampling is indicated when there is failure to improve after 48 hours, when the organism is a resistant pneumococcus treated with vancomycin plus a cephalosporin, in gram-negative bacillary and device-associated infection, and in neonates.[57][6]

Non-Bacterial Meningitis

Aetiology Principal therapy Key evidence
Enterovirus and parechovirus meningitis Supportive care, analgesia, discontinuation of empiric antibiotics once bacterial infection is excluded Self-limiting in immunocompetent hosts[3]
Herpes simplex meningitis or encephalitis Intravenous aciclovir pending PCR results Empiric aciclovir where encephalitic features are present[56]
Tuberculous meningitis, HIV-negative Antituberculous therapy plus adjunctive dexamethasone Dexamethasone reduced the risk of death in adolescents and adults with tuberculous meningitis[59]
Tuberculous meningitis in HIV-positive adults Antituberculous therapy and antiretroviral therapy; adjunctive dexamethasone of unproven benefit In a randomised placebo-controlled trial, death over 12 months occurred in 116 of 263 participants (44.1%) in the dexamethasone group and 126 of 257 (49.0%) in the placebo group (hazard ratio 0.85; 95% CI 0.66 to 1.10; P = 0.22), with serious adverse events in 192 of 263 (73.0%) versus 194 of 257 (75.5%), P = 0.52[60]
Cryptococcal meningitis in HIV Single high dose of liposomal amphotericin B 10 mg/kg with 14 days of flucytosine and fluconazole, followed by fluconazole consolidation and maintenance Ten-week all-cause mortality was 24.8% with the single-dose regimen versus 28.7% with the previous standard of care, meeting non-inferiority with fewer adverse events[61][62]
Neoplastic meningitis Intrathecal or systemic chemotherapy, targeted therapy, and involved-field irradiation Treatment is directed by the primary tumour and performance status[35]
Drug-induced aseptic meningitis Withdrawal of the causative agent and supportive care Diagnosis confirmed by resolution after withdrawal

Procedural / Surgical Therapy

Surgical intervention is not required for uncomplicated community-acquired bacterial meningitis. Procedural and surgical management is nevertheless central to several specific situations.[6][50][62][3]

  • Management of raised intracranial pressure: head elevation, osmotherapy, ventilatory control of PaCO2, and, in selected patients, invasive intracranial pressure monitoring within a neurocritical care pathway
  • Therapeutic lumbar puncture: in cryptococcal meningitis with raised opening pressure, CSF should be drained to reduce the pressure to below 20 cm H2O, with repeated procedures as needed
  • Hydrocephalus: external ventricular drainage for acute obstructive or communicating hydrocephalus, with conversion to a ventriculoperitoneal shunt if CSF diversion is required long term. Hydrocephalus is particularly common in tuberculous meningitis
  • Infected neurosurgical devices: removal or externalisation of infected ventriculoperitoneal shunts, external ventricular drains, deep brain stimulators and intrathecal pumps, combined with systemic antimicrobial therapy, gives higher cure rates than antimicrobial therapy alone. Reimplantation is deferred until CSF cultures are repeatedly negative
  • Intraventricular or intrathecal antimicrobial therapy: reserved for healthcare-associated ventriculitis and meningitis that responds poorly to systemic therapy alone, or for multidrug-resistant gram-negative organisms, using preservative-free formulations
  • Source control of a parameningeal focus: mastoidectomy, drainage of sinusitis, and evacuation of subdural empyema or brain abscess
  • Repair of a cerebrospinal fluid fistula: endoscopic or open repair after imaging localisation in recurrent bacterial meningitis
  • Decompressive craniectomy: considered as a rescue measure for refractory intracranial hypertension or large space-occupying infarction, supported only by observational data

Long-Term Management

  • Audiological assessment: formal hearing testing should be arranged before or shortly after discharge and no later than four weeks after the illness, because post-meningitic cochlear ossification can develop within weeks and narrows the window for effective cochlear implantation. Profound bilateral sensorineural hearing loss warrants urgent referral to an implant programme[5][3]
  • Neurological and neuropsychological follow-up: assessment for cognitive impairment, fatigue, behavioural change, learning difficulties in children, focal deficits and epilepsy; approximately one in five survivors of bacterial meningitis sustains long-term sequelae[5][27]
  • Seizure management: anticonvulsant therapy for acute symptomatic and late unprovoked seizures, with periodic review of the need for continued treatment
  • Assessment for an underlying predisposition after recurrent or unusual disease: complement function including CH50 and AH50, immunoglobulin levels, splenic function, HIV testing, and imaging for a cerebrospinal fluid fistula or inner ear malformation
  • Vaccination after recovery: pneumococcal, meningococcal and Hib vaccination as indicated by the causative organism and host risk factors, since natural infection does not confer reliable protection
  • Rehabilitation: physiotherapy, occupational therapy, speech and language therapy, educational support, and psychological support for patients and families
  • Limb and skin sequelae of meningococcaemia: management of scarring, growth plate injury and amputation-related rehabilitation

