Wellmer, Andreas

[["dc.bibliographiccitation.firstpage","6881"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Infection and Immunity"],["dc.bibliographiccitation.lastpage","6886"],["dc.bibliographiccitation.volume","69"],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Ragheb, J."],["dc.contributor.author","Zysk, G."],["dc.contributor.author","Kunst, T."],["dc.contributor.author","Smirnov, Alexey"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T08:28:39Z"],["dc.date.available","2018-11-07T08:28:39Z"],["dc.date.issued","2001"],["dc.description.abstract","Tumor necrosis factor alpha (TNF-alpha) and TNF-beta are key mediators in bacterial inflammation. We therefore examined the role of TNF-alpha and its two receptors in murine pneumococcal central nervous system infection. TNF-alpha knockout mice and age- and sex-matched controls and TNF receptor (p55 and p75)-deficient mice and heterozygous littermates were infected intracerebrally with a Streptococcus pneumoniae type 3 strain. Mice were monitored until death or were killed 36 h after infection. Bacterial titers in blood, spleen, and brain homogenates were determined. Leukocyte infiltration and neuronal damage were assessed by histological scores. TNF-alpha -deficient mice died earlier than the controls after intracerebral infection although overall survival was similar. TNF-alpha deficiency did not inhibit leukocyte, recruitment into the subarachnoid space and did not lead to an increased density of bacteria in brain homogenates. However, it caused a substantial rise of the concentration of S. pneumoniae cells in blood and spleen. Spleen bacterial titers were also increased in p55- and p75-deficient mice. TNF receptor-deficient mice showed decreased meningeal inflammation. Neuronal damage was not affected by either TNF-alpha or TNT receptor deficiency. In a murine model of pneumococcal peritonitis, 10(2) CFU of S. pneumoniae produced fatal peritonitis in TNF-alpha -deficient, but not wild-type, mice. Early leukocyte influx into the peritoneum was impaired in TNF-alpha -deficient mice. The lack of TNF-alpha or its receptors renders mice more susceptible to S. pneumoniae infections."],["dc.identifier.doi","10.1128/IAI.69.11.6881-6886.2001"],["dc.identifier.isi","000171739200040"],["dc.identifier.pmid","11598062"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16471"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0019-9567"],["dc.title","Effect of deficiency of tumor necrosis factor alpha or both of its receptors on Streptococcus pneumoniae central nervous system infection and peritonitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","909"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Scandinavian Journal of Infectious Diseases"],["dc.bibliographiccitation.lastpage","913"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Prange, J."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Zysk, G."],["dc.contributor.author","Lange, P."],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T09:39:30Z"],["dc.date.available","2018-11-07T09:39:30Z"],["dc.date.issued","2001"],["dc.description.abstract","Increased total CSF lactate is an important indicator differentiating bacterial from aseptic meningitis. Bacteria can produce D- and L-lactate; mammalian cells produce only L-lactate. We measured D- and L-lactate production of Streptococcus pneumoniae, Staphylococcus aureus, Neisseria meningitidis and Escherichia coli in vitro, of S. pneumoniae and E. coli in rabbit experimental meningitis and of various common pathogens in CSF from patients with bacterial meningitis. Despite marked in vitro production of D-lactate by S. aureus (maximum: 4.59 mmol/l; i.e. 34.9% of total lactate), N. meningitidis (4.62 mmol/l; i.e. 98.1%) and E. coli (3.14 mmol/l; i.e. 97.2%), minimal amounts were measured in human S. aureus (0.38 mmol/l; i.e. 1.3% of total lactate) or N. meningitidis (0.28 mmol/l; i.e. 3.9%) and experimental E. coli meningitis (0.75 mmol/l; i.e. 4.4%). In only 9 of 54 human CSF samples did D-lactate exceed 0.15 mmol/l. S. pneumoniae did not produce significant amounts of D-lactate in vitro (maximum; 0.55 mmol/l; i.e. 2.7% of total lactate), in experimental meningitis (0.18 mmol/l; i.e. 3%) or in human cases of meningitis (0.28 mmol/l; i.e. 1.9%). In conclusion, increased total CSF lactate in meningitis consists mainly of L-lactate and originates predominantly from host cells. CSF D-lactate is of limited diagnostic value."],["dc.identifier.isi","000173355800006"],["dc.identifier.pmid","11868764"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33300"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Taylor & Francis As"],["dc.publisher.place","Oslo"],["dc.relation.conference","40th Interscience Conference on Antimicrobial Agents and