Epidemiology, Diagnosis, and Antimicrobial Treatment of Acute Bacterial Meningitis

Brouwer, Matthijs C.; Tunkel, Allan R.; Beek, Diederik van de

doi:10.1128/cmr.00070-09

Cited by 723 publications

(754 citation statements)

References 362 publications

(591 reference statements)

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“…Community-acquired bacterial meningitis is a severe infectious disease with high morbidity and mortality rates (Brouwer et al 2010), and is most commonly caused by Streptococcus pneumoniae (van de Beek et al 2004b). Acquired immunodeficiency previously has been associated with an increased risk of bacterial meningitis (Adriani et al 2013;van Veen et al 2016;Weisfelt et al 2010).…”

Section: Introductionmentioning

confidence: 99%

Bacterial Meningitis in Patients using Immunosuppressive Medication: a Population-based Prospective Nationwide Study

Veen

Brouwer

Ende

et al. 2016

J Neuroimmune Pharmacol

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We studied occurrence, presentation, disease course, effect of adjunctive dexamethasone, and prognosis of bacterial meningitis in patients using immunosuppressive medication. Patients were selected from our nationwide, prospective cohort on community-acquired bacterial meningitis performed from March 1, 2006 through October 31, 2014. Eighty-seven of 1447 episodes (6 %) of bacterial meningitis occurred in patients using immunosuppressive medication, and consisted of corticosteroids in 82 %. Patients with bacterial meningitis using immunosuppressive medication were less likely to present with headache (P = 0.02) or neck stiffness (P = 0.005), as compared those not on immunosuppressive medication. In 46 % of episodes CSF leukocyte count was below 1000/mm 3 . CSF cultures revealed S. pneumoniae in 41 % and L. monocytogenes in 40 % of episodes. Outcome was unfavorable in 39 of 87 episodes (45 %) and death occurred in 22 of 87 episodes (25 %). Adjunctive dexamethasone was administered in 52 of 87 (60 %) episodes, and mortality tended to be lower in those on adjunctive dexamethasone therapy as compared to those without dexamethasone therapy (10 of 52 [19 %] vs 12 of 35 [34 %], P = 0.14). We conclude that bacterial meningitis in patients using immunosuppressive medication is likely to present with atypical clinical and laboratory features, and is often caused by atypical bacteria, mainly L. monocytogenes. Adjunctive dexamethasone is widely prescribed in these patients and was not associated with harm in this study.

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Section: Introductionmentioning

confidence: 99%

Bacterial Meningitis in Patients using Immunosuppressive Medication: a Population-based Prospective Nationwide Study

Veen

Brouwer

Ende

et al. 2016

J Neuroimmune Pharmacol

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“…No homologous sequence of those molecules was detected in Ccs4. Despite abundant epidemiological data that S. pneumoniae is the most common cause of bacterial meningitis [3], only four pneumococcal factors have been reported to contribute to BBB penetration. Furthermore, NanA, CbpA, and RrgA are not considered to be competence-inducible molecules [25].…”

Section: Discussionmentioning

confidence: 99%

“…Infection with the Gram-negative bacterium E. coli is also an important cause of bacterial meningitis [3], and the transmembrane proteins, such as OmpA [31] and YijP [32], contribute to hBMEC adhesion and invasion. OmpA loops, which mediate bacterial entry into hBMECs, have been identified [31,33].…”

Section: Discussionmentioning

confidence: 99%

“…Bacterial meningitis is a significant problem in many areas of the world, especially in developing countries [3], while the mortality rate associated with pneumococcal meningitis has reached 30% in some areas, with sequelae such as hearing loss, focal neurological deficit, and cognitive impairment occurs in approximately 50% of survivors [1,4]. …”