Special Populations

Population Key considerations
Neonates (0-2 months) Group B Streptococcus predominates, accounting for 85% (660/775) of cases in United States surveillance of infants aged 0-2 months. Empiric ampicillin plus cefotaxime or an aminoglycoside; adjunctive dexamethasone is not recommended; prolonged therapy and repeat CSF examination to document sterilisation; cranial imaging for ventriculitis and abscess[25][58]
Infants and children The Bacterial Meningitis Score assists risk stratification in children older than 2 months with CSF pleocytosis but should not be used in critically ill or pretreated patients. Dexamethasone gives the clearest benefit for hearing preservation in H. influenzae type b disease[53][54][58]
Pregnancy Increased susceptibility to Listeria monocytogenes; ampicillin must be included in empiric cover. Avoid fluoroquinolones where alternatives exist; coordinate obstetric and neonatal care
Adults older than 50 years L. monocytogenes and aerobic gram-negative bacilli must be covered; presentation is frequently atypical with lethargy and confusion and without neck stiffness; advanced age is an independent predictor of unfavourable outcome[42][26]
Immunocompromised hosts, including HIV Broader empiric cover with vancomycin plus ampicillin plus cefepime or meropenem; test for cryptococcal antigen, Mycobacterium tuberculosis, syphilis and viral causes; CSF may show minimal pleocytosis despite severe infection[50][62]
Complement deficiency or complement inhibitor therapy Marked excess risk of invasive meningococcal disease including non-groupable strains; requires MenACWY and MenB vaccination and, for some patients on complement inhibitors, antibiotic prophylaxis[31]
Post-neurosurgical patients and those with CSF devices Managed as healthcare-associated ventriculitis and meningitis: staphylococci and aerobic gram-negative bacilli predominate, device removal is usually required, and intraventricular therapy may be needed[6]
Recurrent meningitis Investigate for cerebrospinal fluid fistula, basilar skull fracture, inner ear malformation, cochlear implant, complement deficiency, asplenia, and HSV-2 recurrent (Mollaret) meningitis
Resource-limited settings Case fatality reaches up to 54%; lumbar puncture should be performed as soon as possible and treatment must not be delayed for imaging. The corticosteroid benefit demonstrated in high- and middle-income settings has not been reproduced in low-income settings[27][58][5]

