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

The aims of the present study were to document the epidemiology, clinical features and complications of childhood acute bacterial meningitis (ABM) in The Sudan during both an inter-epidemic (endemic) period (1985-1986), and the 1988 serogroup A epidemic; and to examine the phenotypic and genetic similarities and differences of Neisseria meningitidis strains isolated in The Sudan and Sweden. A new enzyme immunoassay test (Pharmacia Meningitis EIA-Test) was evaluated as a potential rapid diagnostic method for the detection of Haemophilus influenzae (HI) type b, Neisseria meningitidis (MC) and Streptococcus pneumoniae (PNC). The test was found to have good sensitivity (0.86) and specificity (0.95) in the inter-epidemic period; and to be adaptable to the field work in The Sudan during the 1988 MC epidemic. During inter-epidemic (endemic) situations in The Sudan, greater than 90% of childhood ABM was caused by one of the three organisms, HI type b, MC and PNC. HI accounted for 57% of the cases. The peak incidence (76%) of HI cases was in infants (less than 12 months) similar to the situation in other African countries. The overall case fatality ratio was 18.6%. Prospective follow-up of survivors for 3-4 years revealed that an additional 43% either died or had permanent neurological complications, the most prevalent and persistent of which was sensorineural hearing loss recorded in 22% of long term survivors. Post-meningitic children were found to have significantly lower intelligence quotients (92.3 +/- 13.9) than their sibling controls (100.7 +/- 10.2, P = 0.029). Features of the large serogroup A sulphonamide resistant MC epidemic (February-August 1988) in Khartoum are described. An estimated annual incidence of 1,679/100,000 was recorded at the peak of the epidemic. The highest attack rate was in young children less than 5 years, as in many other African countries; nevertheless, a high morbidity was observed in adults (31% of the cases greater than or equal to 20 years). The clinical features, mortality (6.3%) and short term sequelae in Sudanese children were generally within the framework described for MC disease elsewhere. Detailed analysis of MC isolates from Sudan and Sweden by characterizing their electrophoretic enzyme types, DNA restriction endonuclease pattern and outer membrane proteins, revealed that serogroup A MC clone III-1 was responsible of The Sudan epidemic in 1988 and has been the dominant serogroup A organism in Sweden since 1973. The Sudanese strains isolated prior to the epidemic (1985) were clone IV-1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Childhood acute bacterial meningitis in the Sudan: an epidemiological, clinical and laboratory study. 211 7

The soluble form of a bacteriophage-induced endo-N-acetylneuraminidase (Endo-N) specific for hydrolyzing oligo- or poly-alpha-2,8-linked sialosyl units in sources as disparate as bacterial and neural membrane glycoconjugates was purified approximately 10,000-fold and characterized. The enzyme appears homogenous by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and has a subunit Mr 105,000. This corresponds to one of the higher Mr phage proteins which comprises 7.5% (by weight) of the total phage protein. The holoenzyme is active at neutral pH and has a Mr by gel filtration of 328,000, suggesting that the active enzyme is a trimer. Endo-N requires a minimum of 5 sialyl residues (DP5, where DP represents degree of polymerization) for activity. The limit digest products from the alpha-2,8-linked polysialic acid capsule of Escherichia coli K1 are DP4 with some DP3 and DP1,2. DP2-4 do not appear to inhibit depolymerization of polysialic acid. Endo-N digestion of the polysialosyl moiety on neural cell adhesion molecules yields sialyl oligomers with DP3 and DP4. The presence of a terminal sialitol changes both the distribution of limit digestion products and the apparent minimum substrate size. Higher Mr alpha-2,8-linked sialyl polymers (approximately DP200) are better substrates (Km 50-70 microM) than sialyl oligomers of approximately DP10-20 (Km 1.2 mM). Endo-N activity is inhibited by DNA and several other poly-anions tested. An examination of the distribution of intermediate products shows that Endo-N binds and cleaves at random sites on the polysialosyl chains, in contrast to initiating cleavage at one end and depolymerizing processively. Endo-N can serve as a specific molecular probe to detect and selectively modify poly-alpha-2,8-sialosyl carbohydrate units which have been implicated in bacterial meningitis and neural cell adhesion.
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PMID:Purification and properties of a bacteriophage-induced endo-N-acetylneuraminidase specific for poly-alpha-2,8-sialosyl carbohydrate units. 354 9

The successful development and implementation of rational strategies for the prevention of bacterial meningitis should be facilitated by acquiring a more detailed knowledge of its pathophysiology. We have used a biologically relevant rat model of meningitis in conjunction with classical microbial genetics and recombinant DNA technology to investigate the molecular basis of Haemophilus influenzae pathogenicity. These studies aim to define how specific bacterial genes mediate the potential of H. influenzae to colonize the nasopharynx, disseminate within the blood stream and invade the central nervous system. By identifying the state or stages in the pathogenic sequence for which the determinant is critical, this approach should also provide insight into the relevant host defense mechanisms which determine resistance or susceptibility. An understanding of the genetic basis of H. influenzae pathogenicity may develop basic knowledge relevant to the treatment and prevention of bacterial meningitis.
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PMID:Pathogenesis of meningitis: experimental studies on the molecular basis of Haemophilus influenzae infection. 624 9

