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)

Three-hundred and forty-nine cases of acute bacterial meningitis treated during a 25-year period (1949 through 1973) were reviewed to determine the prognostic significance of initial historical, physical and laboratory findings. A poor prognosis was associated with age greater than or equal to 40 years (p less than 0.01), presence of predisposing illness (p less than 0.01), associated illness (p less than 0.01), absence of nuchal ridity (p less than 0.05), and derangement of cerebral function (p less than 0.01). The effects of predisposing illness and moderate cerebral dysfunction were dependent upon age. In contrast, the effects of associated illness, mild or severe cerebral dysfunction, and absent nuchal rigidity were independent of age. Laboratory studies associated with a poor prognosis included an elevated cerebrospinal fluid (CSF) protein (p less than 0.05), a positive CSF smear (p less than 0.05), or culture (p less than 0.01), or bacteremia (p less than 0.01). No prognostic significance could be attributed to race (p greater than 0.05), sex (p greater than 0.05), prior antibiotic therapy (p greater than 0.05), duration of illness before institution of adequate therapy (p greater than 0.05), CSF leukocyte count (p greater than 0.05), frequency of polymorphonuclear leukocytes in CSF (p greater than 0.05), CSF sugar less than or equal to 40 mg/100 ml (p greater than 0.05), or a CSF sugar-simultaneous blood sugar ratio less than or equal to 0.40 (p greater than 0.05).
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PMID:Acute bacterial meningitis: an analysis of factors influencing prognosis. 121 6

Viral meningitis is part of the aseptic meningitis syndrome but must be distinguished from bacterial meningitis on the basis of a careful examination of the CSF and sound clinical judgment. Enteroviruses probably account for the bulk of cases of aseptic meningitis that occur in the United States and which are reported to the Centers for Disease Control each year. The seasonal pattern in the incidence of aseptic meningitis is largely due to the seasonal variation of enteroviral infections. Early on, the CSF in patients with viral meningitis frequently contains a predominance of polymorphonuclear leukocytes and may even have a low glucose level. The presence of neutrophils in the initial CSF sample is especially common in patients with enteroviral infections. A CSF glucose level lower than 50 per cent of a simultaneously drawn blood glucose determination is not uncommon in patients with viral meningitis due to mumps, LCM, and herpes simplex. In a patient with a predominance of polymorphonuclear leukocytes in the initial CSF specimen and in whom a viral infection is suspected, antibiotics may be withheld if a spinal tap is repeated within 12 hours. A shift from polymorphonuclear leukocytes to mononuclear cells makes viral meningitis the likely diagnosis. Both herpes simplex and varicella-zoster may infect the meninges by means of spread from cervical and dorsal root ganglia in a retrograde fashion much the way they spread in an antegrade fashion to the skin. HSV-2 is more likely to cause the clinical syndrome of viral meningitis, while HSV-1 is more likely to cause a meningoencephalitis with serious brain dysfunction. The identification of a specific viral agent in body fluids, especially the CSF, in a patient with aseptic meningitis is of more than academic interest, since it can shorten duration of hospital stay and eliminate unnecessary antimicrobial therapy. The diagnosis of enteroviral infections depends upon the isolation of a virus from CSF, stool, or throat plus a fourfold antibody response in the serum to the viral isolate. The 60-odd serotypes of enterovirus, each with different antigenic determinants, preclude serologic testing alone as a useful diagnostic test to identify the patient infected with coxsackievirus or echovirus. For infections, due to herpes simplex, varicella-zoster, LCM, and arboviruses, a serologic test alone can be useful.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Viral meningitis. 399 Apr 41

Sprague-Dawley rats have a marked age-related susceptibility to Haemophilus influenzae type b that does not correlate with serum bactericidal activity. Eighty percent of 5-day-old animals that survive to 48 h after an intraperitoneal inoculation of a mean lethal dose of bacteria have histologically documented meningitis. Animals surviving the inoculations as infants manifest cerebral dysfunction as adults. This model should facilitate experimental study of bacterial meningitis.
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PMID:Production of Haemophilus influenzae b meningitis in infant rats by intraperitoneal inoculation. 454 33

The EEG of the newborn consists of a mixed activity which varies from 1 to 22/s. Waves in the alpha band may occur, but they indicate cerebral dysfunction if they are seen in a rhythmic uninterrupted sequence. Eight newborns who showed rhythmic alpha activity in their EEG are included in our study. This activity occurred together with rhythmic theta waves or was followed by them as part of ongoing electrographic seizure activity. All newborns studied were very sick. Three suffered from severe perinatal asphyxia with persistent fetal circulation; in addition one of them had bacterial meningitis. Two infants suffered from herpes encephalitis. In those cases the rhythmic alpha activity temporarily showed a certain periodicity. This EEG pattern was also seen in a small for gestational age premature infant who had septicemia and subarachnoid hemorrhage and in two extremely premature babies with intraventricular hemorrhage. Four infants were curarized. All of the others also had clinically observed seizures. Rhythmic alpha-activity in the neonatal EEG represents an electrical seizure discharge. It may also occur in premature infants who suffer from intraventricular hemorrhage. Obviously it does not have a diagnostic value. The prognostic value depends upon the underlying disease and the grade of background suppression in the EEG. Anticonvulsant therapy should be administered early using a sufficient dosage.
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PMID:[Rhythmic alpha activity in the EEG of premature and newborn infants]. 640 15

