Continuing Education Activity

Meningitis refers to inflammation of the meninges, the protective membranes surrounding the brain and spinal cord, and encompasses both infectious and noninfectious causes. Infectious meningitis most commonly arises from bacterial or viral agents, though fungi and parasites can also be responsible. Bacterial meningitis remains a global health concern, with an estimated 2.5 million cases and 300,000 deaths reported worldwide in 2024, despite advances in diagnosis, treatment, and vaccination. Viral and aseptic meningitis, while generally less severe, can still result in significant morbidity. Disruption in vaccination programs, vaccine hesitancy, and global health crises continue to complicate prevention efforts. Rapid identification, prompt antimicrobial therapy, and effective supportive care are critical to reducing mortality and long-term neurological sequelae. This course outlines the global epidemiology, emerging diagnostic technologies, and vaccination strategies for meningitis, essential for improving outcomes.

This activity reviews the diagnostic strategies, evidence-based management, and prevention practices of meningitis. Participants will also gain insight into distinguishing between bacterial, viral, fungal, and parasitic etiologies, interpreting cerebrospinal fluid findings, and implementing appropriate empiric therapies. This activity for healthcare professionals is designed to enhance the learner's competence in identifying meningitis, performing the recommended evaluation, and implementing an appropriate interprofessional approach to managing this condition, thereby improving patient outcomes and safety.

Objectives:

• Identify the causes of meningitis.
• Apply evidence-based diagnostic criteria to evaluate a patient with meningitis.
• Implement timely therapies in suspected bacterial meningitis.
• Apply modalities to improve care coordination among interprofessional team members to improve outcomes for patients affected by meningitis.

Introduction

Meningitis is a broad term encompassing many causes of meningeal irritation and inflammation, both infectious and non-infectious. It describes inflammation of the meningeal layers of the brain and is most often associated with bacteria or viruses. While meningitis can be a life-threatening disorder, particularly bacterial meningitis, other entities can cause meningeal irritation, eg, viruses, systemic inflammatory disorders, certain medications, and even vaccinations, some with good outcomes. Before the era of antibiotics, bacterial meningitis was universally fatal. Nevertheless, even with innovations in diagnosis and treatment, bacterial meningitis can still carry a mortality rate of 25% or greater, particularly in low-income countries. Signs and symptoms of meningeal inflammation have been recorded in countless ancient texts; however, the term "meningitis" did not come into general use until surgeon John Abercrombie defined it in 1828.

Despite breakthroughs in diagnosis, treatment, and vaccination, in 2024, 2.5 million cases of bacterial meningitis were reported worldwide, with 300,000 subsequent deaths.[1][2][3][4] The impact on prevention has been complicated by the increasing number of individuals who oppose routine vaccinations for their families, creating gaps in herd immunity and opportunities for outbreaks. Additionally, natural and man-made disasters have disrupted health care systems and vaccination delivery, with serious consequences for both children and adults.

Viral meningitis and aseptic meningitis are much more common than bacterial meningitis, and while both can potentially cause significant morbidity, these entities tend to be less severe in nature than bacterial meningitis.

Etiology

Meningitis is defined as inflammation of the meninges. The meninges are composed of 3 membranes (the dura mater, arachnoid mater, and pia mater) that line the vertebral canal and skull, enclosing the brain and spinal cord. (see Image. Skull Cross-Section) Encephalitis, on the other hand, is inflammation of the brain parenchyma.[5][6] Unfortunately, in some infections, the infection may not be limited to a portion of the central nervous system (CNS) but instead involves both the meninges and the brain parenchyma. This is termed meningoencephalitis and is more commonly associated with viral than bacterial pathogens.[7] Please see StatPearls' companion resource, "Viral Encephalitis," for further information.  

The infectious etiologic agents of meningitis include bacteria, viruses, fungi, and, less commonly, parasites (see Table 1. Infectious Meningitis Etiologies).

Table

Table 1. Infectious Meningitis Etiologies.