Detection of cytomegalovirus (CMV) DNA by the polymerase chain reaction (PCR) in samples of cerebrospinal fluid (CSF) has been shown to be a sensitive method of diagnosing CMV disease in the central nervous system. Since CMV causes latent infection in white blood cells, an unanswered question is whether detection of latent CMV DNA in the cell fraction of CSF samples by PCR is possible in seropositive patients. In a prospective study, the finding of CMV DNA in CSF of CMV seropositive patients with suspected viral infection of the central nervous system (CNS) was evaluated clinically. Fractionation of 64 CSF samples from seropositive patients was carried out before analysing the samples for CMV DNA by PCR. In four of the five patients who had CMV DNA in the cell pellet and/or supernatant, the clinical data suggested CMV-associated neurological disease. The remaining 59 samples were negative in both pellet and supernatant. In addition, 11 CSF samples with high cell counts from patients with bacterial meningitis were examined for CMV DNA and found to be negative in 10 patients and positive in 1. One hundred thirty two uncentrifuged CSF samples were used as negative controls. The results of the study indicate that detection of CMV DNA in CSF samples by PCR correlated well with disease and was not due to latent CMV infection.
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PMID:Detection of cytomegalovirus DNA in cerebrospinal fluid in immunocompetent patients as a sign of active infection. 756 3

An easy, reproducible and semi-quantitative, non-radioactive method for the analysis of mRNA expression for various cytokines, (i.e., Interleukin (IL)-1 beta, IL-4, IL-6, tumor necrosis factor (TNF)-alpha, lymphotoxin (LT), transforming growth factor (TGF)-beta, interferon (IFN)-gamma and endothelin-1 (ET-1)) in cells from cerebrospinal fluid (CSF) and peripheral blood mononuclear cells (PBMC) has been established. By means of polymerase chain reaction primers that cover a splice junction, amplification of contaminating DNA was omitted. Densitometric scanning of ethidium bromide-stained agarose gels proved to be very sensitive for semiquantitative analysis of PCR products. Serial tenfold dilutions of cDNA revealed a log-linear regression from 10(6) to 10(2) cells under optimal cycle conditions. The intra- and inter-assay variability of the method was below 10%. With this assay, the cytokine expression pattern of as few as 10(4) mononuclear cells from blood or CSF was determined. This method made it possible to detect differences in the cytokine gene expression pattern of mononuclear cells from patients with different neurological diseases. CSF cells from 43 patients with various neurological diseases were analyzed. TNF-alpha, LT, and IL-1 mRNA were prominent in the CSF cells of most patients with bacterial meningitis. TNF-alpha, LT, IFN-gamma and IL-6 mRNAs were detected in patients with active multiple sclerosis, whereas TNF-alpha, IL-6, and endothelin-1 mRNA expression was found frequently in patients with HIV encephalitis. Pro-inflammatory cytokines were rarely detected in CSF cells from patients with non-inflammatory diseases of the central nervous system. In blood mononuclear cells from patients with multiple sclerosis, TNF-alpha mRNA expression was associated with disease activity. The sensitivity, specificity, velocity and reliability of this assay considerably facilitates the analysis of cytokine production in mononuclear cells even in conditions where only a limited number of cells is available for analysis.
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PMID:Semi-quantitative analysis of cytokine gene expression in blood and cerebrospinal fluid cells by reverse transcriptase polymerase chain reaction. 778

Primers specific to conserved and variable regions in the 16S rRNA sequence were selected from the partially sequenced 16S rRNA genes of Neisseria meningitidis, Haemophilus influenzae, Streptococcus pneumoniae, S. agalactiae, and Staphylococcus epidermidis. The PCR assay was divided into two DNA amplifications. The first resulted in a general bacterial amplicon, and the second resulted in a species-specific amplicon. The high specificity of the PCR assay was documented after testing bacteria of 28 different species (133 strains). A total of 304 clinical cerebrospinal fluid samples, including 125 samples from patients with bacterial meningitis, were assayed to investigate the diagnostic sensitivity and specificity for bacterial meningitis. The assay showed high sensitivity (0.94) and specificity (0.96) with the clinical samples, although some false results were obtained, the reasons for which are discussed. With agarose gel electrophoresis for detection of the PCR products, the detection limit for meningococci in cerebrospinal fluid was 3 x 10(2) CFU/ml.
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PMID:Detection of bacterial DNA in cerebrospinal fluid by an assay for simultaneous detection of Neisseria meningitidis, Haemophilus influenzae, and streptococci using a seminested PCR strategy. 785 65

