Adil Abbasi, MD, FACP

Learning Objectives

By the end of this review, the learner should be able to:

• Define meningitis and distinguish it from encephalitis and meningoencephalitis.
• Describe global epidemiology, prevalence, and major causes of morbidity and mortality.
• Explain the pathophysiology of meningitis for different infectious agents.
• Classify meningitis by time course and etiology (bacterial, viral, fungal, tuberculous, parasitic, and non-infectious).
• Recognize typical and atypical symptoms and signs in adults and children.
• Outline a diagnostic approach, including when to perform neuroimaging before lumbar puncture.
• List indications and contraindications for lumbar puncture.
• Interpret CSF findings in normal patients vs. bacterial, viral, fungal, tuberculous, and parasitic meningitis.
• Summarize key principles of treatment for each major type of meningitis.
• Apply knowledge to clinical case scenarios.

Introduction:

Meningitis is an inflammatory process involving the leptomeninges (pia and arachnoid mater) and the cerebrospinal fluid (CSF) within the subarachnoid space. It may be caused by infectious agents (bacteria, viruses, fungi, mycobacteria, parasites) or non-infectious mechanisms such as autoimmune disorders, neoplastic infiltration, and drug reactions (Hersi 2023).

Clinically, meningitis is characterized by combinations of fever, headache, neck stiffness, and altered mental status, but the presentation is often variable and nonspecific (Carter 2022; Mount 2017). 

Epidemiology, Prevalence, Morbidity, and Mortality:

Meningitis remains a major global public health problem. The World Health Organization notes that bacterial meningitis is particularly devastating: around 1 in 6 affected individuals die, and about 1 in 5 survivors have major sequelae such as hearing loss, cognitive impairment, seizures, or limb loss (WHO 2025). 

Recent global data suggest that community-acquired bacterial meningitis accounts for a substantial proportion of severe CNS infections, though overall incidence has decreased substantially in countries that have widely implemented conjugate vaccines against Haemophilus influenzae type b (Hib), Neisseria meningitidis and Streptococcus pneumoniae (van Ettekoven 2024; Hasbun 2017). 

Despite advances in therapy, case-fatality ratios (CFRs) remain significant. Modern cohorts report adult 30-day mortality from bacterial meningitis around 5–15%, with higher mortality in resource-limited settings and in infections due to S. pneumoniae or in older/immunocompromised patients (van de Beek 2004; Kiyani 2021; Makowiecki 2024). 

Viral meningitis is the most common overall type in many regions, typically caused by enteroviruses, and usually carries a much better prognosis with low mortality (Cantu 2023; CDC 2025). 

Pathophysiology

The pathophysiology varies with the pathogen but follows a common framework:

1. Colonization and Invasion

• Many organisms colonize mucosal surfaces (e.g., nasopharynx for N. meningitidis and S. pneumoniae).
• Invasion into the bloodstream (bacteremia, viremia, fungemia) or direct extension from local infections (sinusitis, otitis, skull fractures, neurosurgical procedures) leads to entry into the subarachnoid space (Runde 2023). 

2. Crossing the Blood–Brain or Blood–CSF Barrier

• Pathogens cross via transcellular passage, paracellular routes, or “Trojan horse” mechanisms (e.g., TB and some fungi via infected phagocytes).
• Once in the CSF, host immune surveillance is relatively limited, favoring rapid pathogen proliferation.

3. Inflammatory Cascade

• Bacterial cell wall components (e.g., lipopolysaccharide, teichoic acids) trigger a robust inflammatory response with cytokine release (TNF-α, IL-1β, IL-6).
• Endothelial activation increases blood–brain barrier permeability, leading to vasogenic edema, leukocyte influx, and impaired CSF resorption (Kaddoura 2024). 

4. Raised Intracranial Pressure (ICP) and Ischemia

• Cerebral edema (cytotoxic and vasogenic), increased CSF volume, and impaired venous outflow contribute to elevated ICP and decreased cerebral perfusion.
• Vasculitis, thrombosis, and microvascular injury cause focal ischemia and infarction, contributing to neurologic sequelae (van de Beek 2004). 

