Healthcare-Associated Bacterial Meningitis

Laxmi, Sheethal; Tunkel, Allan R.

doi:10.1007/s11908-011-0190-z

Cited by 17 publications

(7 citation statements)

References 41 publications

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“…18,23,24,28 In contrast to intravenous administration, the direct delivery of polymyxins into the central nervous system (CNS) via the intrathecal (ITH) or intraventricular (IVT) routes appears to be more effective and safer. 29 The ITH/IVT polymyxin dosages suggested by the Infectious Diseases Society of America guidelines (2004) call for administration of at least 125 000 IU/per day; however, in the clinical setting, the dose is often chosen empirically and colistin IT doses of 40 000− 500 000 IU/day have been reported. 30,31 Clinical pharmacokinetic data for ITH/IVT colistin suggests that doses > 65 200 IU/day are necessary to achieve sustained concentrations above the MIC of 2 μg/mL (1 mg of colistin is equal to 30 000 IU) (for susceptible Gram-negative pathogens).…”

Section: Clinical Manifestations Of Polymyxinmentioning

confidence: 99%

Molecular Mechanisms of Neurotoxicity Induced by Polymyxins and Chemoprevention

Dai

Xiao

et al. 2018

ACS Chem. Neurosci.

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Neurotoxicity is one major unwanted side-effects associated with polymyxin (i.e., colistin and polymyxin B) therapy. Clinically, colistin neurotoxicity is characterized by neurological symptoms including dizziness, visual disturbances, vertigo, confusion, hallucinations, seizures, ataxia, and facial and peripheral paresthesias. Pathologically, colistin-induced neurotoxicity is characterized by cell injury and death in neuronal cell. This Review covers our current understanding of polymyxin-induced neurotoxicity, its underlying mechanisms, and the discovery of novel neuroprotective agents to limit this neurotoxicity. In recent years, an increasing body of literature supports the notion that polymyxin-induced nerve damage is largely related to oxidative stress and mitochondrial dysfunction. P53, PI3K/Akt, and MAPK pathways are also involved in colistin-induced neuronal cell death. The activation of the redox homeostasis pathways such as Nrf2/HO-1 and autophagy have also been shown to play protective roles against polymyxin-induced neurotoxicity. These pathways have been demonstrated to be upregulated by neuroprotective agents including curcumin, rapamycin and minocycline. Further research is needed toward the development of novel polymyxin formulations in combination with neuroprotective agents to ameliorate this unwanted adverse effect during polymyxins therapy in patients.

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Section: Clinical Manifestations Of Polymyxinmentioning

confidence: 99%

Molecular Mechanisms of Neurotoxicity Induced by Polymyxins and Chemoprevention

Dai

Xiao

et al. 2018

ACS Chem. Neurosci.

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“…The timing of insertion of a new permanent shunt, when necessary, is not well-defined and differs according to the causative agent [8,16]. Clearly, microbiological clearance has to be achieved before insertion of a new shunt.…”

Section: Management Of Implants and Shunts In Patients With Pnmmentioning

confidence: 99%

Management of post-neurosurgical meningitis: narrative review

Hussein

Bitterman

Shofty

et al. 2017

Clinical Microbiology and Infection

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“…Community-acquired BM (CBM) is distinct from healthcare-associated BM (HBM). HBM has recently been associated with healthcare facilities (HBMF), such as hospitals or nursing homes, and with clinical procedures resulting in post-neurosurgical infection, with or without an implanted, indwelling intracranial device [4][5][6]. Vaccines targeting BM-causing pathogens have been introduced in several countries.…”

Section: Introductionmentioning

confidence: 99%

Bacterial meningitis: Aetiology, risk factors, disease trends and severe sequelae during 50 years in Sweden

et al. 2022

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Background Bacterial meningitis (BM) is a rare but severe infection. Few population‐based studies have characterised BM episodes and sequelae over long periods. Methods This was a population‐based observational cohort study with national coverage, using data on aetiological pathogens, sex, premorbid conditions, steroid pretreatment, severe sequelae and birth, death and diagnosis dates collected from 10,339 patients with BM reported to the National Board of Health and Welfare in Sweden between 1964 and 2014. Results During the 50‐year study period, the incidence of BM decreased in young children, but not in the elderly. The most common cause of BM was pneumococci (34%), followed by Haemophilus influenzae (26%), and meningococci (18%), mainly community acquired. Premorbid conditions were found in 20%. After the H. influenzae type b vaccine was introduced in 1993, the BM incidence decreased by 36%. Following pneumococcal conjugated vaccine introduction in 2009, the incidence and 30‐day mortality from pneumococcal meningitis decreased by 64% and 100%, respectively, in previously healthy children, and the 30‐day mortality decreased by 64% among comorbid adults. The BM incidence in immunosuppressed patients increased by 3% annually post vaccine introduction. The 30‐day mortality was 3% in children and 14% in adults, and the rate of severe sequelae was 44%. On average, patients lost 11 years of healthy life due to BM. Conclusion The introduction of conjugated vaccines into the childhood vaccination program has reduced the incidence of BM in young children, but not in adults. Post vaccine introduction, patients present with more premorbid conditions and other bacterial causes of BM, emphasising the need for a correct diagnosis when treating these infections.

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Healthcare-Associated Bacterial Meningitis

Cited by 17 publications

References 41 publications

Molecular Mechanisms of Neurotoxicity Induced by Polymyxins and Chemoprevention

Molecular Mechanisms of Neurotoxicity Induced by Polymyxins and Chemoprevention

Management of post-neurosurgical meningitis: narrative review

Bacterial meningitis: Aetiology, risk factors, disease trends and severe sequelae during 50 years in Sweden

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