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Meningitis is an inflammation of the protective membranes covering the brain and the spinal cord. Meningitis can have different causes, and discriminating between meningitis etiologies is still considered a hard task, especially when some specific clinical parameters, mostly derived from blood and cerebrospinal fluid analysis, are not completely available. Although less frequent than its viral version, bacterial meningitis can be fatal, especially when diagnosis is delayed. In addition, often unnecessary antibiotic and/or antiviral treatments are used as a solution, which is not cost or health effective. In this work, we address this issue through the use of machine learning-based methodologies. We consider two distinct cases. In one case, we take into account both blood and cerebrospinal parameters; in the other, we rely exclusively on the blood data. As a result, we have rules and formulas applicable in clinical settings. Both results highlight that a combination of the clinical parameters is required to properly distinguish between the two meningitis etiologies. The results on standard and clinical datasets show high performance. The formulas achieve 100% of sensitivity in detecting a bacterial meningitis. [ABSTRACT FROM AUTHOR]

Central nervous system oxygen toxicity (CNS-OT) seizures occur with little or no warning, and no effective mitigation strategy has been identified. Ketogenic diets (KD) elevate blood ketones and have successfully treated drug-resistant epilepsy. We hypothesized that a ketone ester given orally as R,S-1,3-butanediol acetoacetate diester (BD-AcAc(2)) would delay CNS-OT seizures in rats breathing hyperbaric oxygen (HBO(2)). Adult male rats (n = 60) were implanted with radiotelemetry units to measure electroencephalogram (EEG). One week postsurgery, rats were administered a single oral dose of BD-AcAc(2), 1,3-butanediol (BD), or water 30 min before being placed into a hyperbaric chamber and pressurized to 5 atmospheres absolute (ATA) O2. Latency to seizure (LS) was measured from the time maximum pressure was reached until the onset of increased EEG activity and tonic-clonic contractions. Blood was drawn at room pressure from an arterial catheter in an additional 18 animals that were administered the same compounds, and levels of glucose, pH, Po(2), Pco(2), β-hydroxybutyrate (BHB), acetoacetate (AcAc), and acetone were analyzed. BD-AcAc(2) caused a rapid (30 min) and sustained (>4 h) elevation of BHB (>3 mM) and AcAc (>3 mM), which exceeded values reported with a KD or starvation. BD-AcAc(2) increased LS by 574 ± 116% compared with control (water) and was due to the effect of AcAc and acetone but not BHB. BD produced ketosis in rats by elevating BHB (>5 mM), but AcAc and acetone remained low or undetectable. BD did not increase LS. In conclusion, acute oral administration of BD-AcAc(2) produced sustained ketosis and significantly delayed CNS-OT seizures by elevating AcAc and acetone.