Pneumonia Bacterial Publications (38833)
Pneumonia Bacterial Publications
Central line-associated bloodstream infection (CLABSI) rate was 5.1 per 1000 central line days, ventilator-associated pneumonia (VAP) rate was 7.2 per 1000 mechanical ventilator days, and catheter-associated urinary tract infection (CAUTI) rate was 3.9 per 1000 urinary catheter days, all similar to or lower than INICC rates (4.9 [CLABSI]; 16.5 [VAP]; 5.3 [CAUTI]), and higher than CDC/NHSN rates (0.8 [CLABSI]; 1.1 [VAP]; and 1.3 [CAUTI]). Device utilization ratios were higher than INICC and CDC/NHSN rates, except for urinary catheter, which was similar to INICC. Extra length of stay was 8 days for patients with CLABSI, 9.6 for VAP and 5.7 days for CAUTI. Additional crude mortality was 3.0% for CLABSI, 4.4% for VAP, and 16.9% for CAUTI.
DA-HAI rates in our ICUs are higher than CDC/NSHN's and similar to or lower than INICC international rates.
A bronchoalveolar lavage sample was positive via PCR for adenovirus which we suspect exacerbated a pre-existing bacterial pneumonia and led to a severe and non-responsive respiratory failure. His serum adenovirus load was markedly elevated. Treatment was started once the diagnosis of disseminated adenovirus infection was made; however, at that time patient was suffering from refractory hypoxaemia, respiratory acidosis, right heart failure and septic shock. Despite maximal supportive measures our patient ultimately expired over the course of 6 days.
aureus the use of adjunctive AMK-I may enhance bacterial eradication. Herein, we aimed to characterize the in vitro pharmacodynamic (PD) profile of human-simulated ELF exposures of AMK-I against both methicillin-sensitive (MSSA) and -resistant (MRSA) S. aureus.
An in vitro model was used to simulate the resultant ELF pharmacokinetic profile of amikacin after the administration of AMK-I 400 mg q12h. The antibacterial activity of this regimen was tested against 7 S. aureus isolates that display MIC profiles encountered clinically (4 MRSA; MIC range 4-64, 3 MSSA; MIC range 8-16 mg/L). Experiments were conducted over 24 h and samples were taken throughout this period to assess the bacterial density in both control and treatments.
The mean ± SD inoculum 0 h bacterial density was 6.4 ± 0.09 which increased to 8.6 ± 0.19 log10 CFU/mL in the control models by the end of 24 h experiments. Simulated ELF concentrations of AMK-I resulted in a rapid, 5 log10 declined in CFU over the initial 12 h for all MRSA and MSSA isolates. After 12 h, all bacterial counts remained below the limit of detection (LOD, 1.7 log10 CFU/mL) and no regrowth was evident at the end of the study.
AMK-I produced an ELF exposure profile that was rapidly bactericidal against S. aureus displaying typical MICs to amikacin irrespective of their phenotypic profile to methicillin. While the Gram-negative organisms are the target pathogens for AMK-I in the ongoing clinical trials, these data suggest that this adjunctive regimen may also have the potential to eradicate both MSSA and MRSA from lower airway which needs to be further evaluated in randomized-controlled clinical trials.
We aimed to investigate the contribution of thrombin to the host response during pneumonia derived sepsis.
Mice treated with the specific thrombin inhibitor Dabigatran or control chow were infected with the common human sepsis pathogen Klebsiella (K.) pneumoniae via the airways. In subsequent infection experiments, mice were additionally treated with Ancrod to deplete fibrinogen. Ex vivo Klebsiella growth was assessed by incubating human whole blood or specific blood components in various conditions with Klebsiella.
