Meningitis
Meningitis represents a potentially life-threatening clinical syndrome characterized by inflammation of the protective membranes—known as the meninges—surrounding the brain and spinal cord. It is a condition of considerable global health concern, known to affect individuals of all age groups, with neonates, children, and immunocompromised individuals being the most susceptible. The disease may progress rapidly, and if not diagnosed and treated promptly, it can result in significant morbidity or mortality. The primary pathological feature is the infiltration of the subarachnoid space by inflammatory cells, resulting in increased intracranial pressure, brain edema, and potential neurological deficits.
Meningitis may be caused by a range of infectious agents, including bacteria, viruses, fungi, and parasites, as well as by non-infectious causes such as autoimmune disorders, drugs, and malignancies. This multifaceted etiology leads to varying clinical manifestations, prognosis, and treatment strategies, depending on the causative factor. Timely intervention with appropriate antimicrobial therapy, corticosteroids, and supportive measures is critical to improving outcomes.
2. Definition
Meningitis is defined as the inflammation of the leptomeninges, the membranous coverings of the brain and spinal cord, specifically the pia mater and arachnoid mater. The condition results from infection, autoimmune activity, or other inflammatory processes that trigger a cascade of events leading to cellular infiltration, increased cerebrospinal fluid (CSF) protein levels, and alteration of the blood-brain barrier (BBB).
The disease is broadly classified into acute, subacute, and chronic types based on the duration and progression of symptoms. Acute meningitis typically develops within hours to days, subacute over a week to a month, and chronic over a period of more than four weeks.
3. Epidemiology of Meningitis
3.1 Global Burden
Meningitis remains a global health threat, with an estimated 2.5 million cases and over 250,000 deaths annually, according to the World Health Organization (WHO). The highest burden is observed in the “meningitis belt” of Sub-Saharan Africa, stretching from Senegal in the west to Ethiopia in the east. This region is especially susceptible to epidemic outbreaks of meningococcal meningitis, particularly during the dry season when dust and upper respiratory tract infections predispose individuals to infection.
3.2 Age and Risk Factors
- Neonates and Infants: High vulnerability due to immature immune systems.
- Adolescents and Young Adults: Increased incidence of meningococcal disease.
- Elderly and Immunocompromised: Increased risk of Listeria and fungal meningitis.
Risk factors include:
- Lack of vaccination
- Overcrowding (e.g., dormitories, military barracks)
- Immunosuppression
- Head trauma or neurosurgical procedures
- Congenital defects such as spina bifida
4. Etiology of Meningitis
The causative agents of meningitis are highly diverse and can be broadly categorized into infectious and non-infectious etiologies.
4.1 Infectious Causes
Bacterial Meningitis
Common pathogens include:
- Neonates: Group B Streptococcus, Escherichia coli, Listeria monocytogenes
- Children and Adults: Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae type b (Hib)
- Elderly: Listeria monocytogenes
- Post-neurosurgical or trauma: Staphylococcus aureus, Pseudomonas aeruginosa
Viral Meningitis
More benign than bacterial forms. Common viruses:
- Enteroviruses (Coxsackievirus, Echovirus)
- Herpes simplex virus (HSV)
- Varicella zoster virus (VZV)
- Mumps virus
- HIV
Fungal Meningitis
- Cryptococcus neoformans (commonly in immunocompromised, e.g., HIV/AIDS)
- Candida species
- Histoplasma capsulatum
- Coccidioides immitis
Parasitic Meningitis
- Naegleria fowleri: causes primary amoebic meningoencephalitis (PAM)
- Toxoplasma gondii
- Angiostrongylus cantonensis
4.2 Non-Infectious Causes
- Autoimmune diseases (e.g., systemic lupus erythematosus)
- Drug-induced (e.g., NSAIDs, intravenous immunoglobulins)
- Neoplastic meningitis (meningeal carcinomatosis)
- Post-surgical or traumatic causes
- Sarcoidosis
5. Types of Meningitis
5.1 Acute Bacterial Meningitis
This is the most severe and rapidly progressing form. It involves pus-forming bacteria and presents with fever, headache, neck stiffness, photophobia, and altered mental status. Lumbar puncture typically reveals elevated WBC count, increased protein, and decreased glucose levels.
5.2 Viral (Aseptic) Meningitis
Generally self-limiting and mild. It is diagnosed when clinical features of meningitis are present, but CSF cultures are negative for bacteria. Lymphocytic predominance in CSF is typical, and glucose levels are usually normal.
5.3 Chronic Meningitis
Lasts over 4 weeks. Commonly caused by Mycobacterium tuberculosis, Cryptococcus, or neoplastic infiltration. Presents with insidious onset of symptoms including low-grade fever, lethargy, and cranial nerve palsies.
