Coagulation, coma, and outcome in bacterial meningitis – An observational study of 38 adult cases

Kowalik, Maciej Michał; Smiatacz, Tomasz; Hlebowicz, Maria; Pajuro, Robert; H, Trocha

doi:10.1016/j.jinf.2007.02.002

Cited by 12 publications

(6 citation statements)

References 41 publications

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“…This is consistent with the observed difference in pneumococcal meningitis in a human and mouse model [28,39]. In human bacterial meningitis, it has been suggested that dysregulation of coagulation and fibrinolytic pathways, vascular endothelial cell swelling, and vasculitis plays a role in the pathophysiology of hemorrhages [40][41][42][43][44].…”

Section: Discussionsupporting

confidence: 86%

Characterization of a listeria monocytogenes meningitis mouse model

Koopmans

Brouwer

Serón

et al. 2017

Journal of the Neurological Sciences

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Background: Listeria monocytogenes is a common cause of bacterial meningitis. We developed an animal model of listerial meningitis.Methods: In survival studies, C57BL/6 mice received intracisternal injections with different L. monocytogenes sequence type 1 (ST1) colony forming units per milliliter (CFU; n = 48, 10 5 , 10 6 , 10 7 , 10 8 , and 10 9 CFU/ml). Second, mice were inoculated with 10 8 CFU/ml ST1 and sacrificed at 6 h and 24 h (n = 12/group). Outcome parameters were clinical score, CFUs, cyto-and chemokine levels, and brain histopathology. Third, 84 mice were inoculated (10 9 CFU/ml ST1) to determine optimal antibiotic treatment with different doses of amoxicillin and gentamicin. Fourth, mice were inoculated with 10 9 CFU/ml ST1, treated with amoxicillin, and sacrificed at 16 h and 24 h (n = 12/group) for outcome assessment. Finally, time point experiments were repeated with ST6 (n = 24/group). Results: Median survival time for inoculation with 10 8 and 10 9 CFU/ml ST1 was 46 h and 40 h; lower doses of bacteria led to minimal clinical signs of disease. Brain levels of IL-6, IL-17A, and IFN-γ were elevated at 24 h, and IL-1β, IL-6, IL-10, IFN-γ, and TNF-α were elevated in blood at 6 h and 24 h. Histopathology showed increased meningeal infiltration, vascular inflammation of meningeal vessels, hemorrhages, and ventriculitis. In the treatment model, brain levels of IL-6 and IL-17A and blood levels of IL-6 and IFN-γ were elevated. Compared to ST6, infection with ST1 led initially to higher levels of IL-1β and TNF-α in blood and more profound neuropathological damage. At 16 h post inoculation, IL-1β, IL-10, and TNF-α in blood and IL-6, IL17A, TNF-α, and IFN-γ levels in brain were higher in ST1 compared to ST6 without differences in CFUs between STs. At 24 h, neuropathology score was higher in ST1 compared to ST6 (p = 0.002) infected mice. Conclusions: We developed and validated a murine model of listerial meningitis. ST1-infected mice had a more severe inflammatory response and brain damage as compared to ST6-infected mice.

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Section: Discussionsupporting

confidence: 86%

Characterization of a listeria monocytogenes meningitis mouse model

Koopmans

Brouwer

Serón

et al. 2017

Journal of the Neurological Sciences

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“…Three of the patients with intracranial hemorrhage had a intracranial abscess, four patients had cerebral infarctions and two had a hydrocephalus, which are all associated with higher mortality and unfavorable outcome [8], [16], [23]. The underlying pathophysiology of cerebrovascular complications during bacterial meningitis (infarct, venous thrombosis and hemorrhages) is largely unknown but may share common pathophysiological mechanisms: first, there is a dysregulation of both the coagulation and fibrinolytic pathways, not only systemically but also locally in the central nervous system compartment [24], [25], [26]. Second, vascular endothelial cell swelling and activation is a common finding in bacterial meningitis, which leads to release of procoagulant factors and pro-inflammatory cytokines, causing further endothelial activation and swelling [27].…”