5. Pathogen-Specific Features

• Viral meningitis: typically, milder inflammation with lymphocytic predominance and less dramatic BBB disruption.
• Fungal and tuberculous meningitis: granulomatous inflammation, basal exudates, and a more subacute or chronic course, often with cranial neuropathies and hydrocephalus (Thomas 2023). 
• Parasitic / eosinophilic meningitis: marked eosinophilic response to helminths, sometimes with predilection for specific CNS regions.

Types and Classification

By Time Course

• Acute meningitis: symptoms evolve over hours to a few days; often bacterial or viral.
• Subacute meningitis: evolves over days to weeks; typical causes include TB, fungi, and some parasitic infections.
• Chronic meningitis: symptoms for ≥4 weeks; often TB, fungal, carcinomatous, or autoimmune meningitis (Hersi 2023). 

By Etiology

1. Bacterial meningitis (pyogenic)

• Common pathogens: S. pneumoniae, N. meningitidis, Hib (where vaccines not widely used), Listeria monocytogenes, and Gram-negative bacilli (Runde 2023; Mańdziuk 2023). 
• Less common but known cause of meningitis is Lyme disease which is caused by a spirochete “Borrelia burgdorferi”.

2. Viral (aseptic) meningitis

• Most commonly enteroviruses (e.g., echoviruses, coxsackieviruses), followed by herpesviruses (HSV-2, VZV, occasionally HSV-1, EBV), mumps, measles, HIV, arboviruses (e.g., West Nile virus), and others (Cantu 2023; CDC 2025; Meningitis Research Foundation 2025). 

3. Fungal meningitis

• Cryptococcus neoformans (especially in HIV and other immunocompromised patients), Coccidioides spp., Histoplasma spp., and others.

4. Tuberculous meningitis (TBM)

• Caused by Mycobacterium tuberculosis, often with concomitant systemic TB. Characterized by basal meningeal exudates and high risk of hydrocephalus and stroke (Thomas 2023). 

5. Parasitic / eosinophilic meningitis

• Angiostrongylus cantonensis, Gnathostoma spinigerum, Toxocara spp., and others; often associated with CSF eosinophilia.

6. Non-infectious meningitis

• Autoimmune (e.g., lupus), neoplastic (carcinomatous meningitis), and drug-induced (e.g., NSAIDs, IVIG, certain antibiotics). 

Causes and Risk Factors

Age-Based and Risk-Based Etiologies

• Neonates

• Group B Streptococcus (S. agalactiae), E. coli, other Gram-negative rods (e.g., Klebsiella), and Listeria spp. 

• Infants and children >1 month

• S. pneumoniae, N. meningitidis, and (in under-vaccinated populations) Hib (Medscape Pediatric BM 2025; Mańdziuk 2023). 

• Adolescents and young adults

• N. meningitidis is particularly important, often associated with outbreaks in close-contact settings (dormitories, military recruit camps).

• Adults (community-acquired)

• S. pneumoniae is the leading cause in adults and children >1 month (Mańdziuk 2023). 

• Older adults and special risk groups

• S. pneumoniae, Listeria (especially age >50, alcoholism, pregnancy, immunosuppression), Gram-negative bacilli, and staphylococci in post-neurosurgical or trauma settings.

• Immunocompromised hosts

• More likely to have Listeria, Gram-negative bacilli, TBM, cryptococcal and other fungal meningitis, and opportunistic viral infections (e.g., CMV, VZV, HIV-associated). 

Clinical Features (Symptoms and Signs)

Classic Triad and Common Features

The classic presentation of bacterial meningitis consists of:

1. Fever
2. Neck stiffness (nuchal rigidity)
3. Altered mental status

However, these three symptoms are present in only a minority of patients; one study found that 95% of patients with bacterial meningitis had at least two of four features: fever, headache, neck stiffness, or altered consciousness (Carter 2022). 

Other features:

• Severe headache (often diffuse, sometimes described as the “worst headache”)
• Photophobia and phonophobia
• Nausea and vomiting
• Seizures (more common in pneumococcal, TBM, HSV, and focal complications)
• Focal neurologic deficits (cranial nerve palsies, hemiparesis)
• Rash: Petechial or purpuric rash strongly suggests N. meningitidis.
• Signs of raised ICP: decreased level of consciousness, papilledema (late), Cushing triad in severe cases

Meningeal signs (Kernig and Brudzinski) have variable sensitivity and specificity and cannot reliably distinguish bacterial from viral meningitis (Mount 2017). 

