The most common causes of bacterial meningitis
in the U.S. are Streptococcuspneumoniae (61%), Neisseria
meningitidis (16%), group B streptococcus (14%), Haemophilus
influenzae (7%), and Listeria monocytogenes (2%).
The median age of illness has risen to 39 years of age, and the
incidence of bacterial meningitis has declined.1 Changes
in epidemiology have mirrored vaccination practices in adults and
children against H. influenzae, S. pneumoniae,
and N. meningitidis. The incidence of penicillin-resistant S.
pneumoniae has increased, so that in some areas it accounts
for approximately one third of cases.1 These facts
are important because they affect the ED selection of empiric antibiotics
for presumptive bacterial meningitis.
S. pneumoniae, H. influenzae type
b, and N. meningitidis are encapsulated organisms
that invade the host through the upper airway, survive dissemination
through the blood stream, and then gain access to the subarachnoid
space. The subcapsular constituents of these organisms trigger inflammatory
cascades. The brain and meninges, encased in the fixed-volume skull,
become edematous. Cerebrospinal fluid (CSF) drainage is reduced
by interference with flow and absorption by the arachnoid granulations.
Intracranial blood vessels initially expand, increasing the volume
occupied by that compartment. The brain itself swells by several
mechanisms. Disruption of the blood–brain barrier allows
entry of protein and ultimately water (vasogenic edema), while hydrocephalus
forces CSF into the periventricular parenchyma (interstitial edema).
Eventually, cell membrane homeostasis may be compromised, leading
to increased intracellular water (cytotoxic edema).
The sum of these expanded volumes overwhelms the compensatory
displacement of CSF into the more compliant spinal compartment,
and intracranial pressure rises as a result. Because brain perfusion
depends on arterial pressure exceeding intracranial pressure, ischemia
Organisms can also gain entry to the CSF by direct contiguous
spread. Such direct spread may be from infected parameningeal structures
(e.g., brain abscess, otitis media, and sinusitis), traumatic or
congenital communications with the exterior, or neurosurgical procedures.
The bacteriologic characteristics of these infections may vary.
Immunologic deficiency states are increasingly common and predispose
to yet other organisms. The clinical and pathophysiologic effects
of organisms other than S. pneumoniae and N.
meningitidis depend on their capacity to stimulate the
host’s immune response. Important risk factors for bacterial
meningitis are listed in Table 168-1.
Table 168-1 Important
Risk Factors for Bacterial Meningitis |Favorite Table|Download (.pdf)
Table 168-1 Important
Risk Factors for Bacterial Meningitis
|Acute or chronic otitis media|
|Cerebrospinal fluid leak|
|Neurosurgical procedure/head injury|
|Indwelling neurosurgical device/cochlear implant|
|Liver disease |
|Unvaccinated to Haemophilus influenzae type
b, Neisseria meningitidis, or Streptococcus