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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metabolic abnormalities during bacterial meningitis include hypoglycorrhachia and cerebrospinal fluid (CSF) lactate accumulation. The mechanisms by which these alterations occur within the central nervous system (CNS) are still incompletely delineated. To determine the evolution of these changes and establish the locus of abnormal metabolism during meningitis, glucose and lactate concentrations in brain interstitial fluid, CSF, and serum were measured simultaneously and sequentially during experimental pneumococcal meningitis in rabbits. Interstitial fluid samples were obtained from the frontal cortex and hippocampus by using in situ brain microdialysis, and serum and CSF were directly sampled. There was an increase of CSF lactate concentration, accompanied by increased local production of lactate in the brain, and a decrease of CSF-to-serum glucose ratio that was paralleled by a decrease in cortical glucose concentration. Brain microdialysate lactate concentration was not affected by either systemic lactic acidosis or artificially elevated CSF lactate concentration. These data support the hypothesis that the brain is a locus for anaerobic glycolysis during meningitis, resulting in increased lactate production and perhaps contributing to decreased tissue glucose concentration.
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PMID:Lactate and glucose concentrations in brain interstitial fluid, cerebrospinal fluid, and serum during experimental pneumococcal meningitis. 150 Jul 38

The metabolic basis of the encephalopathy associated with acute bacterial meningitis is unknown. The presence of cerebrospinal fluid lactic acidosis and hypoglycorrhachia suggests that intracellular acidosis or cellular energy depletion may play a role. Phosphorus magnetic resonance spectroscopy allows for the noninvasive determination of intracellular pH and relative amounts of phosphate-containing metabolites in humans. In seven normal volunteers, the intracellular pH of a mixed volume of gray and white matter was 7.00 +/- 0.04 (mean +/- SD). The apparent relative intensities of resonances from adenosine triphosphate, phosphocreatine, phosphodiesters and phosphomonoesters, and inorganic phosphate were measured. An encephalopathic patient with pneumococcal meningitis who had severe cerebrospinal fluid lactic acidosis was studied. Brain intracellular pH and relative phosphate metabolite concentrations were normal. Intracellular acidosis and bioenergetic compromise are therefore not causes of encephalopathy in this disease. This also demonstrates that the human brain can maintain tight control of intracellular pH even in the presence of marked extracellular metabolic acidosis.
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PMID:Brain phosphorus magnetic resonance spectroscopy in acute bacterial meningitis. 277 14

We have analyzed cerebral energy metabolism in rabbits with Streptococcus pneumoniae or Escherichia coli meningitis aiming at an increased understanding of the cerebrospinal fluid (CSF) lactacidosis observed in this disease. After intracisternal inoculation of bacteria the lactate concentration in the CSF increased to 9.7 +/- 0.7 (mean +/- SE) mmol/l compared to control values of 3.2 +/- 0.2 mmol/l. Simultaneously sampled brain tissue from parietal cortex, caudate nucleus, and thalamus showed no increase in lactate concentrations. The high-energy phosphate content decreased only marginally, phosphocreatine levels by 11-17% in the cortex and in the caudate nucleus, and adenosine triphosphate concentrations by 15%, but only in the caudate nucleus. Our results indicate that the CSF lactate increase in bacterial meningitis is not primarily linked to cerebral lactacidosis. The decreased concentrations of high-energy phosphates in diseased animals need further study but may be due to increased intracranial pressure and reduced capillary blood flow.
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PMID:Experimental meningitis in the rabbit. II. Cerebral energy metabolism in relation to increased cerebrospinal fluid concentrations of lactate. 330 78

In order to examine the effects of platelet-activating factor (PAF) in complicated Plasmodium falciparum infections, plasma concentrations of lyso-PAF, stable metabolite and principal precursor of PAF, were measured in 25 Vietnamese adults with severe malaria. The concentration of PAF in the cerebrospinal fluid (CSF) was determined in a sub-group of 23 comatose patients and, together with that of lyso-PAF, in the plasma of 20 patients on recovery of consciousness. The concentration of lyso-PAF in the plasma was depressed on admission to hospital (median [range]; 21 [8-143] vs. 293 [215-410] ng/ml in 10 controls; P < 0.001). There was, however, no change in plasma activity of acetylhydrolase which converts PAF to lyso-PAF (P > 0.01 vs. controls) while simultaneous reduction in the concentration of lipoproteins associated with lyso-PAF were less than those of lyso-PAF per se in the plasma. The plasma concentration of lyso-PAF on admission was associated with parasitaemia and the concentration of serum triglycerides (rs = -0.42, P = 0.04 in each case), the latter being consistent with hepatic effects of PAF reported in previous studies. CSF concentrations of PAF on admission were low (2.3 [0.5-7.7] vs. 0.9 [0-2.5] ng/ml after recovery, P < 0.01) compared with values reported previously in bacterial meningitis. Plasma concentrations of lyso-PAF after recovery lay between admission and control values. While increased availability of PAF may reflect parasite burden and may modulate liver-mediated metabolic disturbances such as hypoglycaemia and lactic acidosis, the role of PAF in cerebral malaria is uncertain.
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PMID:The metabolism of platelet-activating factor in severe and cerebral malaria. 858 36