Meningitis is characterized by cerebrospinal fluid (CSF) pleocytosis and a clinical symptom complex of fever, headache, and meningismus. It represents acute purulent infection of the subarachnoid space. The etiologies of meningitis are myriad, with bacteria, viruses, fungi, parasites, and noninfectious causes all being implicated. In addition to community-acquired infection, nosocomial bacterial meningitis should be considered in patients with invasive procedures, complicated head trauma, or systemic bacteremia. This summary will highlight bacterial pathogens as the etiologic agents of acute meningitis.
While cases of bacterial meningitis have decreased over the past several decades as a result of use of Haemophilus influenzae type b conjugate vaccine and polysaccharide pneumococcal vaccine, contemporary studies suggest the incidence is 4-6 cases per 100 000 adults and as high as 80 cases per 100 000 infants aged younger than 2 months. The 3 most common pathogens, Hinfluenzae, Neisseria meningitidis, and Streptococcus pneumoniae, account for > 80% of cases in the adult population. Group B Streptococcus (GBS) accounts for the majority of infections in infants aged younger than 2 months. Mortality is higher for pneumococcal meningitis (as high as 30%) versus non-pneumococcal meningitis (7%-11%).
In developing countries with a high prevalence of pulmonary tuberculosis, Mycobacterium tuberculosis is a common cause of meningitis.
Antecedent history of otitis media, upper respiratory tract infection, pneumonia, gastrointestinal symptoms, or trauma may provide an indication to possible etiologic agents.
Neisseria meningitidis can cause characteristic skin manifestations such as petechiae and palpable purpura.
Patients with Listeria meningitis have an increased risk of seizures and focal neurological deficits early in the course of infection. Rhombencephalitis can occur, manifested as ataxia with cranial nerve palsies and/or nystagmus. Consumption of undercooked or improperly refrigerated food has been linked to sporadic Listeria outbreaks.
Acute bacterial meningitis may manifest as meningitis or meningoencephalitis with or without accompanying sepsis. The classic triad of acute meningitis includes fever, neck stiffness, and altered mental status. These 3 findings at presentation are found in only 44% of patients. However, at least 2 of 4 findings of headache, fever, stiff neck, and altered mentation are seen in 95% of patients. Altered mental status is present in almost two-thirds of patients with bacterial meningitis and is usually absent in viral meningitis unless coincident encephalitis is present. Lethargy or altered level of consciousness is more common in acute bacterial meningitis, with coma seen in up to 20% of patients. Depression of sensorium occurs more commonly with pneumococcal rather than meningococcal meningitis.
Focal cerebral abnormalities to consider include hemiparesis, monoparesis, and aphasia and may be due to stroke, seizures, or both. Cranial nerve palsies may occur, with eighth nerve palsy being most common.
The 3 clinical features on presentation that portend an adverse outcome appear to be the presence of hypotension, altered mental status, and seizures.
Rarely, meningitis may persist for 4 weeks and is then considered chronic meningitis.
Common acute meningitis bacterial pathogens by risk factor: Age younger than 1 month:
Viral meningitis – Culture negative, lymphocytic pleocytosis (when present) with normal CSF glucose. CSF viral polymerase chain reaction (PCR) testing may establish the diagnosis.
Drug-induced aseptic meningitis – Many drugs implicated, especially nonsteroidal anti-inflammatory drugs, antibiotics, OKT3 monoclonal antibodies, and intravenous immunoglobulin. Neutrophils or lymphocytes can dominate CSF, occasionally eosinophils seen.
Paraneoplastic syndrome – Many tumors have been associated with auto-antibody production resulting in meningoencephalitis. CSF and serum testing for antibodies establishes the diagnosis.
Subdural empyema – Suggested by rapid deterioration; associated sinus or mastoid infection or surgery.
Subarachnoid hemorrhage – Look for the presence of red blood cells (RBC) and xanthochromia on CSF.
Stroke – Large strokes may cause meningeal irritation if there is significant necrosis in the brain or hemorrhage. Temporally, the fevers usually present 24-48 hours after stroke.
Delirium tremens – Patients can have confusion, fevers, and rigidity. History of alcohol use, negative cultures, and otherwise bland CSF point toward the diagnosis.
Brain abscess – Symptoms may include headache, fever, and focal neurologic findings.
Paravertebral or epidural abscess – Local inflammation my produce CSF pleocytosis without actual infection of the CSF. Imaging the spine may identify lesion.
