Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The condition of the blood-CSF barrier can be evaluated by the simultaneous quantitation of marker proteins in serum and cerebrospinal fluid. The concentration ratios of albumin and alpha 2-macroglobulin, plotted versus the hydrodynamic radii are used as permeability parameter. There are wide ranging barrier disturbances during the early stages of meningitis. In mumps meningitis only slight disturbances were found, meanwhile in bacterial meningitis the barrier permeability was strongly increased. In both disease groups one may detect secretory fractions of both immunglobulins G and A. In some cases of mumps meningitis a prolonged humoral immune reaction was found.
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PMID:[Blood-cerebrospinal fluid barrier and the local immune response in the course of meningitis in childhood]. 9 99

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

The examination of cerebrospinal fluid has provided useful information for diagnosis of CNS infections. The progress of analytical technology has brought the possibility to detect very small amounts of chemical substances. I thought that new information from brain should be obtained by using modern analytical technology for several substances in CSF. Free amino acid pattern, glutamine, homocarnosine, glutamic acid decarboxylase (GAD), neuron specific enolase (NSE) and 2',5'-oligoadenylic acid synthetase (2-5 A) in CSF have been examined for information of brain injury and dysfunctions. The results are as follows. 1) The individual difference and constancy of free amino acid pattern in CSF were found in children without any neurological diseases. 2) The levels of free amino acids in CSF increased in the acute phase of bacterial meningitis. 3) High levels of glutamine in CSF of children with acute bacterial meningitis were normalized during the recovery phase. 4) A marked imbalance of free amino acids in CSF was found in children with Lennox-Gastaut syndrome. 5) A decrease of homocarnosine levels in CSF was related with the degree of unconsciousness in children suffering from neurological diseases. 6) High GAD activities in CSF were observed in the acute phase of aseptic meningitis and after intrathecal injection of methotrexate for the therapy against meningeal leukemia. 7) High NSE activities in CSF were found in the acute phase of bacterial meningitis, intracranial hemorrhage, encephalopathy and encephalitis. 8) High 2-5A activities CSF were measured in the acute phase of mumps meningitis with subsequent decreases during the recovery phase. These results suggest that several substances in CSF are useful as markers of brain injury and dysfunction.
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PMID:[Cerebrospinal fluid as informative source of the brain]. 201 95

A fourfold or greater increase in titer of complement-fixing (CF) antibodies to Mycoplasma pneumoniae was found in 40.7% of paired sera from 54 patients with bacterial meningitis that had been proven by culture and in 10.3% of 39 patients with other bacteremic infections, but in none of eight patients with whooping cough or 40 patients with mumps meningitis. The CF antigen used was a crude lipid antigen, but comparable antibody increases were found by an enzyme-linked immunosorbent assay using a crude M. pneumoniae protein antigen. Increases were also frequently seen in nonspecific antibodies to the capsular polysaccharide of group A Neisseria meningitidis; these increases were significantly, but not completely, correlated to the nonspecific reactions to the mycoplasmal antigens. The data call for caution in interpreting serologic tests for M. pneumoniae when dealing with diseases not commonly associated with M. pneumoniae.
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PMID:Increase in titers of antibodies to Mycoplasma pneumoniae in patients with purulent meningitis. 680 46

Interferon was detected in the cerebrospinal fluid (CSF) of 26 of 51 children with aseptic meningitis, two of 44 with bacterial meningitis, and four of 118 with miscellaneous conditions including encephalitis, convulsive disorders and leukemia with neurological involvement. The geometric mean titre of interferon in mumps meningitis was seven to eight times higher than that in enteroviral meningitis; however, levels of interferon were not related to the concentration of leukocytes in CSF from these patients. Interferon titres were relatively greater at the height of the febrile response in children with mumps meningitis or enteroviral meningitis. There was no association between the presence of interferon in the CSF and the isolation of mumps virus or an enterovirus from the same specimen. Patients frequently developed homologous antibody one to three days after signs of aseptic meningitis, obscuring the relationship of interferon production to clinical improvement.
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PMID:Interferon in the cerebrospinal fluid of children with central nervous system disorders. 2032 6