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

Hypoglycorrhachia (abnormally low cerebro spinal fluid glucose content) eludes exact numerical definition, largely because of the dynamic equilibrium between blood and CSF glucose. A group of 181 pediatric patients with a CSF glucose less than 50 mg/100 ml or a CSF/blood glucose ratio less than 0.50 were studied. Hypoglycorrhachia was present in patients with bacterial meningitis, aseptic meningitis, meningeal carcinomatosis, subarachnoid hemmorrhage, and hypoglycemia. Markedly diminished CSF glucose values were seen primarily in patients with bacterial meningitis. Higher CSF/blood glucose ratios predominated in those with hypoglycemia and neonates with low-normal blood sugars. Following bacterial meningitis and hypoglycemia, aseptic meningitis (including five children with documented enterovirus meningitis and one with documented mumps meningitis) was the third most common cause of hypoglycorrhachia in children. When readily available, positive CSF viral cultures may allow early cessation of antibiotic therapy in two types of patients with meningitis and hypoglycorrhachia: (1) those receiving previous recent antibiotic therapy, and (2) those with CSF findings more typical of a bacterial meningitis.
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PMID:Hypoglycorrhachia in pediatric patients. 93 86

Excessive extracellular fluid concentrations of the amino acids glutamate and aspartate play an important role in the pathogenesis of neuronal cell damage during hypoxia, hypoglycemia, and seizure. The purpose of these investigations was to test the hypothesis that bacterial meningitis causes progressive increase in excessive extracellular fluid concentrations of excitatory and inhibitory neurotransmitters. To test this hypothesis, Escherichia coli was injected intracisternally in juvenile rabbits after which neurotransmitter concentrations were measured with in vivo microdialysis. The data showed significant elevation of the excitatory amino acids aspartate and glutamate, as well as of the inhibitory neurotransmitters gamma-amino butyric acid and taurine in the excessive extracellular fluid of animals injected with E. coli compared with control animals injected with saline. However, concentrations of these excitatory and inhibitory amino acids rose late in the course of meningitis, at a time when the animals were hypotensive (mean blood pressure < or = 40 mm Hg). These data show that the major increase in excitatory neurotransmitters during experimental meningitis occurs in association with the cerebral ischemia produced by septic shock rather than being produced by the meningitis itself.
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PMID:Effect of experimental Escherichia coli meningitis on concentrations of excitatory and inhibitory amino acids in the rabbit brain: in vivo microdialysis study. 790 33

Excitatory amino acids are increasingly implicated in the pathogenesis of neuronal injury induced by a variety of CNS insults, such as ischemia, trauma, hypoglycemia, and epilepsy. Little is known about the role of amino acids in causing CNS injury in bacterial meningitis. Several amino acids were measured in cerebrospinal fluid and in microdialysis samples from the interstitial fluid of the frontal cortex in a rabbit model of pneumococcal meningitis. Cerebrospinal fluid concentrations of glutamate, aspartate, glycine, taurine, and alanine increased significantly in infected animals. Among the amino acids with known excitatory or inhibitory function, interstitial fluid concentrations of glutamate were significantly elevated (by 470%). Alanine, a marker for anaerobic glycolysis, also increased in the cortex of infected rabbits. The elevated glutamate concentrations in the brain extracellular space suggest that excitotoxic neuronal injury may play a role in bacterial meningitis.
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PMID:Amino acids in cerebrospinal and brain interstitial fluid in experimental pneumococcal meningitis. 809 28

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

Bacterial meningitis is still a major cause of death and disability in children worldwide. With the advent of conjugate vaccines against the three major pathogens, the burden of disease is increasingly concentrated in developing countries that cannot afford the vaccines. Antibiotic resistance is an increasing problem; in developed countries, high-level resistance to beta-lactams among Streptococcus pneumoniae necessitates the addition of vancomycin to third-generation cephalosporins. In many developing countries, the problems are more fundamental. Increasing resistance of S. pneumoniae to penicillin and chloramphenicol and of Haemophilus influenzae to chloramphenicol means that many children with bacterial meningitis receive ineffective treatments, as third-generation cephalosporins are often unavailable or unaffordable. Case fatality rates are as high as 50% and neurological sequelae occur in one-third of survivors. The use of corticosteroids in meningitis is controversial; the evidence that they protect against neurological complications of childhood meningitis (particularly severe hearing loss) is strongest when: meningitis is caused by H. influenzae type b; dexamethasone is given before the first dose of antibiotics; a bactericidal antibiotic such as a third-generation cephalosporin is used; and in the early stages of the infection. There are few controlled clinical trials on which to base recommendations about other adjuvant therapy for meningitis. Avoidance of secondary brain injury from hypoxia, hypotension, hypo-osmolarity and cerebral oedema, hypoglycaemia or convulsions is essential for a good outcome. The problem of bacterial meningitis will only be solved if protein-conjugate vaccines (or other effective vaccine strategies) against S. pneumonia, H. influenzae and epidemic strains of Neisseria meningitidis are available to all the world's children. Making third-generation cephalosporins affordable in the developing world is also a necessary intervention, but better antibiotics will not overcome the problems of poor access to hospitals and late presentation with established brain injury, and will inevitably bring further pressure for antimicrobial resistance.
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PMID:The management of bacterial meningitis in children. 1287 33

Acute encephalitis/encephalopathy is a life-threatening disease, and early diagnosis is important. The acute encephalitis/encephalopathy is characterized by impaired consciousness, delirium, convulsion, pyrexia, vomiting, headache, paralysis and so on. We need to distinguish various diseases with similar symptoms, such as febrile seizure, bacterial meningitis, acute disseminated encephalomyelitis, cerebrovascular disease, non-convulsive status epilepticus, benign convulsion with gastroenteritis, hypoglycemia, inherited metabolic disease, toxicosis, heat attack, somatoform disorder and so on, from acute encephalitis/encephalopathy. We describe the features of these diseases in point of view with difference from acute encephalitis/encephalopathy. A synthetic and prompt evaluation including medical interview, neurological sign, blood examination, computed tomography, magnetic resonance imaging, spinal fluid examination, electroencephalogram, is necessary to diagnose as acute encephalitis/encephalopathy.
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PMID:[Differential diagnosis for diseases similar to acute encephalitis/encephalopathy]. 2140 Aug 45