Bacterial meningitis is a medical emergency requiring prompt recognition and evaluation and urgent institution of appropriate antibacterial therapy. The nature of the causative microorganisms has changed dramatically over time. For example, the introduction and widespread use of the Haemophilus influenzae type b proteinpolysaccharide vaccine has reduced the number of cases of H influenzae meningitis in the United States by 94%, and shifted the median age of patients with meningitis from 15 months to 25 years. 1 The use of the septa-valent pneumococcal protein-polysaccharide vaccine and of the quadrivalent conjugate vaccine against Neisseria meningitidis will likely have additional significant impact in preventing meningitis. In the early 1900s, meningitis due to H influenzae or Streptococcus pneumoniae was invariably fatal. Mortality dropped to 25–35% for S pneumoniae and 5–10% for H influenzae and N meningitidis meningitis after the introduction of sulfonamides followed by penicillin in the 1930s and 1940s. Empiric treatment regimens employing vancomycin and a third generation cephalosporin came into widespread use in the early 1990s, but have had little additional impact on mortality. 2 This failure is not due to inadequate control of bacterial infection, as modern antibiotic regimens sterilize the CSF in 90% of patients within 48 hours. 3 The key to reducing mortality further is likely to lie in interrupting the cascade of events initiated by bacterial entry into the CNS, including triggering of CNS inflammatory responses, oxidative stress, apoptotic cascades, and alterations in microvascular permeability that lead to neuronal death, cerebral edema, and increased intracranial pressure. 4 Currently, dexamethasone is the only adjuvant targeting these events of proven therapeutic benefit. Dexamethasone reduces mortality from S pneumoniae meningitis in adults from 34% to 14%, but has no significant impact on other forms of bacterial meningitis. 5 New therapies based on an understanding of pathophysiology are desperately needed. In the Netherlands, approximately 85% of all patients with bacterial meningitis have CSF and blood isolates sent to the Reference Laboratory for Bacterial Meningitis. Between October 1998 and April 2002, this laboratory identified 1,108 patients with bacterial meningitis, and clinical and laboratory data were ultimately collected on 68% of these cases, encompassing 696 episodes of community-acquired meningitis in 671 patients. Among this group, 51% of cases were due to S pneumoniae, 37% to N meningitidis, 4% to Listeria monocytogenes, and 8% to other organisms. 6 An article in this issue of Neurology® evaluates the occurrence and prognostic relevance of seizures in this cohort. 7

The authors found that seizures occurred in 17% of the 696 meningitis episodes. There were 107 patients with in-hospital seizures, which were generalized in 59%, focal in 20%, and focal with secondary generalization in 21%. These results are similar to the 45–71% distribution for generalized, 16–36% for focal, and 13–14% for focal plus generalized seizures reported by others. 8, 9 In the entire group of patients with seizures, the median number of seizures was 2. Seventy-five percent of seizures occurred before or within 48 hours of hospitalization, paralleling results in other studies indicating that 60–80% of seizures occur within this window. 8, 9 The authors compared the clinical characteristics of patients with and without seizures. Seventy-nine percent of patients with in-hospital seizures and 76% of the smaller group with prehospital seizures had meningitis caused by S pneumoniae (as compared to 46–48% in compa-