Chemotherapy"],["dc.relation.eventlocation","TORONTO, CANADA"],["dc.relation.issn","0036-5548"],["dc.title","D- and L-lactate in rabbit and human bacterial meningitis"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","325"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurocritical Care"],["dc.bibliographiccitation.lastpage","329"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Djukic, M."],["dc.contributor.author","Bottcher, T."],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Brocke, V. V."],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T08:44:15Z"],["dc.date.available","2018-11-07T08:44:15Z"],["dc.date.issued","2005"],["dc.description.abstract","Rifampin, a protein synthesis inhibitor, reduced mortality in a mouse model of meningitis compared to bacteriolytic cephalosporin standard therapy. To assess whether moxifloxacin (known to cause a less rapid bacteriolysis than cephalosporins) can similarly reduce mortality, mice infected with Streptococcus pneumoniae by deep intracerebral injection were treated subcutaneously with either 200 mg/kg of moxifloxacin or ceftriaxone every 8 hours for 5 days (n=49 each). They were then observed for an additional 8 days. Overall mortalities were 35 and 29 in moxifloxacin- and ceftriaxone-treated mice, respectively (p=0.29). Kaplan-Meier survival analysis also revealed no statistically significant differences (p=0.32). Moxifloxacin failed to reduce mortality compared to cephalosporin standard therapy."],["dc.identifier.doi","10.1385/NCC:2:3:325"],["dc.identifier.isi","000231204500015"],["dc.identifier.pmid","16159084"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20158"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Humana Press Inc"],["dc.relation.issn","1541-6933"],["dc.title","Moxifloxacin in experimental Streptococcus pneumoniae cerebritis and meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","137"],["dc.bibliographiccitation.issue","2-3"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","140"],["dc.bibliographiccitation.volume","296"],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Noeske, C."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Munzel, U."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T11:20:54Z"],["dc.date.available","2018-11-07T11:20:54Z"],["dc.date.issued","2000"],["dc.description.abstract","Survivors of bacterial meningitis frequently suffer from long-term sequelae, particularly from learning and memory deficits. For this reason, spatial memory and learning was studied in a mouse model of ceftriaxone-treated Streptococcus pneumoniae meningitis. Persistent deficits of spatial learning despite normal motor function were observed in mice infected with 10(4) colony-forming units (CFU) in 25 mul of saline into the right forebrain in comparison to mice treated with an equal amount of saline. Survivors of meningitis performed significantly worse in memorizing a hidden platform in a Morris water maze. After 2 weeks, the difference between post-meningitis and control mice diminished. Yet, when the platform was moved after 180 days, learning of the new location was still strongly impaired in mice surviving meningitis. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/S0304-3940(00)01645-1"],["dc.identifier.isi","000165859800019"],["dc.identifier.pmid","11109000"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55647"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Spatial memory and learning deficits after experimental pneumococcal meningitis in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","767"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Antimicrobial Agents and Chemotherapy"],["dc.bibliographiccitation.lastpage","770"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Smirnov, Alexey"],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Maier, K."],["dc.contributor.author","Henne, S."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T08:56:14Z"],["dc.date.available","2018-11-07T08:56:14Z"],["dc.date.issued","2000"],["dc.description.abstract","In a rabbit model of Streptococcus pneumoniae meningitis, 5 mg of gemifloxacin mesylate (SB-265805) per kg/h reduced the bacterial titers in cerebrospinal fluid (CSF) almost as rapidly as 10 mg of ceftriaxone per kg/h (Delta log CFU/ml/h +/- standard deviation [SD], -0.25 +/- 0.09 versus -0.38 +/- 0.11; serum and CSF concentrations of gemifloxacin were 2.1 +/- 1.4 mg/liter and 0.59 +/- 0.38 mg/liter, respectively, at 24 h). Coadministration of 1 mg of dexamethasone per kg did not affect gemifloxacin serum and CSF levels (2.7 +/- 1.4 mg/liter and 0.75 +/- 0.34 mg/liter, respectively, at 24 h) or activity (Delta log CFU/ml/h +/- SD, -0.26 +/- 0.11)."],["dc.identifier.doi","10.1128/AAC.44.3.767-770.2000"],["dc.identifier.isi","000085399200049"],["dc.identifier.pmid","10681354"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23091"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0066-4804"],["dc.title","Gemifloxacin is effective in experimental pneumococcal meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1560"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Critical Care Medicine"],["dc.bibliographiccitation.lastpage","1564"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Azeh, I."