Thrombin inhibition by Dabigatran enhanced bacterial outgrowth and spreading, and accelerated mortality. Thrombin inhibition did not influence neutrophil recruitment to the lung or activation or neutrophil extracellular trap formation. Dabigatran reduced D-dimer formation and fibrin deposition in the lung. Fibrin depletion also enhanced bacterial outgrowth and spreading, and thrombin inhibition had no additional effect herein. Both thrombin and fibrin polymerization inhibited ex vivo Klebsiella outgrowth in human whole blood, which was neutrophil dependent and the effect of thrombin required the presence of platelets and platelet protease activated receptor-1. In vivo thrombin inhibition reduced platelet-neutrophil complex formation and endothelial cell activation, but did not prevent sepsis-induced thrombocytopenia or organ damage.
These results suggest that thrombin plays an important role in protective immunity during pneumonia derived sepsis by fibrin polymerization and enhancement of platelet-neutrophil interactions. This article is protected by copyright. All rights reserved.
We described antibiotic prescriptions and evaluated the clinical impact of initial combination antibiotic therapy and de-escalation strategy in patients with VAP caused by P. aeruginosa.
Between 1994 and 2014, all 100 patients with VAP caused by P. aeruginosa in our intensive care unit (ICU) were included in a retrospective cohort study to evaluate the prognostic impact of initial combination antibiotic therapy.
Eighty-five patients received initial combination antibiotic therapy and 15 monotherapy. Nine patients received inadequate initial antibiotic therapy. De-escalation was performed in 42 patients. Thirty-nine patients died in the ICU. Factors independently associated with death were SAPS II score [SAPS II ≥40 versus <40: hazard ratio (HR) 2.49, 95% confidence interval (CI) 1.08-5.70, p = 0.03] and septic shock (HR = 4.80, 95% CI = 1.90-12.16, p < 0.01) at onset of VAP. Initial combination antibiotic therapy (HR = 1.97, 95% CI = 0.56-6.93, p = 0.29) and early de-escalation (HR = 0.59, 95% CI = 0.27-1.31, p = 0.19) had no impact on mortality. In multivariate analysis, the risk for inappropriate initial antibiotic therapy was higher in cases with multi-drug resistant P. aeruginosa [odd ratio (OR) = 7.11, 95% CI = 1.42-35.51, p = 0.02], but lower in cases with initial combination antibiotic therapy (OR = 0.12, 95% CI = 0.02-0.63, p = 0.01).
In our cohort, combination therapy increased the likelihood of appropriate therapy but did not seem to impact on mortality.
Laboratory and two 15-college wrestling invitational meets.
A total of 231 collegiate wrestlers and 8 officials.
In the laboratory-based part of the study, we measured the bacterial load of mats disinfected with 10% bleach, OxiTitan, Benefect, eWater, and KenClean and inoculated with Staphylococcus epidermidis (strain ATCC 12228) at a concentration of 6.5 × 10(4) bacteria/cm(2). In the empirical part of the study, we used these disinfectants during 2 invitational meets and measured mat and participant bacterial load during competition. Participants were swabbed at weigh-in and after their last bout. Mat bacterial load was monitored hourly.
We determined total colony counts and species.
With controlled testing, we observed that products claiming to have residual activity reduced bacterial load by 63% over the course of competition compared with nonresidual agents. Only 4 of 182 participating wrestlers tested positive for methicillin-resistant Staphylococcus aureus , which is the normal population occurrence. The predominant species on mats were skin bacteria ( Staphylococcus epidermidis ) and substantial levels of respiratory bacteria ( Streptococcus pneumonia ), as well as several soil species and a surprisingly low incidence of fecal bacteria ( Escherichia coli ). Disinfectant effectiveness during the meets was consistent with controlled study findings. Cleaning mats with residual disinfectants reduced the average bacterial load by 76% compared with nonresidual cleaners. Using a footbath did not reduce the bacterial load compared with a bleach-cleaned mat, but using alcohol-based hand gel reduced it by 78%.
Best practices based on these data include backward mopping of the mats with a residual disinfectant pulled behind the cleaner, allowing mats to dry before walking on them, having wrestlers use hand gel before each bout, and strongly recommending that all wrestlers receive annual influenza vaccinations.