The following are the most common bacterial causes of meningitis in the United States:

• Streptococcus pneumoniae (highest mortality worldwide); 20% to 30% in adults and 10% in children [8][9]
• Streptococcus agalactiae (group B strep); neonatal incidence in the US after intrapartum prophylaxis began was 0.34 to 0.37 cases per 1,000 live births, and in adults, 0.16 per 1,000,000 people [10][11][12]
• Neisseria meningitidis 
• Haemophilus influenzae 
• Listeria monocytogenes [2][13][14][CDC. Meningococcal Disease Surveillance and Trends. Nov 14 2024]

Less common causes of bacterial meningitis, eg, Staphylococcus aureus, may be found in patients with recent surgery, central lines, and trauma. Mycobacterium tuberculosis should be considered in the differential diagnosis for immunocompromised hosts and in young children with a close contact to an active case of tuberculosis. Borrelia burgdorferi meningitis can occur in individuals who live in or travel to Lyme-endemic areas. Treponema pallidum central nervous system infection can be seen in persons with HIV/AIDS and individuals with multiple sexual partners or a sexual partner with a risk factor. T pallidum can occur at any stage of the infection, from initial onset in primary syphilis to secondary and tertiary syphilis. Escherichia coli, Streptococcus agalactaie (GBS), and Listeria are important pathogens in the neonatal period. Please see StatPearls' companion resource, "Neonatal Meningitis," for further information.

The most common viral agents of meningitis are nonpolio enteroviruses (group A and B coxsackievirus, echoviruses, and parechoviruses).[15] Other viral causes include Mumps, Parechovirus, Herpesviruses (eg, Epstein-Barr virus, herpes simplex virus, and varicella-zoster virus), measles, influenza, and arboviruses (eg, West Nile, La Crosse, Powassan, Jamestown Canyon). Please see StatPearls' companion resource, "Viral Encephalitis," for further information. 

A recently published survey of meningitis in the US found Enterovirus as the predominant cause at 51%, with bacterial meningitis at 14% of total cases.[13] The rest of the identified infectious causes were HSV (8.3%), fungal (2.7%), arboviral (1.1%) and other viruses at 0.8%). The remaining cases were classified as unknown (21%) or noninfectious (3.5%).[13]

Fungal meningitis is typically associated with an immunocompromised host (eg, HIV/AIDS, chronic corticosteroid therapy, and patients with cancer). Throughout the world, regional endemic fungi have been identified, and clinicians should be aware of local pathogens as well as a patient's travel history that may have exposed them to nonendemic fungal pathogens. Medical and surgical procedures can also result in fungal meningitis from contaminated devices and equipment. In 2012, Tainted steroid injections in the US were associated with unusual fungal infections, including meningitis. In 2023, an outbreak of suspected Fusarium solani was associated with cases reported following spinal anaesthesia in 2 private medical clinics in Mexico, where individuals from the US and Canada had travelled for medical procedures.[16] While many fungi can cause meningitis with the right conditions, the most common fungi causing meningitis include:

• Cryptococcus neoformans
• Coccidioides immitis
• Aspergillus
• Candida
• Endemic fungi
• Mucormycosis (more common in patients with diabetes mellitus and transplant recipients; direct extension of sinus infection)

Some parasites may also cause meningitis, often resulting in a predominance of eosinophils in the spinal fluid. Fortunately, such infections are uncommon, but can include:

• Malaria (a common infection in the tropics but an uncommon cause of meningitis)
• Helminths causing eosinophilic meningitis, eg, Angiostrongylus cantonensis (found in Asia and the Pacific regions), Baylisascaris procyonis (associated with raccoon feces), and Gnathostoma spinigerum
• Naegleria fowlerii (the agent causing primary amebic meningoencephalitis)

A number of special circumstances permit organisms outside the typical meningitis pathogens to appear more frequently (see Table 2. Factors with Increased Risk of Atypical Meningitis Pathogens). Any common bacteria or viruses can cause meningitis in immunocompromised individuals, yet clinicians may also encounter pathogens that rarely produce disease in those with intact immune defenses. Fungal organisms exemplify this pattern, particularly Candida species and endemic mycoses that produce milder infections in immunocompetent hosts but still disseminate in individuals with impaired immunity.

