Ventilator-associated pneumonia (VAP) is the leading healthcare-acquired infection among ventilated patients in intensive care units (ICU). VAP is a serious patient complication that results in increased hospital length of stay, cost, morbidity, and mortality. The accumulation of subglottic secretions above the endotracheal tube (ETT) cuff increases the risk of VAP, as these secretions may leak around the cuff of the ETT resulting in aspiration and an increased risk for infection. An in depth literature review was done to determine the effectiveness of subglottic secretion aspiration (by means of specialized ETT tubes with intrinsic suction lumens) in decreasing the incidence rate of VAP. Evidenced-based data were gathered from the CINAHL Plus with Full Text, PubMed, and Cochrane Database of Systematic Reviews databases for this review. VAP guidelines recommend subglottic secretion aspiration as a means to prevent its occurrence. However, important variables such as suction pressure, frequency, secretion viscosity, and ETT cuff pressure and volume need to be considered. The interaction among these variables determines the effectiveness of subglottic secretion removal. The goal of this review was to highlight these interactions and provide evidenced-based information for critical care nurses to expand their understanding of the dynamics involved in subglottic secretion aspiration and how to efficiently use this practice to prevent VAP.

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The study explored the prevalence of biofilm formers and its association with multidrug resistance in Klebsiella Pneumonia, a gram-negative bacterium that has high propensity to form antibiotic resistant strains and forms biofilms. Biofilms are complex microbial community with attributes that vary from planktonic cells. Antibiotic resistance is a property that has shown evidence to be higher in biofilms as compared to planktonic cells. Multi-drug resistance, a higher form of antibiotic resistance, is defined as resistance to at least one agent in three or more antibiotic categories. A single-armed and a two-armed meta-analysis was done to assess prevalence of biofilm formers and to find association between biofilm formation capacity and multi drug resistance. The one-armed meta-analysis revealed 74% (95% CI: 64%-83%) prevalence of biofilm formers among clinical isolates of Klebsiella Pneumonia. The prevalence rate is comparable with that of prevalence rate attained by other bacterium by similar meta-analysis studies. This high prevalence of biofilm formers warrants for a paradigm shift in treatment strategies for treatment of infections. The two-armed meta-analysis showed that there was identical risk of multi drug resistance among the biofilm formers and non-biofilm formers. The result challenges the intrinsic capacity of planktonic cells to resist against antibiotics to achieve multi drug resistance. Further research to update the biofilm formation profiles and to understand the resistance mechanism in commonly occurring bacterial infections in of utmost importance.

Background: After the first COVID-19 infection wave, a constant increase of pulmonary embolism (PE) hospitalizations not linked with active PCR-confirmed COVID-19 was observed, but potential contributors to this observation are unclear. Therefore, we analyzed associations between changes in PE hospitalizations and (1) the incidence of non-COVID-19 pneumonia, (2) the use of computed tomography pulmonary angiography (CTPA), (3) volume depletion, and (4) preceding COVID-19 infection numbers in Germany. Methods: Claims data of Helios hospitals in Germany were used, and consecutive cases with a hospital admission between May 6 and December 15, 2020 (PE surplus period), were analyzed and compared to corresponding periods covering the same weeks in 2016–2019 (control period). We analyzed the number of PE cases in the target period with multivariable Poisson general linear mixed models (GLMM) including (a) cohorts of 2020 versus 2016–2019, (b) the number of cases with pneumonia, (c) CTPA, and (d) volume depletion and adjusted for age and sex. In order to associate the daily number of PE cases in 2020 with the number of preceding SARS-CoV-2 infections in Germany, we calculated the average number of daily infections (divided by 10,000) occurring between 14 up to 90 days with increasing window sizes before PE cases and modeled the data with Poisson regression. Results: There were 2,404 PE hospitalizations between May 6 and December 15, 2020, as opposed to 2,112–2,236 (total 8,717) in the corresponding 2016–2019 control periods (crude rate ratio [CRR] 1.10, 95% CI 1.05–1.15, P < 0.01). With the use of multivariable Poisson GLMM adjusted for age, sex, and volume depletion, PE cases were significantly associated with the number of cases with pneumonia (CRR 1.09, 95% CI 1.07–1.10, P < 0.01) and with CTPA (CRR 1.10, 95% CI 1.09–1.10, P < 0.01). The increase of PE cases in 2020 compared with the control period remained significant (CRR 1.07, 95% CI 1.02–1.12, P < 0.01) when controlling for those factors. In the 2020 cohort, the number of preceding average daily COVID-19 infections was associated with increased PE case incidence in all investigated windows, i.e., including preceding infections from 14 to 90 days. The best model (log likelihood −576) was with a window size of 4 days, i.e., average COVID-19 infections 14–17 days before PE hospitalization had a risk of 1.20 (95% CI 1.12–1.29, P < 0.01). Conclusions: There is an increase in PE cases since early May 2020 compared to corresponding periods in 2016–2019. This surplus was significant even when controlling for changes in potential modulators such as demographics, volume depletion, non-COVID-19 pneumonia, CTPA use, and preceding COVID-19 infections. Future studies are needed (1) to investigate a potential causal link for increased risk of delayed PE with preceding SARS-CoV-2 infection and (2) to define optimal screening for SARS-CoV-2 in patients presenting with pneumonia and PE.