The patient was a 75-year-old male, who simultaneously showed symptoms of bacterial meningitis during steroid treatment for erythroderma and symptoms of respiratory failure. Based on ground-glass shadows in both lungs on chest X ray, bronchoalveolar lavage (BAL) was carried out and strongyloides was detected. In addition to strongyloidiasis, the patient was shown to have the complication of pneumocystis carinii (PC) pneumonia after PC DNA was detected in BAL fluid using a PCR assay. When other causes for immunodeficiency affecting the incidence of opportunistic infection were investigated, the ATL virus was detected in peripheral blood cells and monoclonal amplification was indicated, though the presence of anti-ATL antibody was negative. According to the results, this patient was found to have early stage adult T cell leukemia. In conclusion, we treated this adult T cell leukemia patient who had strongyloidiasis and amplification of PC DNA in BAL and for which the PCR assay, a new technology used for diagnosing PC pneumonia, was considered to be effective.
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PMID:[A case of adult T cell leukemia complicated with strongyloidiasis and amplification of pneumocystis carinii DNA in bronchoalveolar lavage fluid]. 804 Oct 45

The value of DNA single-cell cytometry for the detection of neoplasia in Feulgen-stained cerebrospinal fluid cytological specimens was tested on 34 cases of Non-Hodgkin's lymphoma or leukemia and on 66 cases of viral or bacterial meningitis as a disease control group. The DNA content of 200 randomly chosen nuclei was measured on one pre-existing, cytologically representative slide per case, using a TV-image analysis system TAS-plus (Leitz, Germany). Neoplasia was diagnosed, if at least three nuclei with a DNA content above 5c (5cEE > or = 3) were found. The sensitivity investigating only one slide per case was 79.4% (27/34), the specificity 78.8% (52/66). Three lymphomas and 7 inflammatory cases were classified as suspicious (0 < 5cEE < 3). In 4 lymphoma cases (11.8%) a false-negative diagnosis and in 7 cases (10.6%) of viral meningitis a false-positive diagnosis were made. No false-positive diagnosis occurred in bacterial meningitis. While the false-negative diagnoses may be due to the only slightly increased number of cells in cerebrospinal fluid, no final explanation for increased DNA values after viral infection can be given. Therefore, before using DNA single-cell cytometry to prove the malignant character of lymphocytic pleocytosis in cerebrospinal fluid, viral meningitis has to be clinically excluded.
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PMID:DNA single cell cytometry in lymphocytic pleocytosis of the cerebrospinal fluid. 831 Jul 92

Apoptotic neuronal death and the increase of neuron-specific enolase (NSE) in cerebrospinal fluid (CSF) were studied in a rabbit model of experimental pneumococcal meningitis after treatment with antimicrobial (ceftriaxone) and antiinflammatory agents (dexamethasone, monoclonal antibodies against the beta-subunit of beta 2-integrins [anti-CD18 mAb]). Twenty-four hours after infection, apoptotic cell death was found solely in the granular cell layer of the dentate gyrus. Neurons with DNA fragmentation were quantified with the in situ tailing (IST) reaction. Dexamethasone and anti-CD18 mAb inhibited the NSE increase in CSF significantly (p = 0.003, p = 0.011). After administration of dexamethasone the density of apoptotic neurons was significantly higher than in control animals receiving only ceftriaxone (p = 0.044). The median of the density of apoptotic neurons was lower in the dentate gyrus in animals receiving anti-CD18 mAb and ceftriaxone vs those receiving only ceftriaxone, although the difference did not reach statistic significance (p = 0.058). In conclusion, apoptotic cell death occurs in the dentate gyrus during the early phase of bacterial meningitis. The extent was influenced by antiinflammatory therapy. The systemic administration of glucocorticoids increased the quantity of apoptotic neurons in the dentate gyrus but reduced overall neuronal damage as indicated by low levels of NSE concentration in CSF.
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PMID:Anti-inflammatory treatment influences neuronal apoptotic cell death in the dentate gyrus in experimental pneumococcal meningitis. 864 98

A combination of universal and species-specific primers was used to detect and differentiate by nested polymerase chain reaction (PCR) the four species most commonly causing bacterial meningitis. Primers recognising conserved sequences in the 16S and 23S ribosomal RNA genes were employed to amplify the 16S-23S spacer region from Neisseria meningitidis, Haemophilus influenzae (type b), Streptococcus pneumoniae, and Streptococcus agalactiae (group B streptococcus). The sequence of the most abundant spacer product was determined in each case and used to deduce species-specific primers. A nested PCR using universal primers in the first round and a species-specific primer in the second were able to detect and distinguish between the four common pathogens, in the presence of human DNA. Streptococcus pneumoniae DNA was detected in the cerebrospinal fluid of a meningitis patient with negative culture and Gram-stain results.
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PMID:An approach to the identification of the pathogens of bacterial meningitis by the polymerase chain reaction. 868 87


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