Special Populations

• Neonates and infants

• May present with nonspecific signs: poor feeding, irritability, lethargy, apnea, temperature instability, bulging fontanelle, seizures.

• Elderly and immunocompromised patients

• May have blunted fever and minimal meningeal signs; confusion or delirium can be the dominant feature.

Diagnostic Approach

Initial Assessment and Stabilization

• Ensure airway, breathing, circulation (ABC or CBA per new guidelines).
• Rapidly assess vital signs, level of consciousness (e.g., GCS), and focal neurologic deficits.
• Obtain blood cultures and basic labs (CBC, electrolytes, renal/liver function, coagulation profile, inflammatory markers). 

Meningitis is a medical emergency. In suspected acute bacterial meningitis, guidelines emphasize early empiric antimicrobial therapy, ideally after blood cultures and, when safe, a prompt lumbar puncture (Tunkel 2004; Carter 2022). 

Role of Neuroimaging

CT or MRI of the brain is not mandatory before LP in all patients, but is recommended when there is concern for a mass lesion or markedly raised ICP. Clinical features that should prompt neuroimaging before LP include (Tunkel 2004; Engelborghs 2017; Jane 2023): 

• New focal neurologic deficit (e.g., hemiparesis, aphasia)
• New-onset seizures (particularly within 1 week)
• Moderate to severe impairment of consciousness
• Papilledema or clinical concern for raised ICP
• Known CNS mass lesion, recent neurosurgery, or head trauma
• Significant immunocompromise (e.g., HIV with low CD4, transplant, high-dose steroids)

If none of these are present, immediate LP is generally recommended to expedite diagnosis.

Laboratory Studies

1. Blood tests

• CBC: leukocytosis or leukopenia
• CRP, ESR, procalcitonin: may help distinguish bacterial from viral etiologies (bacterial tend to have higher procalcitonin).
• Blood cultures: positive in a significant proportion of bacterial meningitis cases.

2. Microbiologic tests on CSF (after LP)

• Gram stain and culture
• Cell count and differential
• Glucose, protein, lactate (or LDH proxy), ± CSF pH
• PCR panels for bacterial and viral pathogens
• Acid-fast stain, mycobacterial culture, and nucleic acid amplification for TB
• Fungal stains (India ink for Cryptococcus), fungal culture, cryptococcal antigen
• VDRL/FTA-ABS for neurosyphilis, where indicated 

3. Other tests

• HIV testing when appropriate
• Chest imaging, TB screening, or other systemic work-up for TBM, fungal infection, or neoplastic meningitis.

Lumbar Puncture (LP)

Indications:

Key indications include (AMBOSS 2024; Merck 2024; Stat Pearls 2023): 

• Suspected CNS infections, especially meningitis and encephalitis
• Suspected subarachnoid hemorrhage with negative CT
• Evaluation for demyelinating disease (e.g., multiple sclerosis)
• Evaluation of CNS malignancies and paraneoplastic syndromes
• Suspected idiopathic intracranial hypertension or normal pressure hydrocephalus (for opening pressure and CSF removal)

Contraindications:

Absolute contraindications (Engelborghs 2017; Medscape 2024; Merck 2024; VIM-Book 2024): 

• Evidence of space-occupying lesion with mass effect or posterior fossa mass (on imaging), with risk of herniation.
• Infection at the puncture site (cellulitis, abscess).
• Uncorrected severe coagulopathy or severe thrombocytopenia (e.g., platelets <30 ×10⁹/L, INR >1.5, or very low fibrinogen). 

Relative contraindications:

• Clinical or radiologic suspicion of markedly increased ICP
• Spinal cord mass or deformity at the puncture site
• Hemodynamic instability or respiratory compromise

In suspected acute bacterial meningitis with contraindications to immediate LP, blood cultures should be obtained, and empiric intravenous antibiotics and dexamethasone started before or while arranging neuroimaging and eventual LP (Tunkel 2004). 

Practical Considerations

• Measure opening pressure in the lateral decubitus position when safe and feasible. Normal opening pressure: roughly 10–20 cm H₂O in adults. 
• Collect multiple tubes (usually 3–4) for cell counts, biochemistry, microbiology, and additional tests.
• Avoid traumatic taps (though they are common); if traumatic, interpret CSF cell counts and protein with caution and may correct for RBC count.

