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Item Implementation of intermittent pulse oximetry in low-risk hospitalized bronchiolitis patients(Montana State University - Bozeman, College of Nursing, 2024) Donovan, Alaina Jean; Chairperson, Graduate Committee: Margaret Hammersla; This is a manuscript style paper that includes co-authored chapters.Background: In 2014, the American Academy of Pediatrics (AAP) updated its guidelines, which recommend the utilization of intermittent pulse oximetry (IPOx) in low-risk and non-hypoxemic bronchiolitis patients. IPOx is the utilization of pulse oximetry monitoring intermittently at specified times. The overuse of pulse oximetry has been associated with an increase of hospital length of stay (LOS), alarm burden for RNs, and parental anxiety. Methods: A two-month QI project was implemented in a large Montana hospital's 10-bed inpatient pediatric unit. The project consisted of implementing an Inpatient Bronchiolitis Pathway utilizing IPOx. When criteria were met, IPOx orders were to be placed into the EMR. After each shift, RNs were asked to self-rate their adherence to the IPOx orders. At the end of each month, RNs completed a Likert-style questionnaire that assessed their satisfaction with the pathway and alarm fatigue. Results: During the QI project there were 12 bronchiolitis patients; of those, only eight patients met the necessary criteria. Six out of the eight had IPOx orders placed into the EMR. There was a 75% rate of IPOx order placement for the short and long-term goals. Adherence to the IPOx orders had a success rate of 73% during the month of January and a 57% adherence rate during the month of February. A comparison of mean LOS showed a mean difference of -5.9 hours in January and February of 2024 compared to 2023. The RN questionnaires showed overall satisfaction with the Inpatient Bronchiolitis Pathway and a reduction of alarm fatigue. Conclusion: The implementation of IPOx for inpatient bronchiolitis patients has been shown to decrease hospital LOS, unnecessary interventions, parental anxiety, and alarm fatigue. While the QI project does show possible improvement to LOS, a study with a longer time frame and increased sample size is needed to determine any clinical significance. The questionnaire suggests decreased alarm fatigue with the implementation of IPOx, which shows that even a small change could significantly impact RN alarm burden. Well-defined guidelines and education to staff and parents should be prioritized to continue to improve adherence to IPOx in the bronchiolitis population.Item Aerosol stability of severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2)(Montana State University - Bozeman, College of Agriculture, 2022) Bushmaker, Trenton John; Chairperson, Graduate Committee: Raina K. Plowright and Vincent J. Munster (co-chair); Neeltje van Doremalen and Dylan H. Morris were authors and Myndi G. Holbrook, Amandine Gamble, Brandi N. Williamson, Azaibi Tamin, Jennifer L. Harcourt, Natalie J. Thornburg, Susan I. Gerber, James O. Lloyd-Smith, Emmie de Wit and Vincent J. Munster were co-authors of the article, 'Aerosol and surface stability of SARS-CoV-2 as compared with SARS-CoV-1' in the journal 'New England journal of medicine' which is contained within this thesis.; Claude Kwe Yinda and Dylan H. Morris were authors and Myndi G. Holbrook, Amandine Gamble, Danielle Adney, Cara Bushmaker, Neeltje van Doremalen, Raina K. Plowright, James O. Lloyd-Smith and Vincent J. Munster were co-authors of the article, 'Comparative aerosol stability of SARS-CoV-2 variants of concern' submitted to the journal 'Emerging infectious diseases - CDC' which is contained within this thesis.The routes of transmission of the zoonotic pathogen severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) have been extensively studied to understand the spread at individual and population levels. Aerosol particles produced by infected individuals and the deposition patterns inhaled are known to affect the virulence of bioaerosol pathogens. Droplet nuclei particles (< 5 microns) aerosols typically deposit within the alveolar spaces of the lungs, whereas droplet (>5 microns) aerosols typically deposit within the nasopharyngeal and tracheobronchial regions of the respiratory tract. A few studies have evaluated pulmonary disease following droplet nuclei size particles of SARS-CoV-2 aerosol inhalation in African green monkeys and golden hamsters, concluding that both models have mild respiratory disease representative of human disease. More importantly, human participants with SARS-CoV-2 infections have been studied to look at the generation of particles during breathing, talking, and singing; the study concluded droplet nuclei particles accounted for 85% of the copies of virus produced and play a significant role in transmission. However, the environmental persistence of the aerosolized droplet nuclei particles, and the likely role of environmental persistence in driving transmission, is unknown for SARS-CoV-2. In these studies, we show the changing aerosol stability of SARS-CoV-2 during the supplanting waves of Variants of Concern (VOC). With the determination of viable viral particles characterized over time, we can make inferences about the role VOC and aerosol transmission have in driving population-level pathogen transmission. A secondary objective of these studies was to characterize the role those evolving mutations have had on viral entry and aerosol durability. Our work suggests that aerosol stability may be important in driving some population-level phenomena (e.g., indoor transmission, including superspreader events) but given the short infected-to-naive transmission transit time, the variation in the duration of aerosol stability among VOCs may not explain the difference in transmission rates of VOCs. This data will be useful for assessing the future evolution of aerosol transmission of SARS-CoV-2.Item Initiation and pathogenesis of Staphylococcus aureus Pneumonia following influenza A infection(Montana State University - Bozeman, College of Letters & Science, 2019) Borgogna, Timothy Ryan; Chairperson, Graduate Committee: Jovanka Voyich-Kane; Adrian Sanchez-Gonzalez, Kelly Gorham and Jovanka M. Voyich