Glutamic acid decarboxylase (GAD) activity in cerebrospinal fluid (CSF) was determined in 53 patients with neurological diseases as follows: Epilepsy (n:17), febrile convulsions (n:3), meningoencephalitis (n:17), encephalopathies (n:10), CNS leukemia (n:3), congenital hydrocephalus (n:2) and pseudoileus neonatorum (n:1). Compared with the mean normal value (5.2 +/- 2.5 pmol CO2 formed/hr/ml) reported in Part I, a significant increase of GAD activity in CSF was demonstrated in patients with uncontrolled epileptic seizures (11.4 +/- 3.9 pmol CO2 formed/hr/ml), febrile convulsions (13.5 +/- 8.7), viral meningitis with or without encephalitis (20.3 +/- 13.6), encephalopathies (30.0 +/- 25.9), CNS leukemia (11.1 +/- 5.0), congenital hydrocephalus (20.5 +/- 7.3) and pseudoileus neonatorum (28.6). Markedly high GAD activity was found in patients with CNS leukemia several days after intrathecal injection of methotrexate (39.8 +/- 18.0). On the other hand, significantly low GAD activity was shown in patients with bacterial meningitis or brain abscess (1.3 +/- 1.2). This suggests that some bacterial factors may be inhibitory toward GAD activity in CSF. High GAD activity in CSF may be useful as an indicator of aseptic brain dysfunction, although it was not always correlated with the severity of symptoms.
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PMID:Glutamic acid decarboxylase in cerebrospinal fluid in infancy and childhood Part II. Glutamic acid decarboxylase activity in cerebrospinal fluid of children with neurological diseases. 666 Apr 21

A sample of 22 subjects was studied from a population of adults who had suffered from bacterial meningitis in childhood. Audiovestibular, oculomotor and neuropsychological investigations were performed and quality of life was assessed. An age-matched control group of 20 subjects was recruited. In the meningitis group, nine subjects had abnormal pure tone audiograms. One was previously undiagnosed and a progression was found in four. There was an overrepresentation of subclinical vestibular pathology (6 out of 9 (67%)) in this group. Audiovestibular test results showed a peripheral pattern and oculomotor tests were normal. The quality of life scores of those with hearing loss were significantly higher than those in the control group. Neuropsychological tests of brain dysfunction were abnormal in six out of 22 (27%) who had recovered from meningitis. The prevalence of such dysfunctions was not related to audiovestibular disorder. The quality of life scores of those with brain dysfunctions were similar to those of the control group. The findings of reduced auditory memory and tone level perception in four out of 22 (18%), suggest that lesions of central auditory pathways may follow from bacterial meningitis. The results support the idea that inner ear damage is the major cause of hearing loss after bacterial meningitis. Despite the absence of brainstem involvement, central nervous system lesions with disturbed auditory processing and language functions can be of significance. The high frequency of discrete brain dysfunctions indicate that a thorough neuropsychological investigation is required after bacterial meningitis.
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PMID:Audiovestibular and neuropsychological outcome of adults who had recovered from childhood bacterial meningitis. 969 25

Until the introduction of antibiotics in the 1930s and 1940s, acute bacterial meningitis was fatal in most cases. Since then it has become curable with a variable mortality and morbidity rate for individual pathogens and patients. Neuropathological and clinical studies have shown that a fatal outcome of the disease is often due to central nervous system (CNS) complications including cerebrovascular involvement, brain oedema formation, and hydrocephalus resulting in increased intracranial pressure and seizure activity. During recent years, experimental studies with animal models have substantially increased our knowledge of the interactions of bacterial pathogens with mammalian cells and their entry into the CNS, and the complex pathophysiological mechanisms of brain dysfunction during acute bacterial meningitis. There is now a substantial body of evidence that cytokines, chemokines, proteolytic enzymes, and oxidants are involved in the inflammatory cascade that leads to tissue destruction in bacterial meningitis. Genetic targeting and/or pharmacological blockade of these pathways was beneficial in experimental bacterial meningitis. Apart from dexamethasone, these treatment strategies hold major promise for the adjunctive therapy of acute bacterial meningitis in clinical practice.
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PMID:Pathogenesis and pathophysiology of pneumococcal meningitis. 1246 88

Death and co-morbidity derived from acute bacterial meningitis remain unacceptably high and are mainly related to immune-mediated cerebral dysfunction. Cerebral edema, hydrocephalus and ischaemic cerebrovascular events are severe complications that eventually occur following the activation of a complex network of cytokines, chemokines, proteases and oxidants released after cerebrospinal fluid infection. The caspase pathway appears to play a central role in the induction and amplification of the host inflammatory response. Such overactive immune reactions induce brain cell damage but, importantly, they may potentially be blocked. Several agents have been developed aiming to counteract the deleterious effects of such immune imbalance. These drugs are candidates to become adjuvant therapy against acute bacterial meningitis in the future, in addition to dexamethasone. We review the current state-of-art of bacterial meningitis adjuvant therapy, including caspase inhibitors, antioxidants, poly (ADP-ribose) polymerase inhibitors, inhibitors of lipid peroxidation and metalloproteinase inhibitors.
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PMID:Advances in adjuvant therapy against acute bacterial meningitis. 1557 71

The generation of intense inflammation in the subarachnoid space in response to meningitis-causing bacteria contributes to brain dysfunction and neuronal injury in bacterial meningitis. Microglia, the major immune effector cells in the central nervous system (CNS), become activated by bacterial components to produce proinflammatory immune mediators. In this study, we showed that FimH adhesin, a tip component of type 1 fimbriae of meningitis-causing Escherichia coli K1, activated the murine microglial cell line, BV-2, which resulted in the production of nitric oxide and the release of tumor necrosis factor-alpha. Mitogen-activated protein kinases, ERK and p-38, and nuclear factor-kappaB were involved in FimH adhesin-mediated microglial activation. These findings suggest that FimH adhesin contributes to the CNS inflammatory response by virtue of activating microglia in E. coli meningitis.
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PMID:FimH adhesin of Escherichia coli K1 type 1 fimbriae activates BV-2 microglia. 1603 24