Despite effective antibiotic therapy, pneumococcal meningitis remains a serious disease with a case fatality rate of 15-25%. Furthermore, long term residues affect up to 50% of survivors. One of the most frequent sequelae is sensorineural hearing loss. In a retrospective study of 87 patients with pneumococcal meningitis, hearing impairment occurred in 26% of survivors. Unfortunately, sufficient treatment regimens are still missing. However, recent animal studies of pneumococcal meningitis have provided new insights into the pathology and pathophysiology of meningitis-associated hearing loss. These studies have demonstrated that the bacteria most likely enter the cochlea through the perilymphatic duct. Once arrived in the perilymphatic spaces, they induce a severe suppurative labyrinthitis. Blood-labyrinth barrier disruption develops, hair cells are damaged, and neurons in the spiral ganglion undergo (mostly necrotic) cell death, leading to meningitis-associated hearing loss. Reactive oxygen and nitrogen species, in particular peroxynitrite, seem to be among the crucial mediators of cochlear damage and hearing loss during meningitis. In our rat model of pneumococcal meningitis, adjunctive therapy with the antioxidants and peroxynitrite scavengers Mn(III)tetrakis(4-bencoic acid)-porphyrin (MnTBAP) and N-Acetyl-L-Cystein (NAC) signifi-cantly attenuated acute and long term hearing loss. In several other animal studies of pneumococcal meningitis, adjunctive antioxidant therapy also protected infected animals from intracranial complications. NAC is already in clinical use (e.g., in the treatment of acetaminophen intoxications), and only minor adverse reactions have been reported. Therefore, the use of NAC seems to be a promising future treatment option in pneumococcal meningitis.