Primary Prevention

  • Conjugate vaccination is the principal preventive intervention.
  • Adapted from the recommendations of the United States Centers for Disease Control and Prevention's (CDC's) Advisory Committee on Immunization Practices (ACIP).[31][63][64][65]
Targeted group by age and/or risk factor Primary dose(s) Booster dose(s)
Adolescents aged 11 through 18 years One dose of a quadrivalent meningococcal conjugate vaccine (MenACWY), preferably at age 11 or 12 years. Discuss serogroup B meningococcal vaccination (MenB-FHbp or MenB-4C) for adolescents and young adults aged 16 through 23 years under shared clinical decision-making; the preferred age is 16 through 18 years If the primary dose was given at age 12 years or younger, give a MenACWY booster at age 16 years. If given at age 13 to 15 years, give a MenACWY booster at age 16 to 18 years
First-year college students aged 19 through 21 years living in residence halls If a dose has not been received at age 16 years or later, give one dose of MenACWY. Discuss MenB vaccination as above Give a MenACWY booster if the previous dose was given before age 16 years
Persons with HIV infection Age under 2 years: multidose infant MenACWY-CRM series at 2, 4, 6 and 12 to 15 months, or two doses of an age-appropriate MenACWY at least 12 weeks apart from age 9 to 23 months. Age 2 years and older: two doses of MenACWY 8 to 12 weeks apart Booster 3 years after the primary series if the last dose was given before age 7 years, then every 5 years; boosters every 5 years if the last dose was given at age 7 years or older
Persons with persistent complement component deficiency or receiving a complement inhibitor (eg, eculizumab, ravulizumab) Age-appropriate MenACWY series (two doses 8 to 12 weeks apart from age 2 years) and a complete MenB series (MenB-FHbp at 0, 1 to 2 and 6 months, or MenB-4C as two doses at least 1 month apart) MenACWY boosters every 5 years (or after 3 years if the last dose was before age 7 years). MenB booster 1 year after the primary series, then every 2 to 3 years while risk persists
Persons with functional or anatomic asplenia, including sickle cell disease Age-appropriate MenACWY series and a complete MenB series from age 10 years As for complement deficiency
Microbiologists routinely exposed to Neisseria meningitidis isolates and other persons with prolonged increased exposure One dose of MenACWY and a complete MenB series from age 10 years MenACWY every 5 years; MenB booster 1 year after the primary series, then every 2 to 3 years while risk persists
Travellers to or residents of countries where meningococcal disease is hyperendemic or epidemic, including the African meningitis belt and Hajj pilgrims Age-appropriate MenACWY series or single dose from age 2 years Boost every 5 years if risk continues (after 3 years if the last dose was given before age 7 years)
Persons present during an outbreak caused by a vaccine-preventable serogroup Age-appropriate MenACWY for serogroups A, C, W or Y outbreaks; complete MenB series for serogroup B outbreaks As directed by the responsible public health authority
Pneumococcal prevention, children Routine infant pneumococcal conjugate vaccine series As per the national childhood immunisation schedule
Pneumococcal prevention, adults A single dose of pneumococcal conjugate vaccine for all conjugate-naive adults aged 50 years and older, and for adults aged 19 through 49 years with risk conditions. PCV15, PCV20 and PCV21 are options; PCV15 is followed by PPSV23 Additional doses only as specified for those who began the series with PCV13
Haemophilus influenzae type b prevention Routine infant Hib conjugate vaccine series As per the national childhood immunisation schedule; additional doses for asplenia, complement deficiency and transplantation

Available meningococcal products include the quadrivalent conjugate vaccines MenACWY-CRM and MenACWY-TT, the serogroup B vaccines MenB-FHbp and MenB-4C, and a pentavalent MenABCWY vaccine that may be used when a MenACWY dose and a MenB dose are indicated at the same visit. The quadrivalent meningococcal polysaccharide vaccine (MPSV4, Menomune) has been withdrawn, and MenHibrix (HibMenCY) was discontinued in 2017.[31][63]

Secondary Prevention

Antimicrobial chemoprophylaxis is indicated for individuals who have had close contact with a patient with invasive meningococcal disease during the 7 days before symptom onset and up to 24 hours after the patient starts effective therapy. Prophylaxis should ideally be given within 24 hours of identification of the index case and is of limited value after 14 days. Close contacts include:[31][56]

  • Household members and others sharing sleeping accommodation
  • Child-care and preschool centre contacts
  • Anyone directly exposed to the patient's oral secretions, for example through kissing, mouth-to-mouth resuscitation, endotracheal intubation, or endotracheal tube management
  • Health-care personnel who managed the airway or were directly exposed to respiratory secretions without appropriate personal protective equipment
  • Airline passengers seated directly next to the index patient on a flight lasting 8 hours or longer, or with direct exposure to respiratory secretions
Drug Age group Dosage Duration and route of administration
Rifampicin Children aged under 1 month 5 mg/kg every 12 hours 2 days, oral
Rifampicin Children aged 1 month and older 10 mg/kg every 12 hours (maximum 600 mg) 2 days, oral
Rifampicin Adults 600 mg every 12 hours 2 days, oral
Ciprofloxacin Adults 500 mg Single oral dose
Ceftriaxone Children aged under 15 years 125 mg Single intramuscular dose
Ceftriaxone Adults 250 mg Single intramuscular dose
Azithromycin Children 10 mg/kg (maximum 500 mg) Single oral dose; alternative where ciprofloxacin-resistant meningococci circulate
Azithromycin Adults 500 mg Single oral dose; alternative where ciprofloxacin-resistant meningococci circulate

Ceftriaxone is preferred in pregnancy. Rifampicin is avoided in pregnancy, interacts with hormonal contraception and many other drugs, and should not be used in patients with severe hepatic disease. Where ciprofloxacin-resistant Neisseria meningitidis has been identified locally, ciprofloxacin should be replaced by an alternative agent. Rifampicin chemoprophylaxis is also indicated for selected household contacts of patients with invasive Haemophilus influenzae type b disease when an incompletely vaccinated or immunocompromised child is present in the household. Index patients treated with an agent that does not reliably eradicate nasopharyngeal carriage, such as penicillin monotherapy, should themselves receive eradication therapy before discharge.[31][56]