Additional scenarios emphasize the role of normal flora in disease development, especially when foreign bodies, eg, ventriculoperitoneal shunts, remain in place. Disruption of normal host barriers also provides pathogens with access to the central nervous system. Brain or spinal surgery, penetrating trauma involving the face or sinuses, congenital spinal deformities with sinus tracts, and abnormal cribiform plate defects all create pathways that enable bacterial entry into the central nervous system.

Table

Table. Factors with Increased Risk of Atypical Meningitis Pathogens.

Epidemiology

The epidemiology of meningitis is complex, especially when considering the overlap with encephalitis, which is sometimes difficult to separate in viral meningitis cases. The incidence of meningitis also varies widely worldwide, with 0.9 cases per 100,000 population in high-income countries and 80 cases/100,000 population in low-income countries.[26] Case fatalities and poor outcomes are likewise disparate across the globe, with the highest mortalities in low-income nations (54%), and survivors experiencing neurologic deficits.

In the US, the annual incidence of bacterial meningitis is approximately 0.9 cases/100,000 population with a case fatality rate of 14.3%.[27][26] Viral meningitis exhibits seasonal patterns in temperate climates and year-round patterns in tropical regions.[15][28] In 2017, the US recorded approximately 75,000 cases of viral-related meningitis, mostly due to Enteroviruses (particularly coxsackieviruses, echoviruses, and parechoviruses).[13]

The highest incidence of bacterial meningitis worldwide is in an area of sub-Saharan Africa dubbed “the meningitis belt,” stretching from Ethiopia to Senegal.[29][30][31] As many as 80 cases per 100,000 exist in this area, with mortalities reaching over 50%.[31][WHO. Guidelines on Meningitis Diagnosis, Treatment, and Care. 10 Apr 2025]

Bacterial Meningitis

While bacterial meningitis can occur in healthy individuals of all ages, certain risk factors increase susceptibility. Clinicians need to be aware of these factors and perform a complete clinical history to determine if any of these factors are present. Many, but not all, of these conditions may predispose to bacteremia and lead to meningitis, including:

• Chronic medical disorders (renal failure, diabetes, adrenal insufficiency, cystic fibrosis)
• Extremes of age, notably children under 5 and adults over 60
• Undervaccination
• Immunosuppressed states: iatrogenic (particularly for those taking biologics such as TNF-α inhibitors), transplant recipients, congenital immunodeficiencies, AIDS
• Living in crowded conditions
• Exposures:

  • Travel to endemic areas (southwestern US for cocci or northeastern US for Lyme disease)
  • Vectors (mosquitoes, ticks)
• Alcohol use disorder
• Presence of a ventriculoperitoneal shunt or other foreign material
• Surgical or traumatic disruption of the meninges
• Congenital disabilities
• Bacterial endocarditis
• Malignancy
• Dural defects
• Intravenous drug use
• Sickle cell anemia
• Splenectomy

Viral Meningitis

Worldwide data show viral meningitis occurring far more frequently than bacterial meningitis, with reported incidence ranging from at least 0.26 to 17 cases per 100,000 individuals.[32] In the US, enteroviral meningitis accounts for an estimated 75,000 cases annually and represents the most common viral form.[33] Temperate regions exhibit a seasonal pattern, with increased cases in summer and autumn, whereas tropical and subtropical regions report year-round activity.[WHO. Guidelines on Meningitis Diagnosis, Treatment, and Care. 10 Apr 2025] Travelers visiting these regions during winter may still contract viral meningitis, requiring clinicians to remain aware of this risk. Many causative viruses spread through fecal-oral transmission, close contact with infected individuals, or exposure to vectors such as ticks and mosquitoes.

