Bakteryjne zapalenie opon mózgowych II: patofizjologia

Bacteria such as Neisseria meningitidis colonize the nasopharynx and invade the bloodstream, eventually reaching cerebral vessels. They penetrate the blood-brain barrier or blood-cerebrospinal fluid barrier through the vascular endothelium or choroid plexus to reach the subarachnoid space. Bacterial virulence factors like polysaccharide capsules help resist immune defenses during this invasion.

Bacterial components like lipopolysaccharides and teichoic acids trigger activation of microglia and astrocytes in the subarachnoid space. These cells secrete proinflammatory cytokines including TNF-α, IL-1β, and IL-6, which increase adhesion molecule expression and recruit neutrophils into the cerebrospinal fluid, amplifying the inflammatory cascade.

Proinflammatory cytokines increase vascular permeability, causing vasogenic edema as plasma leaks into the extracellular space. Cytotoxic edema develops from inflammatory injury causing intracellular swelling of neurons and glia. Interstitial edema results from impaired cerebrospinal fluid reabsorption at arachnoid villi, collectively elevating increased intracranial pressure and impairing cerebral perfusion.

Vascular inflammation triggers endothelial activation and neutrophil-mediated injury, promoting microthrombi formation that reduces cerebral blood flow. This vascular injury causes ischemic neuronal damage by limiting oxygen delivery to brain tissue. The combination of barrier disruption, edema, and reduced perfusion creates a cascade leading to rapid disease progression.

The subarachnoid space has limited immune surveillance, allowing bacteria to multiply rapidly after crossing the blood-brain barrier. Cerebrospinal fluid lacks robust antimicrobial defenses compared to blood, enabling bacterial components to accumulate and trigger intense local inflammation. This environment facilitates the pathogenic cascade characteristic of bacterial meningitis.

Vasogenic edema occurs from increased vascular permeability allowing plasma leakage into extracellular space. Cytotoxic edema results from inflammatory injury causing intracellular swelling of neurons and glia. Interstitial edema develops from impaired cerebrospinal fluid reabsorption at arachnoid villi due to inflammatory exudates, potentially contributing to hydrocephalus.

Bacterial virulence factors such as polysaccharide capsules resist phagocytosis and complement-mediated killing, enabling pathogens to survive in the bloodstream and reach the central nervous system. Once in the subarachnoid space, bacterial components like lipopolysaccharides and teichoic acids trigger immune activation, initiating the inflammatory cascade that characterizes meningitis pathophysiology.