Pathogenesis of meningitis Risk factors for pathogen entry include immunocompromised state (HIV positive, cancer, chemotherapy patients, etc.), bacteremia, viremia, endocarditis, asplenia, site-specific infections (pneumonia, sinusitis, otitis media), and cranial injury. Following pathogen invasion, the immune system is activated, which produces the complications and clinical features of meningitis. Immune cells and the damaged endothelial cells release matrix metalloproteinases (MMPs), cytokines, and nitric oxide (NO). MMPs and NO induce vasodilation in the cerebral vasculature. Cytokines and chemokines induce capillary wall changes in the blood brain barrier (BBB) leading to the expression of more leukocyte receptors, which increases white blood cell (WBC) binding and extravasation. Further damage to the meninges and endothelial cells increases cytotoxic reactive oxygen species production, which damages pathogens as well as the nearby cells. Collectively, these changes lead to an elevated intracranial pressure (ICP), cerebral edema, meningeal irritation, and neuronal death. #Meningitis #Pathophysiology #Pathogenesis