Other Meningitis Etiologies

Fungal and parasitic etiologies appear far less frequently, yet recent reports highlight outbreaks linked to procedural exposures. One outbreak involved a pathogenic fungus associated with surgical procedures performed under spinal epidural anesthesia in Mexico, followed by care in Mexico or Texas. Approximately 25 cases caused by Fusarium solani species complex were identified from cerebrospinal fluid. Among 212 US residents at risk from these procedures, clinicians identified 14 suspected cases, 11 probable cases, and 2 confirmed cases, with 3 fatalities attributed to the organism.[34]

Aseptic meningitis, defined as meningeal inflammation without a positive bacterial culture, is typically diagnosed based on cerebrospinal fluid pleocytosis marked by a white cell count exceeding 5 cells/mm³. All pathogens discussed above may yield negative cultures, particularly when antibiotics are administered before the lumbar puncture. Please see StatPearls' companion resource, "Aseptic Meningitis," for further information. Potential causes of aseptic meningitis include:

• Certain medications, particularly non-steroidal anti-inflammatory drugs (NSAIDs), antibiotics (especially penicillin class drugs and sulfamides), intravenous gamma globulin (IVIg), and monoclonal antibody preparations, are associated with aseptic meningitis.
• Neoplastic meningitis may result from metastasis of cancers elsewhere in the body, lymphomas, and leukemias.
• Systemic inflammatory diseases can affect the central nervous system, eg, systemic lupus erythematosus (SLE), Bechet disease, sarcoidosis, and polyangiitis.
• Vaccination may cause meningeal irritation with the initial administration, especially with varicella-zoster, MMR, rabies, influenza, and pertussis vaccines (aseptic meningitis following vaccination from reactivation of the vaccine strain has also been reported in the case of VZV).[35][36][37]

Pathophysiology

Infection of the meninges typically begins through hematogenous dissemination, neuronal transport, or direct contiguous spread from an adjacent infected site. The invading pathogen and the host immune response generate a complex cascade of events capable of worsening clinical outcomes. Bacterial meningitis develops when organisms colonizing the nasopharynx penetrate the mucosa and enter the bloodstream, either directly or through engulfment by immune cells with subsequent transport to the CNS. Once within the subarachnoid space, these organisms replicate and trigger inflammation across the subarachnoid and ventricular compartments.

Viral meningitis follows a similar sequence; after initial infection, a secondary viremia often seeds the CNS. Host responses involving humoral and cellular mediators, eg, IL-1, IL-6, TNF, reactive oxygen intermediates, matrix metalloproteinases, and related factors, arise to control the infection.[38] Alterations in the cerebral vasculature subsequently disrupt the blood-brain barrier, generating global and focal edema and ischemia that contribute to structural and functional brain injury. Progressive inflammation correlates closely with pathophysiologic changes and neuronal damage.[26][39]

Crosstalk within the neuroimmune axis underscores the intricate relationship between host and pathogen. Experimental mouse models demonstrate that Streptococcus pneumoniae and Streptococcus agalactiae can utilize meningeal neuronal pathways. By exploiting nociceptors responsible for pain signaling, these organisms gain CNS access. Genetically engineered mice lacking these receptors show reduced bacterial loads and diminished inflammatory responses in meningitis models.[40] Although confirmation in humans remains incomplete, a similar mechanism may operate. Viral pathogens, eg, rabies and herpesviruses, also use neuronal routes to enter the CNS.[41][42]

Direct inoculation of pathogens into the CNS may occur through trauma, neurosurgical procedures, or implantation of foreign bodies, eg, ventriculoperitoneal shunts used in hydrocephalus management. Contiguous extension can arise from uncontrolled infections in neighboring structures, including otitis media, mastoiditis, or sinusitis. Rare congenital disabilities affecting the blood-brain barrier, eg, midline cribiform plate anomalies or lumbosacral abnormalities involving dural sinus tracts or meningoceles, may also permit localized bacterial entry into the CNS and cause meningitis.[43]

History and Physical

Bacterial Meningitis Clinical Features

Bacterial meningitis presents with considerable variation depending on age and immune status. Most affected individuals appear acutely ill upon seeking medical evaluation, while viral or fungal meningitis often produces a less toxic appearance despite the presence of headache, fever, and neck stiffness. Clinicians generally encounter 1 of 3 presentation patterns in bacterial meningitis.