Section: Introductionmentioning

confidence: 99%

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Competence-induced protein Ccs4 facilitates pneumococcal invasion into brain tissue and virulence in meningitis

et al. 2018

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Streptococcus pneumoniae is a major pathogen that causes pneumonia, sepsis, and meningitis. The candidate combox site 4 (ccs4) gene has been reported to be a pneumococcal competence-induced gene. Such genes are involved in development of S. pneumoniae competence and virulence, though the functions of ccs4 remain unknown. In the present study, the role of Ccs4 in the pathogenesis of pneumococcal meningitis was examined. We initially constructed a ccs4 deletion mutant and complement strains, then examined their association with and invasion into human brain microvascular endothelial cells. Wild-type and Ccs4-complemented strains exhibited significantly higher rates of association and invasion as compared to the ccs4 mutant strain. Deletion of ccs4 did not change bacterial growth activity or expression of NanA and CbpA, known brain endothelial pneumococcal adhesins. Next, mice were infected either intravenously or intranasally with pneumococcal strains. In the intranasal infection model, survival rates were comparable between wild-type strain-infected and ccs4 mutant strain-infected mice, while the ccs4 mutant strain exhibited a lower level of virulence in the intravenous infection model. In addition, at 24 hours after intravenous infection, the bacterial burden in blood was comparable between the wild-type and ccs4 mutant strain-infected mice, whereas the wild-type strain-infected mice showed a significantly higher bacterial burden in the brain. These results suggest that Ccs4 contributes to pneumococcal invasion of host brain tissues and functions as a virulence factor.

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“…Countries of the African ‘meningitis belt’ have for over 100 years experienced large meningococcal meningitis epidemics [2–4]. Multilocus sequence typing (MLST) of carriage and disease isolates has shown that between the late 1980s and 2010, epidemic waves of colonization and disease were mainly associated with hypervirulent serogroup A clones with the sequence types (ST) 5, 7, and 2859 [5–8].…”

Section: Introductionmentioning

confidence: 99%

Spontaneous point mutations in the capsule synthesis locus leading to structural and functional changes of the capsule in serogroup A meningococcal populations

Ispasanie

Micoli²,

Lamelas

et al. 2018

Virulence

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Whole genome sequencing analysis of 100 Neisseria meningitidis serogroup A isolates has revealed that the csaABCD-ctrABCD-ctrEF capsule polysaccharide synthesis locus represents a spontaneous point mutation hotspot. Structural and functional properties of the capsule of 11 carriage and two disease isolates with non-synonymous point mutations or stop codons in capsule synthesis genes were analyzed for their capsular polysaccharide expression, recognition by antibodies and sensitivity to bactericidal killing. Eight of eleven carriage isolates presenting capsule locus mutations expressed no or reduced amounts of capsule. One isolate with a stop codon in the O-acetyltransferase gene expressed non-O-acetylated polysaccharide, and was not recognized by anti-capsule antibodies. Capsule and O-acetylation deficient mutants were resistant to complement deposition and killing mediated by anti-capsular antibodies, but not by anti-lipopolysaccharide antibodies. Two capsule polymerase mutants, one carriage and one case isolate, showed capsule over-expression and increased resistance against bactericidal activity of both capsule- and lipopolysaccharide-specific antibodies. Meningococci have developed multiple strategies for changing capsule expression and structure, which is relevant both for colonization and virulence. Here we show that point mutations in the capsule synthesis genes substantially contribute to the repertoire of genetic mechanisms in natural populations leading to variability in capsule expression.

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Epidemiology, Diagnosis, and Antimicrobial Treatment of Acute Bacterial Meningitis

Cited by 723 publications

References 362 publications

Bacterial Meningitis in Patients using Immunosuppressive Medication: a Population-based Prospective Nationwide Study

Bacterial Meningitis in Patients using Immunosuppressive Medication: a Population-based Prospective Nationwide Study

Competence-induced protein Ccs4 facilitates pneumococcal invasion into brain tissue and virulence in meningitis

Spontaneous point mutations in the capsule synthesis locus leading to structural and functional changes of the capsule in serogroup A meningococcal populations

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