CSF Findings

Typical Patterns

The following table summarizes typical CSF patterns. Individual patients may show overlaps, especially early in disease or after partial treatment. Data are adapted and synthesized from major clinical references (Merck Manual, AAFP, NCBI Bookshelf, RCH guideline, Geek Medics, and TBM studies). 

(Note: Values are approximate and should be interpreted in clinical context)

Treatment

Important: The following outlines general principles and is for educational purposes. Actual therapy must follow current guidelines and local resistance patterns and be individualized by clinicians.

General Principles in Acute Bacterial Meningitis

1. Immediate empiric therapy

• Start empiric IV antibiotics as soon as possible when bacterial meningitis is suspected—ideally after blood cultures and, if not delayed by imaging, after LP.
• Empiric regimens typically include:

• A third-generation cephalosporin (e.g., cefotaxime or ceftriaxone) to cover S. pneumoniae, N. meningitidis, and many Gram-negative organisms.
• Vancomycin to cover cephalosporin-resistant S. pneumoniae.
• Ampicillin is often added in older adults, pregnant patients, and immunocompromised hosts to cover Listeria (Tunkel 2004; Runde 2023). 

2. Adjunctive corticosteroids

• Dexamethasone given before or with the first dose of antibiotics reduces mortality and neurologic sequelae in pneumococcal meningitis, especially in high-income settings (Tunkel 2004; van de Beek 2004). 

3. Targeted therapy

• Once CSF culture/PCR identifies the pathogen and susceptibilities, narrow therapy accordingly (e.g., penicillin or ceftriaxone for susceptible meningococcal or pneumococcal strains).

4. Supportive and ICU care

• Management of raised ICP, seizures, hemodynamic instability, and electrolyte disturbances.
• Hearing evaluation and rehabilitation for survivors with sensorineural hearing loss.

Viral Meningitis

• Many cases, especially enteroviral meningitis, are self-limited and managed with supportive care (analgesia, hydration, monitoring). 
• Acyclovir is recommended for suspected or confirmed HSV or VZV meningitis/encephalitis.
• Treat underlying HIV, CMV, or other specific viral infections per guidelines.

Fungal Meningitis

• Cryptococcal meningitis: typically treated with induction therapy using an amphotericin B–based regimen plus flucytosine, followed by high-dose fluconazole consolidation and maintenance, and careful management of ICP.
• Coccidioidal or histoplasma meningitis: azole therapy (e.g., fluconazole, itraconazole, or other agents) or amphotericin B depending on severity and guidelines.

Tuberculous Meningitis (TBM)

• Requires prolonged combination anti-tuberculous therapy (e.g., isoniazid, rifampin, pyrazinamide, ethambutol initially) with adjustments based on susceptibility and drug interactions.
• Adjunctive corticosteroids improve survival in many TBM patients.
• Early recognition and treatment are crucial due to high risk of disability and death. 

Parasitic / Eosinophilic Meningitis

• Therapy depends on the organism: often anthelminthic agents (e.g., albendazole) plus corticosteroids to reduce inflammatory symptoms in selected cases.
• Some forms (e.g., Naegleria fowleri primary amoebic meningoencephalitis) require aggressive multi-drug therapy and still have very high mortality.

Lyme meningitis.

• The infection with Borrelia burgdorferi (the bacteria that causes Lyme disease) can spread to the nervous system and cause Lyme neuroborreliosis.
• One of the main forms of neuroborreliosis is Lyme meningitis, an inflammation of the meninges.
• Lyme meningitis usually has a subacute onset – symptoms develop over days to weeks, not hours.

• Often causes: Headache, Neck stiffness (may be milder), Fatigue, malaise, sometimes low-grade fever, Often associated facial nerve palsy (Bell’s palsy) or other cranial neuropathies, especially in children and young adults in endemic areas.

CSF typically shows:

• Elevated white cells, usually lymphocytic rather than neutrophilic
• Mild–moderate ↑ protein
• Normal or mildly ↓ glucose

Diagnosis is confirmed with Lyme serology and/or CSF antibody testing for Borrelia (depending on local protocols).

Treatment:

• Usually treated with IV ceftriaxone or high-dose IV/PO penicillin or doxycycline for several weeks, depending on guidelines and patient factors.
• Prognosis is generally good with timely treatment, though headaches and fatigue can take time to resolve.