The first involves an insidious course over several days, marked by worsening headache and fever before meningeal signs emerge, a pattern frequently associated with Streptococcus pneumoniae. The second involves a more rapid evolution of classic meningitis symptoms over a 1- to 2-day period, often seen with Haemophilus influenzae type B. The third presents with septic shock and rapid decompensation over a few hours, a scenario commonly linked to Neisseria meningitidis with concomitant meningococcemia. Typical symptoms include fever, neck stiffness, and photophobia, while nonspecific symptoms, eg, headache, dizziness, confusion, delirium, irritability, and nausea or vomiting, often accompany the illness. Indicators of increased intracranial pressure—altered mental status, neurologic deficits, and seizures—signal a worse prognosis. A thorough history should address relevant risk factors, followed by a focused physical examination. Laboratory testing and imaging support diagnostic confirmation, but must not delay immediate initiation of appropriate antimicrobial therapy.

Pediatric Presentations

In infants beyond the neonatal period, as well as older children and adults, the physical examination concentrates on detecting focal neurologic deficits and signs of meningeal irritation, including Brudzinski and Kernig signs. The Brudzinski sign appears when neck flexion triggers reflex hip flexion due to meningeal irritation, although this finding remains uncommon.[44] Kernig sign occurs more frequently; passive knee extension with the hip flexed elicits pain or resistance beyond 135 degrees of extension. These signs warrant further evaluation but do not conclusively diagnose or exclude meningitis. A complete skin examination may reveal petechiae or purpura, which can suggest meningococcal infection but also occur in other severe systemic illnesses associated with disseminated intravascular coagulation. Cranial nerve abnormalities develop in roughly 10% to 20% of individuals with meningitis.

Neonates and young infants exhibit subtler or atypical findings. Presentations may include fever or hypothermia, reduced oral intake, lethargy, excessive sleep, irritability, or a bulging fontanelle. Paradoxical irritability—characterized by distress during handling with relative calm when left undisturbed—may also appear. Clinicians should gather a complete perinatal history and obtain laboratory studies that may include testing for CMV, toxoplasmosis in the setting of exposure to raw meat or cat litter, HIV, syphilis, and review of birth-parent vaccine status. Several causes of meningitis are vaccine-preventable, including pneumococcus, Haemophilus influenzae type B, meningococcus, measles, and varicella. Tuberculosis transmission from birth parent to infant can occur; when risk factors exist, both require testing, and infants need prophylaxis if the birth parent or household contact has active disease, with repeat testing after 3 months. Please see StatPearls' companion resource, "Tuberculosis in Children," for further information.

Evaluation

Suspicion for meningitis arises from a detailed history and targeted physical examination, while definitive confirmation relies solely on cerebrospinal fluid (CSF) analysis. Cerebrospinal fluid evaluation includes Gram stain, white blood cell count, glucose, protein, and culture, with polymerase chain reaction (PCR) or other rapid molecular diagnostics used when available (see Image. Cerebrospinal Fluid Gram Stain).[45] Newer biomarkers can complement standard testing, and inflammatory markers, eg, C-reactive protein and procalcitonin, may support diagnostic accuracy.[46] MALDI-TOF technology has transformed the rapid identification of bacterial and certain fungal pathogens in bloodstream infections, yet its performance with cerebrospinal fluid has only recently been explored and has not matched the reliability of culture-based methods.[47] Although rapid diagnostic platforms reduce ongoing laboratory costs and technologist demands, the initial investment may pose challenges for some institutions. Cerebrospinal fluid is obtained through lumbar puncture, and clinicians should measure opening pressure whenever possible.[48]