Section: Discussionmentioning

confidence: 99%

Intracerebral Hemorrhages in Adults with Community Associated Bacterial Meningitis in Adults: Should We Reconsider Anticoagulant Therapy?

et al. 2012

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ObjectiveTo study the incidence, clinical presentation and outcome of intracranial hemorrhagic complications in adult patients with community associated bacterial meningitis.MethodsNationwide prospective cohort study from all hospitals in the Netherlands, from 1 March 2006, through 31 December 2010.ResultsOf the 860 episodes of bacterial meningitis that were included, 24 were diagnosed with intracranial hemorrhagic complications: 8 upon presentation and 16 during clinical course. Clinical presentation between patients with or without intracranial hemorrhage was similar. Causative bacteria were Streptococcus pneumoniae in 16 patients (67%), Staphylococcus aureus in 5 (21%), Pseudomonas aeruginosa and Listeria monocytogenes both in 1 patient (4%). Occurrence of intracranial hemorrhage was associated with death (63% vs. 15%, P<0.001) and unfavorable outcome (94% vs. 34%, P<0.001). The use of anticoagulants on admission was associated with a higher incidence of intracranial hemorrhages (odds ratio 5.84, 95% confidence interval 2.17–15.76).ConclusionIntracranial hemorrhage is a rare but devastating complication in patients with community-associated bacterial meningitis. Since anticoagulant therapy use is associated with increased risk for intracranial hemorrhage, physicians may consider reversing or temporarily discontinuing anticoagulation in patients with bacterial meningitis.

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“…The pathogenesis of cerebral infarction remains unclear and is the subject of ongoing research, which has focused largely on two areas: first, the dysregulation of the coagulation and fibrinolytic pathways, not only systemically but also locally, as exemplified by the upregulation of PAI-1 and elevated levels of prothrombin fragments F1 and -2 and soluble tissue factor in the CSF of patients with pneumococcal meningitis (264,525,536); and second, endothelial cell dysfunction, which may lead to localized swelling and release of procoagulant factors and proinflammatory cytokines. Also, endothelin, which is one of several potent vasoactive peptides, has been shown to be elevated in CSF during acute stages of infection (33,251,389).…”

Section: Cerebrovascular Complicationsmentioning

confidence: 99%

Pathogenesis and Pathophysiology of Pneumococcal Meningitis

et al. 2011

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SUMMARY Pneumococcal meningitis continues to be associated with high rates of mortality and long-term neurological sequelae. The most common route of infection starts by nasopharyngeal colonization by Streptococcus pneumoniae , which must avoid mucosal entrapment and evade the host immune system after local activation. During invasive disease, pneumococcal epithelial adhesion is followed by bloodstream invasion and activation of the complement and coagulation systems. The release of inflammatory mediators facilitates pneumococcal crossing of the blood-brain barrier into the brain, where the bacteria multiply freely and trigger activation of circulating antigen-presenting cells and resident microglial cells. The resulting massive inflammation leads to further neutrophil recruitment and inflammation, resulting in the well-known features of bacterial meningitis, including cerebrospinal fluid pleocytosis, cochlear damage, cerebral edema, hydrocephalus, and cerebrovascular complications. Experimental animal models continue to further our understanding of the pathophysiology of pneumococcal meningitis and provide the platform for the development of new adjuvant treatments and antimicrobial therapy. This review discusses the most recent views on the pathophysiology of pneumococcal meningitis, as well as potential targets for (adjunctive) therapy.

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Coagulation, coma, and outcome in bacterial meningitis – An observational study of 38 adult cases

Cited by 12 publications

References 41 publications

Characterization of a listeria monocytogenes meningitis mouse model

Characterization of a listeria monocytogenes meningitis mouse model

Intracerebral Hemorrhages in Adults with Community Associated Bacterial Meningitis in Adults: Should We Reconsider Anticoagulant Therapy?

Pathogenesis and Pathophysiology of Pneumococcal Meningitis

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