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Case Scenarios

Case 1 – Acute Bacterial (Meningococcal) Meningitis

Presentation:
A 19-year-old college student presents with 12 hours of high fever, severe headache, photophobia, vomiting, and progressive confusion. On exam: T 39.5°C, HR 120, BP 100/60, neck stiffness, petechial rash on the legs, GCS 13, no focal deficits.

Key points:

• Young adult in a close-living setting with fever, headache, neck stiffness, altered mental status, and petechial rash strongly suggests meningococcal meningitis (N. meningitidis).
• There are no obvious focal neurological deficits or known risk factors for mass lesion, so immediate LP is generally acceptable without prior imaging, depending on local protocols. 
• Blood cultures and LP are performed; empiric IV antibiotics and dexamethasone are started immediately.
• CSF: ↑ opening pressure, turbid fluid, WBC 3000/µL (90% neutrophils), protein 250 mg/dL, glucose 25 mg/dL (serum 100 mg/dL → ratio 0.25), Gram-negative diplococci seen.

Teaching message:
Rapid recognition and treatment of suspected meningococcal meningitis are lifesaving. Close contacts require chemoprophylaxis according to public health guidelines.

Case 2 – Subacute Tuberculous Meningitis

Presentation:
A 55-year-old man with poorly controlled diabetes and recent weight loss presents with 3 weeks of headache, low-grade fever, night sweats, and gradual cognitive decline. He has mild neck stiffness and right abducens nerve palsy.

Key points:

• Subacute course with constitutional symptoms and cranial neuropathy suggests TBM or fungal meningitis. 
• MRI shows basal meningeal enhancement and mild hydrocephalus. LP after neuroimaging: opening pressure 28 cm H₂O; CSF protein 300 mg/dL; glucose 25 mg/dL (serum 100 mg/dL, ratio 0.25); WBC 250/µL with lymphocytic predominance; AFB stain negative; TB PCR pending.
• Despite negative initial AFB smear, high clinical suspicion and typical CSF profile justify empiric anti-TB therapy plus corticosteroids while awaiting culture or NAAT confirmation.

Teaching message:
TBM often presents sub acutely with basal meningitis and cranial neuropathies. Diagnostic tests may be insensitive; treatment should not be delayed when suspicion is high. 

Case 3 – Cryptococcal Meningitis in HIV

Presentation:
A 40-year-old man with untreated HIV infection (CD4 ~40 cells/µL) presents with 2 weeks of worsening headache, low-grade fever, and blurred vision. He is oriented but slow to respond. No focal deficits; mild papilledema on fundoscopic exam.

Key points:

• Advanced HIV, subacute headache, and papilledema raise suspicion for cryptococcal meningitis.
• Brain imaging is performed first to assess for mass lesions and degree of hydrocephalus.
• LP reveals markedly elevated opening pressure (e.g., 35 cm H₂O), clear CSF, WBC 40/µL (lymphocytic), protein 120 mg/dL, glucose 35 mg/dL, serum 80 mg/dL (ratio 0.44). India ink stain shows encapsulated yeasts; cryptococcal antigen is positive. 
• Treatment includes amphotericin B plus flucytosine and serial LPs or other measures to manage elevated ICP, followed by consolidation and maintenance therapy with fluconazole.

Teaching message:
In immunocompromised patients, chronic or subacute meningitis with high opening pressure and lymphocytic CSF should prompt evaluation for fungal etiologies such as Cryptococcus.

Chapter Summary (Bullets)