The following additional testing, if available, should be performed based on the suspected etiology:

• Viral: Multiplex and specific PCRs for West Nile and other arboviral agents, herpes viruses, mumps, and measles (can be used for patients with suspected viral meningitis) [49]
• Fungal

  • Latex agglutination or lateral flow on CSF is considered the new gold standard for diagnosing cryptococcal disease in the CNS.[50] 
  • Biomarkers, eg, beta D-glucan and galactomannan, may be helpful when used in combination with standard methods.[51] 
  • Newer research has expanded information on appropriate cutoff values for noncryptococcal fungal CSF pathogens and continues to improve specific diagnoses.[52] 
  • CSF fungal culture, India ink stains may be applied if other methods are not available, but cultures are time-consuming. India ink staining requires an experienced operator; sensitivity is lower early in the disease; however, with an inexperienced operator, specificity is 94% to 100%.[50]
• Mycobacterial: CSF Acid-fast bacilli smear and culture, GeneXpert or Xpert Ultra or other PCR-based testing, TB loop-mediated isothermal amplification (LAMP) assay (if available) [53]
• Syphilis: CSF VDRL
• Lyme disease: CSF burgdorferi antibody for local synthesis (culture and PCR for Lyme CNS disease not recommended due to low sensitivity and specificity)

Ideally, the CSF sample should be obtained before initiating antimicrobials. However, when bacterial meningitis is suspected and the patient is severely ill, antibiotics should be initiated before performing the lumbar puncture. PCR-based testing has made significant strides in diagnosing meningitis pathogens, even if the person received antibiotics before the CSF evaluation.

Computed Tomography of the Head Before Lumbar Puncture

Debate continues regarding the need for cranial computed tomography (CT) scanning before lumbar puncture in community-acquired meningitis. Concern about brain herniation frequently prompts clinicians to image before collecting cerebrospinal fluid. Current recommendations from the Infectious Disease Society of America and the European Society of Clinical Microbiology and Infectious Diseases support cranial CT before lumbar puncture in patients with features suggesting a more complicated course, including altered mental status with a Glasgow Coma Scale below 10, previous central nervous system disease, new-onset seizures within the previous week, focal neurologic deficits, papilledema, severe immunocompromise, and relevant comorbidities in adults older than 60.[54][55][56][57] In patients without these risk factors, CT scanning before lumbar puncture often delays timely therapy and increases healthcare costs without improving safety.[58][59]

A normal head CT does not rule out elevated intracranial pressure or impending herniation. When clinical findings signal a risk for herniation, clinicians should forgo lumbar puncture and begin treatment immediately, regardless of imaging results. Blood work should include blood cultures, serum electrolytes due to the frequent occurrence of the syndrome of inappropriate antidiuretic hormone secretion, serum glucose, and renal and hepatic function tests. Additional studies should reflect the specifics of the patient’s presentation and medical history.

Treatment / Management

All causes of meningitis require supportive care, including airway management, fever control, adequate hydration, and seizure management if needed. Antimicrobial therapy should be rapidly provided for all cases of meningitis as soon as the diagnosis is made.[60][61][62] 

The antibiotic is selected based on the presumed organism causing the infection until diagnostic results are available. The clinician must take into account the patient's demographics and past medical history to provide the best antimicrobial coverage. Various empiric therapies are recommended based on various clinical factors (see Table 3).[26][55][57][63][WHO. Guidelines on Meningitis Diagnosis, Treatment, and Care. 10 Apr 2025]

Table

Table 3. WHO Guidelines on Empiric Therapy for Bacterial Meningitis .

Clinicians should also consider the addition of rifampin if dexamethasone has been given to the patient. Once the agent has been identified, the therapy should be narrowed to target the organism with the best choice of antibiotics for the patient's age, allergies, and medications that may cause drug-drug interactions (see Table 4).[57]

Table

Table 4. Targeted Meningitis Antimicrobial Therapies.

Consider adding rifampin if the ceftriaxone MIC is greater than 2 µg/L.

