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What is meningitis?
Meningitis is an inflammation
of the leptomeninges and underlying subarachnoid cerebrospinal fluid (CSF). It can be useful to divide symptom onset into
acute, subacute, and chronic categories. Unlike subacute (1-7 d) or chronic (>7 d) meningitis,
which have myriad infectious and noninfectious etiologies, acute meningitis (<24 h) is almost always a bacterial infection caused
by one of several organisms. Depending on age and general condition, these gravely ill patients present acutely with signs
and symptoms of meningeal inflammation and systemic infection of less than 1 day's duration. Patients may decompensate quickly
and require emergency care, including antimicrobial therapy, within 30 minutes of emergency department (ED) presentation.
Meningitis is an infection of the fluid of a person's spinal cord and the fluid that surrounds the
brain. People sometimes refer to it as spinal meningitis. Meningitis is usually caused by a viral or bacterial infection.
Knowing whether meningitis is caused by a virus or bacterium is important because the severity of illness and the treatment
differ. Viral meningitis is generally less severe and resolves without specific treatment, while bacterial meningitis can
be quite severe and may result in brain damage, hearing loss, or learning disability. For bacterial meningitis, it is also
important to know which type of bacteria is causing the meningitis because antibiotics can prevent some types from spreading
and infecting other people. Before the 1990s, Haemophilus influenzae type b (Hib) was the leading cause of bacterial meningitis,
but new vaccines being given to all children as part of their routine immunizations have reduced the occurrence of invasive
disease due to H. influenzae . Today, Streptococcus pneumoniae and Neisseria meningitidis are the leading causes of bacterial
meningitis.
Pathophysiology:
A number of factors influence the development of bacterial meningitis, including virulence of the strain,
host defenses, and bacteria-host interactions.
Bacterial seeding usually occurs by hematogenous spread. In those without an identifiable source of
infection, local tissue and bloodstream invasion by bacteria colonized in the nasopharynx may be a common source. Rarely,
infected contiguous structures invade via septic thrombi or osteomyelitic erosion; meningeal seeding also may occur with a
direct bacterial inoculate during trauma, neurosurgery, or instrumentation. Meningitis in the newborn is transmitted vertically
from colonized pathogens in the maternal intestinal or genital tract or horizontally from nursery personnel or caregivers
at home.
Once in the CSF, the paucity of antibodies, complement components, and white blood cells (WBCs) allows
the bacterial infection to flourish. Bacterial cell wall components initiate a cascade of complement- and cytokine-mediated
events that result in at least 3 critical events: increased permeability of the blood-brain barrier, cerebral edema, and presence
of toxic mediators in the CSF. Replicating bacteria, increasing numbers of inflammatory cells, cytokine-induced disruptions
in membrane transport, and increased vascular and membrane permeability perpetuate the infectious process and account for
the characteristic changes in CSF cell count, pH, lactate, protein, and glucose. Exudates extend throughout the CSF, particularly
to the basal cisterns, damaging cranial nerves (eg, cranial nerve VIII, with resultant hearing loss), obliterating CSF pathways
(causing obstructive hydrocephalus), and inducing vasculitis and thrombophlebitis (causing local brain ischemia).
As intracranial pressure (ICP) continues to rise and brain edema progresses, CNS autoregulatory processes
begin to fail. This pivotal event may occur when the transient increase in cerebral blood flow (CBF) reverses and begins to
decrease. CBF reduction correlates with the patient's decreasing alertness and changes in mental status.
Without medical intervention, the cycle of decreasing CBF, worsening cerebral edema, and increasing
ICP proceeds unchecked. Ongoing endothelial injury may result in vasospasm and thrombosis, further compromising CBF, and may
lead to stenosis of large and small vessels. Systemic hypotension (septic shock) also may impair CBF, and the patient soon
dies from systemic complications or from diffuse CNS ischemic injury.
The pathophysiologies of nonbacterial pathogens are less well understood. Fungal meningitis is thought
to unfold in a manner similar to but less acute than bacterial meningitis.
Clinical manifestration
Distinguishing acute, subacute, and chronic meningitis helps identify the
pathogen. Approximately 25% of patients with bacterial meningitis present acutely within 24 hours of onset of symptoms. Other
patients with bacterial meningitis and most patients with viral meningitis present with subacute neurologic symptoms developing
over 1-7 days. Chronic symptoms lasting longer than 1 week suggest meningitis caused by some viruses as well as tuberculosis,
syphilis, fungi (especially cryptococci), and carcinomatous meningitis.
- Classic symptoms (not evident in infants or seen often in the elderly) include the following:
- Nuchal rigidity (generally not present in children <1 y or in patients with altered mental status)
- Prodromal upper respiratory infection (URI) symptoms (viral and bacterial)
- Seizures (30-40% in children, 20-30% in adults)
- Focal neurologic symptoms (including focal seizures)
- Altered sensorium (confusion may be sole presenting complaint, especially in elderly)
- Lethargy and/or change in level of alertness
- Poor feeding and/or vomiting
- Respiratory distress, apnea, cyanosis
- Partially treated meningitis: As many as 40% of patients with meningitis were treated previously with
oral antibiotics. Seizures may be the sole presenting symptom; fever and changes in level of alertness or mental status occur
less commonly than in untreated meningitis.
- Low-grade ventriculitis associated with ventriculoperitoneal shunt: Patients may have a less dramatic
presentation than those with acute meningitis, with headache, nausea, minimal fever, and malaise.
- Fungal meningitis: Headache, low-grade fever, and lethargy are the primary symptoms; the course may
be mild with fluctuating symptoms, especially in immunocompromised patients.
- Tuberculous meningitis: Fever, weight loss, night sweats, and malaise, with or
without headache and meningismus are common symptoms; this infection may follow a protracted course with vague, nonspecific
presentation.
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