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  50. ↑ 50.00 50.01 50.02 50.03 50.04 50.05 50.06 50.07 50.08 50.09 van de Beek D, Cabellos C, Dzupova O, Esposito S, Klein M, Kloek AT, Leib SL, Mourvillier B, Ostergaard C, Pagliano P, Pfister HW, Read RC, Sipahi OR, Brouwer MC (2016). "ESCMID guideline: diagnosis and treatment of acute bacterial meningitis". Clin Microbiol Infect. 22 Suppl 3: S37–S62. doi:10.1016/j.cmi.2016.01.007. PMID 27062097.
  51. ↑ Tansarli GS, Chapin KC (2020). "Diagnostic test accuracy of the BioFire FilmArray meningitis/encephalitis panel: a systematic review and meta-analysis". Clin Microbiol Infect. 26 (3): 281–290. doi:10.1016/j.cmi.2019.11.016. PMID 31760115.
  52. ↑ Leber AL, Everhart K, Balada-Llasat JM, Cullison J, Daly J, Holt S, Lephart P, Salimnia H, Schreckenberger PC, DesJarlais S, Reed SL, Chapin KC, LeBlanc L, Johnson JK, Soliven NL, Carroll KC, Miller JA, Dien Bard J, Mestas J, Bankowski M, Enomoto T, Hemmert AC, Bourzac KM (2016). "Multicenter Evaluation of BioFire FilmArray Meningitis/Encephalitis Panel for Detection of Bacteria, Viruses, and Yeast in Cerebrospinal Fluid Specimens". J Clin Microbiol. 54 (9): 2251–2261. doi:10.1128/JCM.00730-16. PMID 27335149.
  53. ↑ 53.0 53.1 Nigrovic LE, Kuppermann N, Macias CG, Cannavino CR, Moro-Sutherland DM, Schremmer RD, Schwab SH, Agrawal D, Mansour KM, Bennett JE, Katsogridakis YL, Mohseni MM, Bulloch B, Steele DW, Kaplan RL, Herman MI, Bandyopadhyay S, Dayan P, Truong UT, Wang VJ, Bonsu BK, Chapman JL, Kanegaye JT, Malley R (2007). "Clinical prediction rule for identifying children with cerebrospinal fluid pleocytosis at very low risk of bacterial meningitis". JAMA. 297 (1): 52–60. doi:10.1001/jama.297.1.52. PMID 17200475.
  54. ↑ 54.0 54.1 Nigrovic LE, Malley R, Kuppermann N (2012). "Meta-analysis of bacterial meningitis score validation studies". Arch Dis Child. 97 (9): 799–805. doi:10.1136/archdischild-2012-301798. PMID 22764093.
  55. ↑ Hasbun R, Abrahams J, Jekel J, Quagliarello VJ (2001). "Computed tomography of the head before lumbar puncture in adults with suspected meningitis". N Engl J Med. 345 (24): 1727–1733. doi:10.1056/NEJMoa010399. PMID 11742046.
  56. ↑ 56.0 56.1 56.2 56.3 56.4 56.5 56.6 McGill F, Heyderman RS, Michael BD, Defres S, Beeching NJ, Borrow R, Glennie L, Gaillemin O, Wyncoll D, Kaczmarski E, Nadel S, Thwaites G, Cohen J, Davies NW, Miller A, Rhodes A, Read RC, Solomon T (2016). "The UK joint specialist societies guideline on the diagnosis and management of acute meningitis and meningococcal sepsis in immunocompetent adults". J Infect. 72 (4): 405–438. doi:10.1016/j.jinf.2016.01.007. PMID 26845731.
  57. ↑ 57.0 57.1 57.2 57.3 57.4 Tunkel AR, Hartman BJ, Kaplan SL, Kaufman BA, Roos KL, Scheld WM, Whitley RJ (2004). "Practice guidelines for the management of bacterial meningitis". Clin Infect Dis. 39 (9): 1267–1284. doi:10.1086/425368. PMID 15494903.
  58. ↑ 58.0 58.1 58.2 58.3 58.4 58.5 Brouwer MC, McIntyre P, Prasad K, van de Beek D (2015). "Corticosteroids for acute bacterial meningitis". Cochrane Database Syst Rev. 2015 (9): CD004405. doi:10.1002/14651858.CD004405.pub5. PMID 26362566.