Steroid Therapy

Some evidence suggests that steroids can be beneficial for outcomes in high-income countries. A recent Cochrane review suggested a reduction in adverse neurological outcomes but not in mortality for adults with S pneumoniae, H influenzae, and N meningitidis meningitis.[65] In children, steroids were associated with a reduction of severe hearing impairment only in cases of H influenzae meningitis, type B.[65] If steroids are used, they should be given before or concurrently with the first dose of antibiotics.

Increased Intracranial Pressure

If the patient develops clinical signs of increased intracranial pressure (altered mental status, neurologic deficits, nonreactive pupils, bradycardia), interventions to maintain cerebral perfusion include:

• Elevation of the head of the bed to 30 degrees
• Induction of mild hyperventilation in the intubated patient
• Administration of osmotic diuretics such as 25% mannitol or 3% saline

Chemoprophylaxis

Chemoprophylaxis is indicated for close contacts of a patient diagnosed with N meningitidis and H influenzae type B meningitis. Close contacts include housemates, significant others, close schoolmates or teammates, those who have shared utensils, and health care practitioners in proximity to secretions (providing mouth-to-mouth resuscitation or intubating/suctioning without a facemask). The hospital epidemiologist and health department can provide further guidance for those who need prophylaxis.

Antibiotic chemoprophylaxis for N meningitidis includes rifampin, ciprofloxacin, or ceftriaxone, and for H influenzae type B, rifampin.

Differential Diagnosis

The diagnosis of meningitis is generally straightforward, but there are some entities that may be confused with meningitis, especially at both ends of the age spectrum. Encephalitis may also mimic meningitis and can occur concurrently with meningitis, making it difficult to separate the conditions. Severe rheumatologic disease with vasculitis can mimic meningitis, but infection is also a risk for such patients and should be evaluated with LP.[66][67] Clinicians must consider the following conditions in the differential diagnosis of unclear cases:

• Stroke
• Subdural hematoma
• Subarachnoid hemorrhage
• Primary brain tumors
• Metastatic brain disease
• Brain abscess (might coexist with meningitis)
• Encephalitis
• Vasculitis
• Migraine

Prognosis

Outcomes depend on patient characteristics, eg, age and immune status, but also vary by etiologic organism. In the US, the overall annual case fatality rate for bacterial meningitis in 2010 was 14.3%. (Please refer to the Complications section for more information.)

Pathogen-specific mortality rate includes the following:[27]

• Streptococcus pneumoniae meningitis: case fatality rate, 17.9%
• Neisseria meningitidis meningitis: case fatality rate, 10.1%
• Group B Streptococcus meningitis: case fatality rate, 11.1%
• H. influenzae meningitis: case fatality rate, 7%
• Listeria monocytogenes meningitis: case fatality rate, 18.1% [27]

Complications

Despite improvements in diagnosis and management, meningitis continues to be a severe disease with mortality and long-term consequences. For survivors of meningitis, complications can be severe and lifelong. Young children (younger than 1 year) may have short-term complications of subdural effusions that rarely need drainage as they spontaneously resolve, but long-term complications in children can be debilitating.[68] 

A comprehensive cohort study in Sweden of over 36,000 children followed for 35 years revealed a higher risk of cognitive disabilities, seizures, hearing loss, motor function disorders, visual disturbances, behavioral and emotional disorders, and injuries to the intracranial structures compared to age, sex, and residence-matched controls. A 2010 meta-analysis of pediatric patients reported a median risk of sequelae post-discharge of 19.9%. In this study, the most common organism isolated was H influenzae, followed by S pneumoniae. The most common sequelae were hearing loss (6%), followed by behavioral difficulties (2.6%), cognitive difficulties (2.2%), motor deficits (2.3%), seizure disorder (1.6%), and visual impairment (0.9%).[69] 

Bacterial meningitis in adults, primarily caused by S pneumoniae, can have devastating consequences.[70] Adult survivors of meningitis also can experience complications, including hearing loss, cerebrovascular complications, and focal neurological complications, including the following:

