Sensorineural hearing loss (SNHL) is the most common sequel of bacterial meningitis (BM) and is observed in up to 30% of survivors when the disease is caused by Streptococcus pneumoniae. BM is the single most important origin of acquired SNHL in childhood. Anti-inflammatory dexamethasone holds promises as potential adjuvant therapy to prevent SNHL associated with BM. However, in infant rats, pneumococcal meningitis (PM) increased auditory brainstem response (ABR) thresholds [mean difference= 54 decibels sound pressure level (dB SPL)], measured 3 wk after infection, irrespective to treatment with ceftriaxone plus dexamethasone or ceftriaxone plus saline (p< 0.005 compared with mock-infected controls). Moreover, dexamethasone did not attenuate short-and long-term histomorphologic correlates of SNHL. At 24 h after infection, blood-labyrinth barrier (BLB) permeability was significantly increased in infected animals of both treatment groups compared with controls. Three weeks after the infection, the averaged number of type I neurons per square millimeter of the Rosenthal's canal dropped from 0.3019±0.0252 in controls to 0.2227±0.0635 in infected animals receiving saline (p< 0.0005). Dexamethasone was not more effective than saline in preventing neuron loss (0.2462±0.0399; p> 0.05). These results suggest that more efficient adjuvant therapies are needed to prevent SNHL associated with pediatric PM.