Staphylococcus aureus causes chronic bacterial pneumonias that are resistant to antimicrobial treatment and carry a high burden of morbidity and mortality. S. aureus persists in the lung by assuming adaptive phenotypes like biofilms, which protect the bacteria from antibiotics and host bacterial clearance. It is well established that staphylococcal adaptation to the host is often driven by immune pressure, but the specific factors that drive S. aureus persistence in the setting of chronic lung infection have not been fully elucidated. One of the critical processes that drives immune cell function is metabolism. In addition to fueling the bioenergetic needs of the cell and competing with pathogens for key resources, immune cell metabolism also generates key regulatory metabolites that can either bolster or dampen inflammation in a process known as immunometabolism. The role of these regulatory immune metabolites in staphylococcal pneumonias has not been explored. This thesis addresses the hypothesis that immune metabolites play an important role in the pathogenesis of S. aureus pneumonias, not only by regulating immune cell function but also by promoting bacterial adaptation to the lung. In Chapter 1, we examine the current understanding of the pathogenesis of staphylococcal lung infections and review the role of immune metabolites in regulating inflammation. In Chapter 2, we describe the methods we used to test our hypothesis. In Chapter 3, we define the immunometabolic response to S. aureus in the lung, identifying the anti-inflammatory metabolite itaconate as one of the most upregulated metabolites in the infected airway. We determine that itaconate production is triggered by bacterial PAMPs, and is driven by host mitochondrial stress in response to bacterial metabolism. We also discover that neutrophils are the main source of itaconate during staphylococcal pneumonia. In Chapter 4, we investigate the impact of itaconate on neutrophils, the major immune cell responsible for controlling S. aureus infection. We establish that itaconate impedes bacterial clearance and limits neutrophil bacterial killing. This occurs through two major mechanisms, including inhibition of neutrophil glycolysis, which impairs neutrophil survival during infection, and inhibition of the oxidative burst. We find that neutrophil itaconate production is still beneficial to the host, as it promotes protective, anti-oxidant and anti-cell death pathways in the epithelial and endothelial cells that are critical for respiration. In Chapter 5, we investigate the impact of itaconate on the metabolic adaptation of S. aureus to the host. We use longitudinal clinical isolates from a patient with chronic staphylococcal pneumonia to define how clonal strains adapt to the inflamed, itaconate-laden lung. The isolates demonstrate that there is selection for strains with reduced bioenergetics but increased biofilm formation. These metabolic changes are recapitulated by exposing a non-adapted S. aureus strain to itaconate, which inhibits staphylococcal bioenergetics via glycolysis, and causes increased utilization of pathways that produce biofilms. Our data demonstrate that the host immune metabolite itaconate promotes bacterial persistence during staphylococcal pneumonia by impeding bacterial clearance and promoting bacterial biofilm formation. In Chapter 6, we discuss the potential impact of these findings, particularly on the current efforts to develop itaconate as an anti-inflammatory therapeutic, and offer directions for future studies that can further explore how metabolic pathways that normally control inflammation can influence pathogen persistence in the host.

Aims: The purpose of this thesis was to synthesize the current literature on alpha amylase as an emerging biomarker of microaspiration in mechanically ventilated patient. Methods: The methodology included a review and synthesis of pertinent research articles from 1981-2018, written in English language. Criteria for inclusion in the review were all articles that evaluated α- amylase in tracheal secretions or bronchoalveolar lavage fluid (BAL) as a diagnostic tool for identifying microaspiration. The search yielded 11 studies that were reviewed. Findings: The findings suggest that once aspiration occurs, the duration of α-amylase in the lungs requires further exploration to assist in interpretation of positive values. After these values are identified they need be used consistently used throughout practice of mechanically ventilated patients. Inconsistencies in the defining parameters of α-amylase were used with the thirteen studies. Conclusion: Testing amylase levels can require financial stability, standardized training, and timeliness of collecting the specimen. Alpha-amylase is a biomarker of microaspiration. Further research should be conducted to evaluate the biomarker capabilities of α-amylase to assist in early identification and/or prevention of microaspiration in mechanically ventilated patients. Implications for nursing policy practice, education, and considerations for upcoming research of α-amylase were reviewed with limitations to the study.

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