Key Concepts
Introduction
Meningitis is inflammation of the meninges (pia mater and arachnoid) and the cerebrospinal fluid (CSF) within the subarachnoid space. Bacterial meningitis is most dangerous: organisms (Neisseria meningitidis, Streptococcus pneumoniae, Group B Streptococcus in neonates, Listeria monocytogenes in elderly/immunocompromised) reach the meninges hematogenously or via direct extension. Bacteria multiply rapidly in the protein-rich, complement-poor CSF environment. Bacterial cell wall components (lipopolysaccharide, peptidoglycan) trigger an intense inflammatory cascade: cytokine release (TNF-alpha, IL-1, IL-6) increases blood-brain barrier permeability, allowing neutrophil migration into the CSF. This inflammatory exudate increases CSF viscosity and obstructs CSF reabsorption at the arachnoid granulations, causing communicating hydrocephalus and elevated intracranial pressure (ICP). Cerebral edema (vasogenic from BBB breakdown, cytotoxic from neuronal injury, and interstitial from obstructed CSF flow) further elevates ICP. Vasculitis of meningeal blood vessels can cause cortical infarction. Viral meningitis (most commonly enteroviruses) causes lymphocytic pleocytosis in CSF and is generally self-limited. Mortality in bacterial meningitis is 15-25% even with treatment. On the exam, writers often pair stable-sounding options with unstable data—notice the mismatch before you commit. If the stem names a license or role, reread that...