Bacterial Meningitis

Bacterial meningitis is a severe infectious disease involving inflammation of the meninges, the protective membranes surrounding the brain and spinal cord. It occurs when pathogenic bacteria cross the blood–brain barrier and enter the cerebrospinal fluid. Common causative organisms include Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae type b, Listeria monocytogenes, and Escherichia coli K1. The exact route of entry varies by pathogen and host condition.

Routes of Entry into the Central Nervous System

Pathogenic bacteria typically reach the meninges through hematogenous spread, direct extension, or anatomical defects. Hematogenous dissemination is the most common route, where bacteria colonize mucosal surfaces (such as the nasopharynx or gastrointestinal tract), breach the epithelial barrier, and enter the bloodstream. From there, they cross the blood–brain barrier using adhesins and invasins.

Adhesion and Invasion of Epithelial Cells

The pathogenesis of N. meningitidis begins with colonization of the nasopharyngeal epithelium. Type IV pili and specific outer membrane proteins mediate strong adhesion to epithelial cell surfaces. Once anchored, the bacteria disrupt tight junctions between epithelial cells, compromising barrier integrity. This disruption allows the bacteria to traverse the epithelial layer and gain entry into the bloodstream.

Immune Evasion and Endotoxin Release

In the bloodstream, N. meningitidis releases outer membrane vesicles containing Lipid A, a toxic component of its lipooligosaccharide (LOS) layer. Lipid A acts as an endotoxin, provoking a robust immune response characterized by cytokine release, inflammation, and vasodilation. While this inflammatory reaction contributes to disease symptoms, some bacterial cells evade immune clearance by residing within macrophages and other phagocytic cells. These immune cells inadvertently transport the bacteria to the blood–brain barrier.

Penetration of the Blood–Brain Barrier and Meningeal Inflammation

Specialized adhesins facilitate the attachment of N. meningitidis to endothelial cells of the blood–brain barrier. The bacteria then penetrate into the cerebrospinal fluid (CSF), where they multiply and trigger a strong inflammatory response. This inflammatory process, driven by immune cell recruitment and mediator release, results in swelling of the meninges and the characteristic symptoms of meningococcal meningitis, including headache, fever, and neck stiffness.