  59. ↑ Thwaites GE, Nguyen DB, Nguyen HD, Hoang TQ, Do TT, Nguyen TC, Nguyen QH, Nguyen TT, Nguyen NH, Nguyen TN, Nguyen NL, Nguyen HD, Vu NT, Cao HH, Tran TH, Pham PM, Nguyen TD, Stepniewska K, White NJ, Tran TH, Farrar JJ (2004). "Dexamethasone for the treatment of tuberculous meningitis in adolescents and adults". N Engl J Med. 351 (17): 1741–1751. doi:10.1056/NEJMoa040573. PMID 15496623.
  60. ↑ Donovan J, Bang ND, Imran D, Nghia H, Burhan E, Huong D, Hiep N, Ngoc L, Thanh DV, Thanh NT, Wardhani A, Maharani K, Gasmara CP, Hanh N, Oanh P, Estiasari R, Thu D, Kusumaningrum A, Dung LT, Giang DC, Ha D, Lan NH, Chau N, Nguyet N, Geskus RB, Thuong N, Kestelyn E, Hamers RL, Phu NH, Thwaites GE (2023). "Adjunctive Dexamethasone for Tuberculous Meningitis in HIV-Positive Adults". N Engl J Med. 389 (15): 1357–1367. doi:10.1056/NEJMoa2216218. PMID 37819954 Check |pmid= value (help). Vancouver style error: initials (help)
  61. ↑ Jarvis JN, Lawrence DS, Meya DB, Kagimu E, Kasibante J, Mpoza E, Rutakingirwa MK, Ssebambulidde K, Tugume L, Rhein J, Boulware DR, Mwandumba HC, Moyo M, Mzinganjira H, Kanyama C, Hosseinipour MC, Chawinga C, Meintjes G, Schutz C, Comins K, Singh A, Muzoora C, Jjunju S, Nuwagira E, Mosepele M, Leeme T, Siamisang K, Ndhlovu CE, Hlupeni A, Mutata C, van Widenfelt E, Chen T, Wang D, Hope W, Boyer-Chammard T, Loyse A, Molloy SF, Youssouf N, Lortholary O, Lalloo DG, Jaffar S, Harrison TS (2022). "Single-Dose Liposomal Amphotericin B Treatment for Cryptococcal Meningitis". N Engl J Med. 386 (12): 1109–1120. doi:10.1056/NEJMoa2111904. PMID 35320642 Check |pmid= value (help).
  62. ↑ 62.0 62.1 62.2 "Guidelines for diagnosing, preventing and managing cryptococcal disease among adults, adolescents and children living with HIV". World Health Organization. 2022. Retrieved 2026-08-09.
  63. ↑ 63.0 63.1 Collins JP, Crowe SJ, Ortega-Sanchez IR, Bahta L, Campos-Outcalt D, Loehr J, Morgan RL, Poehling KA, Schillie S (2024). "Use of the Pfizer Pentavalent Meningococcal Vaccine Among Persons Aged ≥10 Years: Recommendations of the Advisory Committee on Immunization Practices - United States, 2023". MMWR Morb Mortal Wkly Rep. 73 (15): 345–350. doi:10.15585/mmwr.mm7315a4. PMID 38635488 Check |pmid= value (help).
  64. ↑ Kobayashi M, Leidner AJ, Gierke R, Farrar JL, Morgan RL, Campos-Outcalt D, Schechter R, Poehling KA, Long SS, Loehr J, Cohen AL (2024). "Use of 21-Valent Pneumococcal Conjugate Vaccine Among U.S. Adults: Recommendations of the Advisory Committee on Immunization Practices - United States, 2024". MMWR Morb Mortal Wkly Rep. 73 (36): 793–798. doi:10.15585/mmwr.mm7336a3. PMID 39264843 Check |pmid= value (help).
  65. ↑ Kobayashi M, Leidner AJ, Gierke R, Xing W, Accorsi E, Moro P, Kamboj M, Kuchel GA, Schechter R, Loehr J, Cohen AL (2025). "Expanded Recommendations for Use of Pneumococcal Conjugate Vaccines Among Adults Aged ≥50 Years: Recommendations of the Advisory Committee on Immunization Practices - United States, 2024". MMWR Morb Mortal Wkly Rep. 73 (5152): 1174–1181. doi:10.15585/mmwr.mm735152a4. PMID 39773952 Check |pmid= value (help).


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