• Meningitis is inflammation of the leptomeninges and CSF, caused by infectious and non-infectious processes.
• Bacterial meningitis remains a major global cause of death and disability, despite vaccines and improved care; viral meningitis is more common but usually milder.
• Pathophysiology involves meningeal invasion, blood–brain barrier disruption, inflammatory cytokine cascades, cerebral edema, and raised ICP.
• Classification can be based on time course (acute, subacute, chronic) and etiology (bacterial, viral, fungal, tuberculous, parasitic, autoimmune, neoplastic, drug-induced).
• Age and risk factors strongly influence the likely pathogen: group B strep and Gram-negative rods in neonates; S. pneumoniae and N. meningitidis in older children and adults; Listeria, TB, and fungi in older or immunocompromised patients.
• Classic features of bacterial meningitis include fever, headache, neck stiffness, and altered mental status, but presentations vary; absence of the full triad does not exclude meningitis.
• Lumbar puncture with CSF analysis is essential for diagnosis unless contraindicated; neuroimaging is reserved for patients with signs of increased ICP, focal deficits, or other risk factors.
• Contraindications to LP include mass lesions with mass effect, infection at the puncture site, and significant coagulopathy or severe thrombocytopenia.
• CSF patterns differ across etiologies: bacterial meningitis typically shows high opening pressure, high protein, low glucose, high lactate/LDH, and neutrophilic pleocytosis; viral meningitis often shows normal glucose and lymphocytic pleocytosis; fungal and TBM generally have lymphocytic pleocytosis, markedly elevated protein, and low glucose; parasitic meningitis often shows eosinophilic CSF.
• Treatment of acute bacterial meningitis requires rapid empiric IV antibiotics plus adjunctive dexamethasone in suspected pneumococcal disease, then targeted therapy based on culture/PCR results.
• Viral meningitis is usually managed supportively, with antivirals for HSV/VZV; fungal, TB, and parasitic meningitis require pathogen-specific regimens and often prolonged therapy.
• Early recognition, timely LP, prompt therapy, and attention to complications (ICP, seizures, hearing loss) are key determinants of outcome.

References (Author–Year Format)

Note: All references are presented in author–year style and correspond to the in-text citations above.

• Carter, E., & Ho, D. (2022). The management of acute meningitis: An update. Clinical Medicine (London). PMC
• Cantu, R. M., & colleagues. (2023). Viral meningitis. StatPearls (NCBI Bookshelf). NCBI
• Centers for Disease Control and Prevention (CDC). (2025). About Viral Meningitis. CDC
• Engelborghs, S., et al. (2017). Consensus guidelines for lumbar puncture in patients with neurological diseases. European Journal of Neurology. PMC
• Hasbun, R., et al. (2017). Epidemiology of meningitis and encephalitis in the United States. Clinical Infectious Diseases, 65(3), 359–363. OUP Academic
• Hersi, K., & colleagues. (2023). Meningitis. StatPearls (NCBI Bookshelf). NCBI
• Jane, L. A., & O’Donnell, C. (2023). Lumbar puncture. StatPearls (NCBI Bookshelf). NCBI
• Kaddoura, R., et al. (2024). Post-meningitic syndrome: Pathophysiology and long-term consequences. International Journal of Molecular Sciences, 25(20), 11053. MDPI
• Kiyani, M., et al. (2021). Outcomes and health care resource utilization of adult meningitis. Journal of the Neurological Sciences. PMC
• Mańdziuk, J., & colleagues. (2023). Streptococcal meningitis. StatPearls (NCBI Bookshelf). NCBI
• Makowiecki, M., et al. (2024). Factors associated with in-hospital mortality in adult bacterial meningitis. Journal of Clinical Medicine, 13(24), 7845. MDPI
• Mount, H. R., & Boyle, S. D. (2017). Aseptic and bacterial meningitis: Evaluation, treatment, and prevention. American Family Physician, 96(5), 314–322. AAFP
• Prasad, N., et al. (2025). The epidemiology of bacterial meningitis in the United States after vaccine implementation. Open-access cohort study. PMC
• Runde, T. J., & Kruse, B. (2023). Bacterial meningitis. StatPearls (NCBI Bookshelf). NCBI
• Shahan, B. D., & Waldman, A. L. (2021). Cerebrospinal fluid analysis. American Family Physician, 103(7), 422–428. AAFP
• Thomas, J., et al. (2023). The spectrum of cerebrospinal fluid findings in tuberculous meningitis. Journal of Clinical Neurology. PMC
• Tunkel, A. R., et al. (2004). Practice guidelines for the management of bacterial meningitis. Clinical Infectious Diseases, 39(9), 1267–1284. OUP Academic
• van de Beek, D., et al. (2004). Clinical features and prognostic factors in adults with bacterial meningitis. New England Journal of Medicine, 351(18), 1849–1859. New England Journal of Medicine
• van Ettekoven, C. N., et al. (2024). Global case fatality of bacterial meningitis during an 80-year period. JAMA Network Open. JAMA Network
• World Health Organization (WHO). (2025). Meningitis – Key Facts. World Health Organization