• Increased intracranial pressure from cerebral edema caused by increased intracellular fluid in the brain. Several factors are involved in the development of cerebral edema, including increased blood-brain barrier permeability and cytotoxicity from cytokines, immune cells, and bacteria.
• Hydrocephalus
• Cerebrovascular complications
• Focal neurologic deficits

Viral meningitis generally has a much better prognosis than bacterial or fungal meningitis, but in some cases, a progression to encephalitis and severe neurologic consequences occurs.[33] Poor outcomes are associated more often with the acquisition of Enteroviruses or Parechoviruses at a very young age, resulting in high mortality in neonates from hepatic necrosis and meningoencephalitis.[71] However, even older children (18-42 months at acquisition) who experienced Enterovirus or Parechovirus infection had ongoing issues, with a third of the studied cohort in New Zealand showing developmental delays.[72]

Consultations

Meningitis is a severe infection with dire consequences if not handled correctly. Consultants should be utilized to help ensure the best possible outcomes when caring for a patient with meningitis, especially one with an unusual pathogen, a confusing presentation, severe allergies, or immunocompromise. Infectious disease specialists can be invaluable for assistance in these circumstances. Other consultants may be needed as noted below:

• Adult or pediatric intensivists
• Neurology to aid in seizure management and subsequent follow-up management
• Neurosurgery when there is suspicion of progression to a brain abscess
• Rheumatology and heme/oncology in case of noninfectious cause
• Rehabilitative medicine and physical/occupational therapy for needs following recovery
• Audiologist for hearing assessments following bacterial meningitis infections
• Hospital infection control personnel
• Local health department 

Pearls and Other Issues

Differentiating between bacterial, viral, and fungal meningitis may be difficult. CSF analysis may not be conclusive, and cultures do not always yield an answer immediately. Multiplex and specific PCR panels are available and provide information in a few hours. Given the morbidity and mortality, clinicians should initiate empiric antibiotic therapy and admit all those with suspected meningitis to the hospital on droplet precautions until the pathogen is identified and appropriate antibiotics have been given for 24 hours. While proper care during the infection is critical for the best outcome, prevention with vaccination is key to limiting these infectious agents wherever possible. Clinicians and public health personnel need continued vigilance in addressing increasing misinformation and poor vaccination uptake for preventable diseases. Currently available vaccines that can prevent meningitis include the HiB vaccine against Haemophilus influenzae, the pneumococcal vaccine against Streptococcus pneumoniae, and meningococcal vaccines against Neisseria meningitidis. 

Enhancing Healthcare Team Outcomes

Meningitis represents inflammation of the meninges surrounding the brain and spinal cord and may result from bacterial, viral, fungal, or parasitic infections, as well as non-infectious causes. Bacterial meningitis remains the most severe form, with significant global morbidity and mortality despite advances in antimicrobial therapy and vaccination. Rapid recognition and treatment initiation are essential to prevent irreversible neurological damage and death. Vaccine hesitancy, healthcare disruptions, and emerging pathogens continue to challenge prevention and early intervention efforts.

Effective management of meningitis requires a coordinated, interprofessional approach. Physicians, general practitioners, and advanced practitioners must promptly identify symptoms, perform diagnostic testing, and initiate evidence-based antimicrobial therapy. Nurses play a critical role in patient monitoring, education, and supportive care, while pharmacists ensure accurate dosing and evaluate drug interactions. Collaborative communication among all team members enhances patient safety, minimizes diagnostic delays, and improves outcomes. Public health officials play a key role in identifying individuals in the community who may require prophylaxis against meningitis. This is especially important during outbreak situations. Local health officials should always be notified of any meningitis case. Interprofessional coordination and adherence to evidence-based protocols strengthen team performance and advance patient-centered care.

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Disclosure: Debbie Tristram declares no relevant financial relationships with ineligible companies.

Disclosure: Noah Kondamudi declares no relevant financial relationships with ineligible companies.