Bacterial meningitis begins with the entry of organisms into the well-defended subarachnoid space. The ability to infect the subarachnoid space is not shared equally by all bacteria. The dominance of three organisms— S. pneumoniae, H. influenzae type b, and N. meningitidis—which cause over two-thirds of bacterial meningitis, is no accident. These encapsulated organisms share the ability to invade the host through the upper airway, survive dissemination through the bloodstream, and then gain access to the subarachnoid space. The subcapsular constituents of these organisms are a strong trigger of inflammatory cascades in the host. Inflammation produces the clinical picture of fever, meningismus, and eventually altered mental status, which are the hallmarks of the disease. 4

Stimulation of pain-sensitive structures in meninges and posterior spinal roots leads to headache and meningeal signs. The brain and meninges, encased in the fixed-volume skull, become edematous. Cerebrospinal fluid (CSF) drainage is reduced by interference with its flow in the subarachnoid pathways as well as its absorption by the arachnoid granulations. Hence, the quantity of CSF increases, causing communicating or noncommunicating hydrocephalus. 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. Since brain perfusion depends on arterial pressure's exceeding tissue pressure (in this case intracranial pressure), ischemia may develop. Diminished perfusion is all the more likely, since the vascular supply is burdened with an inflammatory infiltrate whose functional and structural consequences include faulty autoregulation, inflammatory narrowing, and a prothrombotic milieu. There are some variations on the pathophysiologic themes described above. For example, organisms sometimes gain entry to the CSF, not by hematogenous seeding, but through direct contiguity. 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 neurosurgery. 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, H. influenzae type b, and N. meningitidis depend on their capacity to stimulate the host's immune processes and the host's response.5

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