Bacterial meningitis is an important cause of mortality and morbidity despite advances in antimicrobial therapy. A key factor that contributes to the high prevalence of this condition is the incomplete understanding of its pathogenesis. Most cases of bacterial meningitis develop as a result of haematogenous spread, but it is unclear how circulating bacteria cross the blood–brain barrier, and how bacterial entry into the central nervous system results in inflammation and in complications such as pleocytosis, blood–brain barrier disruption and neuronal injury. Recent studies have shed light on the pathogenic mechanisms of bacterial translocation across the blood–brain barrier and the meningitis-associated complications. I propose that bacterial translocation, a key step for the development of meningitis, is the result of specific bacteria–host interactions, and that its complications are the result of multiple host responses to the invading microorganism.