87 and 0.27 μg/mL (P. multocida) and 0.70 and 0.85 μg/mL (A. pleuropneumoniae) for broth and serum MICs, respectively. PK/PD modelling of in vitro time-kill curves established broth and serum breakpoint values for area under curve (AUC0-24 h )/MIC for three levels of inhibition of growth, bacteriostasis and 3 and 4 log10 reductions in bacterial count. Doses were then predicted for each pathogen, based on Monte Carlo simulations, for: (i) bacteriostatic and bactericidal levels of kill; (ii) 50% and 90% target attainment rates (TAR); and (iii) single dosing and daily dosing at steady-state. For 90% TAR, predicted daily doses at steady-state for bactericidal actions were 1123 mg/kg (P. multocida) and 43 mg/kg (A. pleuropneumoniae) based on serum MICs. Lower TARs were predicted from broth MIC data; corresponding dose estimates were 95 mg/kg (P. multocida) and 34 mg/kg (A. pleuropneumoniae).
castellanii shares some traits with macrophages, in particular the ability to phagocyte bacteria, we have studied the uptake and the fate of the bacteria after contact with the two phagocytic cells. In our conditions, K. pneumoniae growth was increased in coculture in presence of A. castellanii or Thp-1 macrophagic cells and bacterial development was also increased by A. castellanii supernatant. In addition, we showed that the presence of the bacteria had a negative effect on the macrophages whereas it does not affect amoeba viability. Using gentamicin, which kills bacteria outside cells, we showed that only macrophages were able to internalize K. pneumoniae. This result was confirmed by electron microscopy. We have consequently reported some differences in bacterial uptake and internalization between a free living amoeba and macrophagic cells, highlighting the fact that results obtained with this amoebal model should not be extrapolated to the relationships between K. pneumoniae and macrophages.
Sixty patients diagnosed with IPF were prospectively enrolled, together with 20 matched controls. Subjects underwent bronchoalveolar lavage (BAL) and peripheral whole blood was collected into PAXgene tubes for all subjects at baseline. For IPF subjects additional samples were taken at 1, 3, and 6 months and (if alive) a year. Gene expression profiles were generated using Affymetrix Human Gene1.1ST Arrays.
Network analysis of gene expression data identified two gene modules that strongly associate with a diagnosis of IPF, BAL bacterial burden (determined by 16S quantitative PCR) and specific microbial OTUs, as well as lavage and peripheral blood neutrophilia. Genes within these modules that are involved in the host defence response include NLRC4, PGLYRP1, MMP9, DEFA4. The modules also contain two genes encoding specific antimicrobial peptides (SLPI and CAMP). Many of these particular transcripts were associated with survival and showed longitudinal over expression in subjects experiencing disease progression, further strengthening their relationship with disease.
Integrated analysis of the host transcriptome and microbial signatures demonstrates an apparent host response to the presence of an altered or more abundant microbiome. These responses remain elevated on longitudinal follow up, suggesting that the bacterial communities of the lower airways may be acting as persistent stimuli for repetitive alveolar injury in IPF.
Cathelicidins are a class of antimicrobial peptide found in humans, mice, and rats, among others. Known as LL-37 in humans and cathelin-related antimicrobial peptide (CRAMP) in rodents, cathelicidins are produced by many different cells, including macrophages, neutrophils, and epithelial cells. The role of cathelicidins is somewhat confounding, as they exhibit both pro-and anti-inflammatory activity. A major obstacle in the study of cathelicidins is the inability of exogenous LL-37 or CRAMP to mimic the activity of their endogenous counterparts. Nevertheless, studies have shown that LL-37 is recognized by multiple receptors, and may stabilize or modulate Toll-like receptor signaling. In addition, cathelicidins play a role in apoptosis, inflammasome activation, and phagocytosis. However, many studies are revealing the dual effects of cathelicidins. For example, CRAMP appears to be protective in models of group A Streptococcus skin infection, pneumonia, and meningitis, but detrimental in cases of severe bacterial infection, such as septic shock. It is becoming increasingly clear that the activity of cathelicidins is modulated by complex interactions with the microenvironment, as well as the disease background. This article reviews what is currently known about the activity of cathelicidins in an attempt to understand their complex roles in systemic diseases.