Effects of Time of Arrival on Trauma Patient Outcomes.

BACKGROUND: Arriving during "off hours" to the hospital can put patients at greater risk of complications or mortality given lesser staff. Our goal was to investigate this in trauma patients with an Injury Severity Score (ISS) of >15. We hypothesized that the patients admitted late at night and/or during the weekend, would have worse outcomes, delays to the operating room (OR), and longer lengths of stay (LOS) compared to those who arrive on a weekday during the day. METHODS: We performed a retrospective study from 8/1/2019 to 8/1/2022 of all trauma patients with an ISS >15 at our Level 1 Trauma Center. Patients <18 years, dead on arrival, or transferred out were excluded. Univariate and multivariable analysis were performed comparing weekday vs weekend arrivals, day vs night shift arrivals, and with patients grouped as weekday day, weekday night, weekend day, and weekend night. The primary outcome was mortality. RESULTS: 953 patients met inclusion criteria. The patients that arrived on the weekend and at night were significantly younger than their counterparts. A significantly greater percentage of Black patients arrived during night shift. Mortality, hospital LOS, and ICU LOS did not differ based on day or time of arrival. CONCLUSION: Contrary to our hypothesis, our study did not find a significant difference in outcomes when evaluating based on a patient's time of arrival. This gives credence that our mature trauma center can provide the same level of care despite the time of a severely injured patient's time of arrival.

Distribution of Hay-Hole Covers Prevents Injuries from Falls Through Hay Holes.

Hay-holes are openings on the second floor of barns used to drop feed to ground level. Hay-hole falls (HHFs) are a unique problem among Anabaptist communities, especially for children. To follow-up on our previous study that created the Anabaptist Youth Trauma Prevention Consortium with distribution of 231 hay-hole covers in South Central Pennsylvania, we compared a five-year period before cover distribution with the 5-year period after. Data were stratified by phase: Before Cover Implementation (BC): 1/2011-12/2016, After Cover Implementation (AC): 1/2017-12/2021. 49 patients met inclusion criteria. There was a 47% decrease in the number of HHF from the BC phase to the AC phase, suggesting that cover distribution has significantly impacted HHF incidence. Further investigation is needed to elucidate the long-term impact of cover distribution and to guide future interventions, such as another round of cover distribution or improvements in the design of these covers for long-term use.

The Short-chain Fatty Acid Propionic Acid Activates the Rcs Stress Response System Partially through Inhibition of d-Alanine Racemase.

The Enterobacterial Rcs stress response system reacts to envelope stresses through a complex two-component phosphorelay system to regulate a variety of environmental response genes, such as capsular polysaccharide and flagella biosynthesis genes. However, beyond Escherichia coli, the stresses that activate Rcs are not well-understood. In this study, we used a Rcs system-dependent luminescent transcriptional reporter to screen a library of over 240 antimicrobial compounds for those that activated the Rcs system in Serratia marcescens, a Yersiniaceae family bacterium. Using an isogenic rcsB mutant to establish specificity, both new and expected activators were identified, including the short-chain fatty acid propionic acid, which is found at millimolar levels in the human gut. Propionic acid did not reduce the bacterial intracellular pH, as was hypothesized for its antibacterial mechanism. Instead, data suggest that the Rcs-activation by propionic acid is due, in part, to an inactivation of alanine racemase. This enzyme is responsible for the biosynthesis of d-alanine, which is an amino-acid that is required for the generation of bacterial cell walls. Consistent with what was observed in S. marcescens, in E. coli, alanine racemase mutants demonstrated elevated expression of the Rcs-reporter in a d-alanine-dependent and RcsB-dependent manner. These results suggest that host gut short-chain fatty acids can influence bacterial behavior via the activation of the Rcs stress response system. IMPORTANCE The Rcs bacterial stress response system responds to envelope stresses by globally altering gene expression to profoundly impact host-pathogen interactions, virulence, and antibiotic tolerance. In this study, a luminescent Rcs-reporter plasmid was used to screen a library of compounds for activators of Rcs. Among the strongest inducers was the short-chain fatty acid propionic acid, which is found at high concentrations in the human gut. This study suggests that gut short-chain fatty acids can affect both bacterial virulence and antibiotic tolerance via the induction of the Rcs system.

Antibiotics Used in Empiric Treatment of Ocular Infections Trigger the Bacterial Rcs Stress Response System Independent of Antibiotic Susceptibility.

The Rcs phosphorelay is a bacterial stress response system that responds to envelope stresses and in turn controls several virulence-associated pathways, including capsule, flagella, and toxin biosynthesis, of numerous bacterial species. The Rcs system also affects antibiotic tolerance, biofilm formation, and horizontal gene transfer. The Rcs system of the ocular bacterial pathogen Serratia marcescens was recently demonstrated to influence ocular pathogenesis in a rabbit model of keratitis, with Rcs-defective mutants causing greater pathology and Rcs-activated strains demonstrating reduced inflammation. The Rcs system is activated by a variety of insults, including ß-lactam antibiotics and polymyxin B. In this study, we developed three luminescence-based transcriptional reporters for Rcs system activity and used them to test whether antibiotics used for empiric treatment of ocular infections influence Rcs system activity in a keratitis isolate of S. marcescens. These included antibiotics to which the bacteria were susceptible and resistant. Results indicate that cefazolin, ceftazidime, polymyxin B, and vancomycin activate the Rcs system to varying degrees in an RcsB-dependent manner, whereas ciprofloxacin and tobramycin activated the promoter fusions, but in an Rcs-independent manner. Although minimum inhibitory concentration (MIC) analysis demonstrated resistance of the test bacteria to polymyxin B and vancomycin, the Rcs system was activated by sub-inhibitory concentrations of these antibiotics. Together, these data indicate that a bacterial stress system that influences numerous pathogenic phenotypes and drug-tolerance is influenced by different classes of antibiotics despite the susceptibility status of the bacterium.