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

Infectious meningitis in adults was reviewed to establish the frequency of meningitis due to each causative agent and to reexamine the laboratory parameters that help to distinguish aseptic, bacterial, and mycobacterial meningitis. Aseptic meningitis occurred 2.2 times more often than bacterial and mycobacterial meningitis combined. The most common nonviral causative agent was the pneumococcus (23 cases) followed by the tubercle bacillus (11 cases) and the meningococcus (5 cases). Cerebrospinal fluid (CSF) Gram stain was the most useful study to rule in a bacterial cause: 89% of cases of bacterial meningitis had a positive initial Gram stain. Hyponatremia occurred in 73% of cases of tuberculous meningitis; hyponatremia combined with a negative Gram stain was highly suggestive of a tuberculous cause. One third of all patients with tuberculous and aseptic meningitis had a predominance of neutrophils in the CSF. No patient with aseptic meningitis had a CSF while count higher than 2,800 cells/cu mm or a CSF protein value higher than 250 mg/100 ml. Other reviews confirm this if cases due to lymphocytic choriomeningitis (LCM) are excluded. One patient with tuberculous meningitis in this series, and none of those cases reviewed, had a CSF white count higher than 1,200 cells/cu mm. Only 3.7% of the patients with aseptic meningitis had hypoglycorrhachia. Series reporting exclusively disease due to mumps and LCM have a higher frequency of hypoglycorrhachia.
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PMID:Recent survey of infectious meningitis in adults: review of laboratory findings in bacterial, tuberculous, and aseptic meningitis. 126 6

In order to establish the epidemiologic features of infectious meningitis in the adult population in our environment, the experience of the Department of Neurology of the Hospital del Rey during the 3-year period, from 1984 to 1986, has been analyzed. Three-hundred-ninety episodes were handled, of which, 51% were acute bacterial meningitis, 45% were acute lymphocytic meningitis, 26% were tuberculous meningitis, 1% were brucellar meningitis and 0.5% were due to Candida albicans. Acute bacterial meningitis predominated in winter, whereas acute lymphocytic meningitis predominated in summer (p less than 0.001). Forty-seven percent of acute bacterial meningitis were due to Neisseria meningitidis and 14.5% of acute lymphocytic meningitis with virologic study, were due to Herpesviridae. The mortality rate of acute bacterial meningitis was 8.5% and that of tuberculous meningitis was 10%. In order to emphasize the importance of these processes, the main epidemiologic data are compared with that of other studies.
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PMID:[Infectious meningitis in the adult: 3-year clinical experience]. 262 82

During a one year period tumour necrosis factor-alpha (TNF-alpha) was prospectively determined in the cerebrospinal fluid of 49 patients with infectious meningitis. TNF-alpha was found in the cerebrospinal fluid of 15 of 18 patients with bacterial meningitis. In 11 patients who had cerebrospinal fluid positive for TNF-alpha it was detected in only one serum (in low concentration). There was no significant correlation between the concentration of TNF-alpha in cerebrospinal fluid and the patient's age, duration of illness and fever, body temperature, and serum C reactive protein. However, cerebrospinal fluid protein concentrations of greater than or equal to 2 g/l and leucocyte values of greater than or equal to 2.5 X 10(9)/l were more often associated with high TNF-alpha concentrations (greater than or equal to 500 pg/ml). In contrast with bacterial meningitis, none of the 31 samples of cerebrospinal fluid from patients with viral meningitis was positive for TNF-alpha. Thus this investigation supports the conclusion, drawn from animal studies on TNF-alpha in the cerebrospinal fluid, that the presence of TNF-alpha is indicative of bacterial meningitis. Absence of TNF-alpha cerebrospinal fluid, however, was found here not to exclude a bacterial aetiology of the infection.
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PMID:Tumour necrosis factor-alpha in infectious meningitis. 281 47

The anaphylatoxin C5a has been implicated in the pathogenesis of bacterial meningitis as a potent mediator of inflammation in the subarachnoid space. We investigated the expression of the receptor for C5a (C5aR) in brains of mice with experimental Listeria monocytogenes (LM) meningoencephalitis. In the course of the disease, infiltrating cells in the meninges and the ventricles were found to express C5aR mRNA and protein. In the brain parenchyma, very low constitutive C5aR expression was seen on pyramidal neurons and Purkinje cells. However, in LM-infected mice, a dramatic increase in C5aR expression occurred on neurons starting 6 h after infection and was maximal between 24 and 36 h. TNF-alpha was identified as an essential mediator of neuronal C5aR expression, since mice lacking the genes for TNF and lymphotoxin-alpha (TNF/lymphotoxin-alpha -/- mice) showed significantly attenuated C5aR expression after LM infection. Furthermore, i.p. injection of recombinant TNF-alpha induced enhanced C5aR expression in the brains of TNF/lymphotoxin-alpha -/- mice and in normal animals even in the absence of a bacterial infection. We also assessed the levels of anaphylatoxin C5a in the cerebrospinal fluid of patients with infectious meningitis. C5a was detected in all patients with bacterial meningitis (n = 9), in 6 of 18 patients with aseptic meningitis, and in 1 of 66 control patients. The finding of TNF-alpha-mediated C5aR expression on neurons in experimental Listeria meningitis and the detection of the ligand, C5a, in the cerebrospinal fluid of human patients with infectious meningitis present new directions in the investigation of the pathophysiologic sequelae leading to secondary brain damage.
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PMID:TNF-alpha-mediated expression of the receptor for anaphylatoxin C5a on neurons in experimental Listeria meningoencephalitis. 921 5

