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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 may develop.

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

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