Bacterial meningitis begins with colonization of the nasopharynx by pathogens (Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae type b, Listeria monocytogenes in neonates/elderly). Bacteremia develops, and organisms cross the blood-brain barrier through receptor-mediated transcytosis or during disruption of the BBB. Within the CSF, bacteria replicate rapidly due to minimal immune defenses (low complement, few immunoglobulins). Bacterial cell wall components trigger release of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), causing neutrophilic infiltration, increased BBB permeability, vasogenic edema, and disrupted CSF flow (interstitial edema). Cytotoxic edema follows as neurons are directly damaged. The cascade results in elevated ICP, reduced cerebral perfusion, and risk of uncal herniation. The nurse coordinates emergent antibiotic administration, performs serial neurological assessments, manages ICP, implements isolation protocols, and coordinates prophylaxis for close contacts.