The evaluation of TNF-alpha and CRP in cerebrospinal fluid (CSF) concentrations determining in the differential diagnosis of infectious meningitis was shown. The highest concentrations of these parameters were detected in the group of patients with bacterial meningitis. The findings correlated with the severity of clinical course of bacterial meningitis and with the routine determined laboratory data of CSF. Usefulness of examination CSF for TNF-alpha and CRP in differential diagnosis of meningitis was underlined, especially in cases, where routine parameters of CSF are not conclusive.
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PMID:[Evaluation of tumor necrosis factor and C-reactive protein level determination in cerebrospinal fluid of meningitis and encephalitis]. 942 22

Chemokines constitute a constantly growing family of small inflammatory cytokines. They have been implied in many different diseases of the CNS including trauma, stroke and inflammation, e.g., multiple sclerosis. In this review we focus on the role of chemokines in infectious meningitis of bacterial or viral origin. In experimental bacterial meningitis induced by Listeria monocytogeneses both CXC and CC chemokines namely MIP-1alpha, MIP-1beta and MIP-2 are produced intrathecally by meningeal macrophages and leukocytes which infiltrate into the CNS. In patients with bacterial meningitis, IL-8, GROalpha, MCP-1, MIP-1alpha and MIP-1beta are detectable in the CSF. These chemokines contribute to CSF mediated chemotaxis on neutrophils and PBMC in vitro. In viral meningitis IL-8, IP-10 and MCP-1 are identified in the CSF to be responsible for chemotactic activity on neutrophils, PBMC and activated T cells. Taken collectively these data indicate that the recruitment of leukocytes in infectious meningitis involves the intrathecal production of chemokines.
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PMID:Chemokines and chemotaxis of leukocytes in infectious meningitis. 962 95

A hallmark of infectious meningitis is the invasion of leukocytes into the subarachnoid space. In experimental meningitis triggered by tumor necrosis factor-alpha and interleukin-1beta, the interaction of leukocytes with endothelial cells and the subsequent migration of the cells through the vessel wall can be inhibited by an antibody to the junctional adhesion molecule (JAM). In contrast to the cytokine-induced meningitis model, anti-JAM antibodies failed to prevent leukocyte influx into the central nervous system after infection of mice with Listeria monocytogenes or lymphocytic choriomeningitis virus. Furthermore, in bacterial meningitis, anti-JAM IgG antibodies, but not Fab fragments, caused disruption of the endothelium. Likewise complement-dependent antibody-mediated cytotoxicity was observed in cultured brain endothelial cells treated with anti-JAM IgG but not with its Fab fragment.
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PMID:Antibodies to the junctional adhesion molecule cause disruption of endothelial cells and do not prevent leukocyte influx into the meninges after viral or bacterial infection. 1095 Aug 2

The pathogenesis of tuberculous meningitis is still unclear. Recently, vascular endothelial growth factor (VEGF) was found to be associated with inflammatory diseases and we found the increased serum level of VEGF in pulmonary tuberculosis. We hypothesized that VEGF might be associated with the pathogenesis of tuberculous meningitis and measured serum and cerebrospinal fluid (CSF) levels of VEGF in 28 patients with tuberculous meningitis and 31 non-tuberculous infectious meningitis patients (13 bacterial meningitis patients, eight fungal meningitis patients and 10 patients with viral meningitis) before therapy. We examined the CSF VEGF levels 3 months after in 12 tuberculous meningitis patients. The serum and CSF levels of VEGF were significantly higher in tuberculous meningitis than in other meningitis. The decrease in titer of CSF VEGF paralleled the clinical improvement of tuberculous meningitis. Immunohistochemical staining of autopsied brains demonstrated the presence of VEGF in the inflammatory mononuclear cells of the dense fibroconnective tissue both in the subarachnoid space and surrounding the vasculitis lesion. We found the expression of VEGF in tuberculous meningitis and think that VEGF reflects its activity.
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PMID:Expression of vascular endothelial growth factor in tuberculous meningitis. 1141 75

We examined whether or not NF-kappaB, a factor that regulates expression of the genes that code for pro-inflammatory cytokines, is activated in cerebrospinal fluid (CSF) cells to investigate the production of pro-inflammatory cytokines by CSF cells in patients with meningitis. Western blotting demonstrated that NF-kappaB was more activated in CSF cells of patients with bacterial meningitis than in those of patients with aseptic meningitis. NF-kappaB was hardly activated in carcinomatous meningitis. The NF-kappaB activation in CSF cells of patients with meningitis tended to be correlated with the CSF interleukin-6 concentration. Our data suggested that CSF cells produce pro-inflammatory cytokines through NF-kappaB activation in meningitis, and that increased NF-kappaB activation in CSF cells indicate infectious meningitis rather than carcinomatous meningitis.
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PMID:NF-kappaB activation in cerebrospinal fluid cells from patients with meningitis. 1239 10

Subarachnoid hemorrhage is the most common cause of cerebral salt wasting syndrome. There are few reports of this condition in infectious meningitis. We describe a patient with hyponatremia and bacterial meningitis. Hyponatremia rapidly improved after administration of sodium chloride. The purpose of this report is to alert clinicians to the fact that hyponatremic patients with central nervous system disease do not necessarily have a syndrome of inappropriate secretion of antidiuretic hormone (SIADH), but may have cerebral salt wasting syndrome. By contrast with SIADH, the treatment requires saline administration.
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PMID:[Cerebral salt wasting syndrome in bacterial meningitis]. 1788 8


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