were co-authors of the article, 'A precise pathogen delivery and recovery system for murine models of secondary bacterial pneumonia' in the journal 'JOVE Journal of visualized experiments' which is contained within this dissertation.; Bennett Hisey, Emily Heitman, Joshua J. Obar, Nicole Meissner and Jovanka M. Voyich were co-authors of the article, 'Secondary bacterial pneumonia by Staphylococcus aureus following influenza A infection is saeR/S dependent' in the journal 'Journal of infectious diseases' which is contained within this dissertation.; Madison M. Collins, Kyle A. Glose, Kyler B. Pallister, Tyler K. Pallister and Jovanka M. Voyich were co-authors of the article, 'Uncovering the executioner: disruption of pulmonary surfactant by influenza A triggers Staphylococcus aureus Pneumonia' which is contained within this dissertation.Infection influenza A virus (IAV) leads to increased host susceptibility to secondary bacterial pneumonia. In cases such as these, Staphylococcus aureus (S. aureus) has emerged as the dominant bacterial pathogen associated with severe infection outcomes. S. aureus is a common commensal of the anterior nares and is frequently trafficked into the lower respiratory tract through inhalations, micro-aspirations, and direct mucosal dispersion. Despite recurrent exposure to the lungs and the capacity to cause severe disease, cases of S. aureus pneumonia are rare in immunocompetent hosts. Previous efforts interrogating S. aureus secondary bacterial pneumonia have largely focused on the immunomodulation that occurs during the antecedent influenza infection and have ignored the virulence contributions of the bacterial pathogen. To that end, we developed a murine model of secondary pneumonia to investigate S. aureus pathogenesis following influenza A infection. We identify that secondary bacterial pneumonia by S. aureus is dependent on the activation of the two-component regulatory system (TCS) SaeR/S. Further, studies demonstrated that in the absence of IAV infection the healthy lung environment suppresses virulence gene expression. Characterization of the lung environment revealed that the lipid constituents of pulmonary surfactant suppress S. aureus virulence production. Our data provide a model of secondary bacterial pneumonia wherein infection with IAV significantly reduces surfactant lipid concentrations within the lungs. The reduction of pulmonary surfactant lipids leads to a loss of S. aureus virulence suppression and rapid activation of the major virulence regulator saeR/S. Taken together, these data provide a strong rational for the low incidence of primary S. aureus pneumonia and the increased severity of S. aureus pneumonia following antecedent influenza A infection. Furthermore, these data highlight possible pulmonary surfactant replacement therapies that may significantly alleviate secondary bacterial pneumonia morbidity and mortality.Item Adaptive immunity to Chlamydia pneumoniae respiratory infection(Montana State University - Bozeman, College of Agriculture, 2000) Day, Thomas GordonItem The alveolar macrophage in pulmonary infection : a comparison of permissiveness to infection with an obligate and a facultative intracellular pathogen(Montana State University - Bozeman, College of Agriculture, 2013) Calverley, Matthew David; Chairperson, Graduate Committee: Allen G. Harmsen; Allen G. Harmsen, Sara Erickson, and Amanda J. Read were co-authors of the article, 'Resident alveolar macrophages are susceptible to and permissive of Coxiella burnetii infection' in the journal 'PLoS ONE' which is contained within this thesis.; Robert A. Cramer and Allen G. Harmsen were co-authors of the article, 'The facultative intracellular pathogen Cryptococcus neoformans proliferates primarily extracellularly early in in vivo infection' submitted to the journal 'mBio' which is contained within this thesis.The lung must mount an effective immune response to pathogenic challenge while controlling attendant tissue damage. Central to this co-ordination are the immunomodulatory effects exerted by the pulmonary environment on the local alveolar macrophages (AMs). Moreover, intracellular pathogens are known to exploit the host immune system. For this reason, we hypothesized that the resident AM would comprise a vulnerable population of cells capable of being exploited by intracellular pathogens. To test this hypothesis, we investigated the role of the AM during pulmonary infection with either the obligate intracellular bacterium Coxiella burnetii or the facultative intracellular fungus Cryptococcus neoformans. We showed [1] that resident AM are indeed the cell-type most susceptible to infection with C. burnetii. These resident AM remain infected up to twelve days, serving as a permissive niche that supports bacterial survival. Additionally, a subset of infected AMs underwent a characteristic phenotypic change in response to infection, resulting in an increased expression of surface integrin CD11b and continued expression of surface integrin CD11c. We conclude that C. burnetii is capable of exploiting the pulmonary environmental effects on the resident AM allowing for exploitation of the AM as a susceptible and permissive niche for infection. In the context of C. neoformans infection, we found that only a restricted population of C. neoformans replicated in AMs. The majority of C. neoformans that replicated in vivo did so extracellularly and the extent of extracellular replication exceeded intracellular replication of the yeast. In fact, the majority of intracellular fungal load in AMs at 48 hours post-infection was attributable to the uptake of extracellular C. neoformans from 24 to 48 hours post-infection. Thus, unlike C. burnetii, C. neoformans does not appear to exploit the pulmonary environmental effects on the resident AM during establishment of infection. Through the identification of the AM as a susceptible and permissive niche for C. burnetii infection and the finding that C. neoformans replicates primarily extracellularly during early pulmonary infection, we have both filled a deficiency in the previous knowledge base and set the stage for future studies into the induction of subsequent adaptive immune responses during these varied infections.