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Wellhausen, M."],["dc.contributor.author","Koenig, B."],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T10:20:11Z"],["dc.date.available","2018-11-07T10:20:11Z"],["dc.date.issued","2002"],["dc.description.abstract","Objective: The release of proinflammatory components from bacteria depends on the mode of action of the antibacterial therapy used. We studied whether this influences mortality in experimental sepsis. Design. In a lethal murine model of Staphylococcus aureus sepsis, animals were randomly assigned to receive the protein synthesis inhibitor clindamycin (CLI) or the beta-lactam ceftriaxone (CRO). Setting. Therapy was introduced subcutaneously 5 hrs after intraperitoneal injection of 107 colony forming units of S. aureus American Type Culture Collection 29213 and was continued every 8 hrs for 3 days. Measurements and Results: Survival was higher in mice receiving CLI (29/50 animals [58%]) than in mice receiving CRO (16/50 animals [32%]; p = 015). Mice treated with CRO died earlier than mice receiving CLI (p = .002). Eight hours after the first antibiotic dose, the motor performance of mice receiving CRO had deteriorated more than it did for mice receiving CLI (p = .009). Higher levels of tumor necrosis factor-alpha were measured in serum (p = .027) and peritoneal fluid (p = .001) of CRO-treated mice. In vitro, CLI released smaller amounts of staphylococcal enterotoxin A than CRO. Conclusions: Antibiotic treatment of Gram-positive sepsis with a protein synthesis inhibitor decreases morbidity and mortality compared with a bacteriolytic compound. This may be caused by a reduction of the concentrations of proinflammatory/toxic bacterial components and cytokines."],["dc.identifier.doi","10.1097/00003246-200207000-00027"],["dc.identifier.isi","000176841100027"],["dc.identifier.pmid","12130979"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41828"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0090-3493"],["dc.title","Protein synthesis inhibiting clindamycin improves outcome in a mouse model of Staphylococcus aureus sepsis compared with the cell wall active ceftriaxone"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2095"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","The Journal of Infectious Diseases"],["dc.bibliographiccitation.lastpage","2098"],["dc.bibliographiccitation.volume","181"],["dc.contributor.author","Bottcher, T."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Smirnov, A. V."],["dc.contributor.author","Fakhrjanali, F."],["dc.contributor.author","Mix, E."],["dc.contributor.author","Pilz, J."],["dc.contributor.author","Zettl, Uwe K."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T10:48:14Z"],["dc.date.available","2018-11-07T10:48:14Z"],["dc.date.issued","2000"],["dc.description.abstract","Bacterial compounds induce the production of reactive oxygen species (ROS) in meningitis. Rifampin releases smaller quantities of proinflammatory compounds from Streptococcus pneumoniae than do beta-lactam antibiotics. Therefore, rabbits infected intracisternally with S. pneumoniae were treated intravenously either with rifampin 5 mg/kg/h or ceftriaxone 10 mg/kg/h (n = 9 each). Before initiation of antibiotic treatment, a strong positive correlation between ROS production of cerebrospinal fluid (CSF) phagocyte populations and bacterial CSF titers was observed (granulocytes: r(s) = .90, P < .0001; monocytes: r(s) = .81, P < .0001). CSF leukocytes from rifampin-treated rabbits produced less ROS (monocytes at 2 h after initiation of treatment: P = .045; at 5 h: P = .014; granulocytes at 5 h: P = .036) than did leukocytes from animals receiving ceftriaxone. The CSF malondialdehyde concentrations and the density of apoptotic neurons in the dentate gyrus were lower in rifampin- than in ceftriaxone-treated animals (P = .002 and .005). The use of rifampin to reduce the release of ROS and to decrease secondary brain injury appears promising."],["dc.identifier.doi","10.1086/315518"],["dc.identifier.isi","000087923900038"],["dc.identifier.pmid","10837202"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48141"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Univ Chicago Press"],["dc.relation.issn","0022-1899"],["dc.title","Rifampin reduces production of reactive oxygen species of cerebrospinal fluid phagocytes and hippocampal neuronal apoptosis in experimental Streptococcus pneumoniae meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","490"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","European Journal of Clinical Microbiology & Infectious Diseases"],["dc.bibliographiccitation.lastpage","493"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Fleischer, H."],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Munzel, U."