5.4 Fungal Meningitis
More prevalent in immunocompromised patients, especially with HIV/AIDS. Symptoms develop slowly and include headache, fever, and confusion. Diagnosis relies on India ink staining, cryptococcal antigen, and culture.
5.5 Parasitic Meningitis
Rare but fatal. Naegleria fowleri, the “brain-eating amoeba,” causes PAM with fulminant progression leading to death within days.
6. Causes of Meningitis
6.1 Pathophysiological Mechanisms
The pathogenesis begins with the invasion of the central nervous system (CNS) via:
- Hematogenous spread (most common)
- Contiguous spread from sinusitis, otitis media
- Direct inoculation through trauma, surgery
This leads to:
- Activation of host immune response
- Release of pro-inflammatory cytokines like IL-1, TNF-α
- Breakdown of the blood-brain barrier
- Cerebral edema, increased intracranial pressure
- Reduced cerebral perfusion and possible ischemic injury
7. Clinical Manifestations
Classic Triad
- Fever
- Neck stiffness
- Altered mental status
Other symptoms:
- Headache
- Photophobia
- Vomiting
- Seizures
- Focal neurological signs
- Petechial rash (especially in meningococcal meningitis)
In infants:
- Bulging fontanelle
- Poor feeding
- Hypotonia
- Irritability
8. Diagnosis of Meningitis
8.1 Clinical Evaluation
- History and physical examination
- Kernig’s and Brudzinski’s signs (meningeal irritation)
8.2 Laboratory Tests
- Lumbar puncture (CSF analysis)
- Opening pressure
- Cell count and differential
- Protein and glucose concentration
- Gram stain and culture
- PCR for viral DNA
- Antigen detection tests (e.g., cryptococcal antigen)
| Type | WBC count | Protein | Glucose | Gram stain |
| Bacterial | High (neutrophils) | High | Low | Often positive |
| Viral | Moderate (lymphocytes) | Mildly elevated | Normal | Negative |
| Tuberculous | High (lymphocytes) | High | Low | AFB stain |
| Fungal | High (lymphocytes) | High | Low | India ink or Ag test |
8.3 Imaging
- CT or MRI before lumbar puncture in patients with:
- Papilledema
- New-onset seizures
- Altered sensorium
- Immunocompromised states
9. Treatment of Meningitis
9.1 Empirical Antimicrobial Therapy
Empirical treatment should be initiated immediately after CSF collection:
| Age Group | Empirical Antibiotics |
| Neonates | Ampicillin + Gentamicin or Cefotaxime |
| Children & Adults | Ceftriaxone + Vancomycin |
| >50 years or immunocompromised | Ceftriaxone + Vancomycin + Ampicillin (for Listeria) |
| Post-surgical/trauma | Vancomycin + Cefepime or Meropenem |
- Duration:
- Neisseria meningitidis: 7 days
- H. influenzae: 7-10 days
- Streptococcus pneumoniae: 10-14 days
- Listeria or Gram-negative bacilli: ≥21 days
9.2 Corticosteroids
- Dexamethasone 0.15 mg/kg every 6 hours for 4 days
- Shown to reduce neurological sequelae, particularly in S. pneumoniae meningitis
9.3 Supportive Treatment
- Antipyretics
- Anticonvulsants (if seizures)
- Oxygen and IV fluids
- Intracranial pressure management
9.4 Specific Treatments
- Fungal meningitis: Amphotericin B + Flucytosine followed by Fluconazole
- Tubercular meningitis: HRZE regimen (Isoniazid, Rifampin, Pyrazinamide, Ethambutol) + steroids
- Viral meningitis: Supportive care; Acyclovir for HSV
10. Prevention of Meningitis
Vaccination
- Hib vaccine
- Pneumococcal conjugate vaccine (PCV13, PPSV23)
- Meningococcal vaccines (MenACWY, MenB)
- BCG vaccine for tuberculosis
Prophylaxis
- Close contacts of meningococcal meningitis cases: Rifampin, Ciprofloxacin, or Ceftriaxone
- Hib exposure in unvaccinated children: Rifampin prophylaxis
11. Complications and Prognosis
- Early complications: Seizures, hydrocephalus, cerebral infarction
- Late complications: Hearing loss, cognitive impairment, motor deficits
- Mortality:
- Bacterial meningitis: 5–30%
- Viral meningitis: <1%
- Fungal and tubercular forms: higher in immunocompromised
Conclusion
Meningitis continues to be a major public health challenge due to its rapid onset, high mortality, and potential for permanent neurological damage. A nuanced understanding of the different forms of meningitis, their etiology, and appropriate therapeutic interventions is critical for timely and effective management. Advancements in molecular diagnostics, antimicrobial therapy, and vaccination strategies have significantly improved the prognosis of this devastating disease. Nonetheless, the persistent prevalence in low-resource settings and the emergence of antibiotic resistance call for continued vigilance, public health initiatives, and global collaboration to combat meningitis comprehensively.