Nitric oxide production during bacterial and viral meningitis in children.

Abstract

Nitric oxide is very likely to play a role in physiopathological mechanisms of bacterial meningitis. As shown by in vitro studies, nitric oxide is toxic to endothelial cells, as well as to neurones, and thus may be responsible for neurological sequelae in bacterial meningitis. Increased level of nitric oxide can also inhibit mitochondrial respiration, enhancing anaerobic glycolysis. Twenty-seven children with documented bacterial meningitis, 73 with viral (mumps and enteroviral) meningitis, and 51 controls were studied. All children with bacterial meningitis were given cefotaxime (200 mg/kg per day). Glucose and protein concentrations and cerebrospinal fluid cell counts were determined routinely, as well as nitrite and nitrate levels. The levels of nitrite and nitrate in cerebrospinal fluid on admission were higher in patients with bacterial meningitis than in controls or in children with viral meningitis. In 10 patients, dexamethasone therapy (0.4 mg/kg every 12 h for 2 days) was started about 10 min before the first antibiotic dose. A significantly lower nitrite concentration was observed after 24-48 h of treatment compared with non-steroid-treated patients. Significant positive correlations between the nitrite and granulocyte counts and the protein concentration in cerebrospinal fluid were found in all patients with meningitis. Increased nitric oxide production in cerebrospinal fluid during the acute phase of bacterial meningitis may result from the inflammatory process and tissue injury. Dexamethasone administered before the first parenteral antibiotic dose seems to reduce nitric oxide production in the cerebrospinal fluid during bacterial meningitis.