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T08:54:47Z"],["dc.date.available","2018-11-07T08:54:47Z"],["dc.date.issued","2001"],["dc.description.abstract","In order to study the release of DNA from Streptococcus pneumoniae in vitro during spontaneous growth and treatment with ceftriaxone or rifampin, a semiquantitative polymerase chain reaction was used. During spontaneous growth, high concentrations of bacterial DNA were released. Exposure to 10 mug/ml of ceftriaxone decreased the DNA release, in median, by 19 times (P=0.03 vs. spontaneous growth). Treatment with 10 mug/ml of rifampin led to a reduction of DNA release, in median, by a factor of 49 (P=0.03 vs. ceftriaxone; six experiments performed on different days)."],["dc.identifier.isi","000170686200008"],["dc.identifier.pmid","11561806"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22749"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0934-9723"],["dc.title","Reduced release of DNA from Streptococcus pneumoniae after treatment with rifampin in comparison to spontaneous growth and ceftriaxone treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2169"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Antimicrobial Agents and Chemotherapy"],["dc.bibliographiccitation.lastpage","2172"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Smirnov, Alexey"],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Ragheb, J."],["dc.contributor.author","Prange, J."],["dc.contributor.author","Schutz, Ekkehard"],["dc.contributor.author","Wettich, K."],["dc.contributor.author","Kalich, S."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T08:53:31Z"],["dc.date.available","2018-11-07T08:53:31Z"],["dc.date.issued","2001"],["dc.description.abstract","In a rabbit model of Streptococcus pneumoniae meningitis single doses of 10 and 2.5 mg of the glycopeptide LY333328 per kg of body weight reduced bacterial titers in cerebrospinal fluid (CSF) almost as rapidly as ceftriaxone at 10 mg/kg/h (changes in log CPU, -0.29 +/- 0.21 and -0.26 +/- 0.22 versus -0.34 +/- 0.15/ml/h). A dose of 1 mg/kg was bacteriostatic (change in log CPU, 0.01 +/- 0.11/ml/h). In two animals receiving LY333328 at a dose of 40 mg/kg the bacterial titers were reduced by 0.54 and 0.51 log CFU/ml/h. The penetration of CSF by LY333328 was 1 to 5%. The concentrations of lipoteichoic and teichoic acids in CSF and neuronal damage were similar in ceftriaxone- and LY333328-treated animals."],["dc.identifier.doi","10.1128/AAC.45.7.2169-2172.2001"],["dc.identifier.isi","000169416800043"],["dc.identifier.pmid","11408247"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22430"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0066-4804"],["dc.title","Activity of LY333328 in experimental meningitis caused by a Streptococcus pneumoniae strain susceptible to penicillin"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6504"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Infection and Immunity"],["dc.bibliographiccitation.lastpage","6508"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Zysk, G."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Kunst, T."],["dc.contributor.author","von Mering, M."],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T09:52:27Z"],["dc.date.available","2018-11-07T09:52:27Z"],["dc.date.issued","2002"],["dc.description.abstract","Pneumolysin, neuraminidases A and B, and hyaluronidase are virulence factors of Streptococcus pneumoniae that appear to be involved in the pathogenesis of meningitis. In a murine model of meningitis after intracerebral infection using mutants of S. pneumoniae D39, only mice infected with a pneumolysin-deficient strain were healthier at 32 and 36 h, had lower bacterial titers in blood at 36 h, and survived longer than the D39 parent strain. Cerebellar and spleen bacterial titers, meningeal inflammation, and neuronal damage scores remained uninfluenced by the lack of any of the virulence factors."],["dc.identifier.doi","10.1128/IAI.70.11.6504-6508.2002"],["dc.identifier.isi","000178675100075"],["dc.identifier.pmid","12379738"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36126"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0019-9567"],["dc.title","Decreased virulence of a pneumolysin-deficient strain of Streptococcus pneumoniae in murine meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]