AimTo evaluate the association between nursing diagnoses, in-hospital mortality and length of stay in adults hospitalized with decompensated heart failure.MethodsA prospective longitudinal study conducted between April 2018 and July 2019. Data were collected from medical records of patients admitted to the emergency department of a large cardiovascular teaching hospital. Sociodemographic and clinical variables, along with nursing diagnoses based on NANDA-I classification, were extracted. Cox proportional hazards regression identified factors associated with mortality, while generalized linear regression with a gamma distribution assessed predictors of length of stay. Discriminatory performance of nursing diagnoses for mortality was evaluated using ROC curve analysis.FindingsA total of 155 patients were included (mean age 62.6 years; 58.7% male); 29 (18.7%) died and 126 (81.3%) were discharged, with a median hospital stay of 5 days. Age, chronic kidney disease, and lower serum sodium were independent prognosis of mortality. The number of nursing diagnoses showed poor discriminative ability for mortality prediction (AUC = 0.59). However, each additional nursing diagnosis was associated with a 6.3% increase in hospital stay (p < 0.05). Patients with acute coronary syndrome or hypertension had on average, 20% shorter hospital stays.ConclusionThe number of nursing diagnoses was independently associated with longer hospitalization, suggesting that these assessments capture care complexity beyond traditional medical diagnoses. Integrating nursing diagnostic information into prognostic models may improve care planning and resource allocation for patients with decompensated hear failure.Implications for nursing knowledgeNursing diagnoses offer additional insights into patient complexity and can enhance clinical decision-making, staffing strategies, and individualized care planning to improve hospital outcomes.

Fecal microbiota transplantation (FMT) has shown efficacy for the treatment of ulcerative colitis but with variable response between patients and trials. The mechanisms underlying FMT's therapeutic effects remains poorly understood but is generally assumed to involve engraftment of donor microbiota into the recipient's microbiome. Reports of microbial engraftment following FMT have been inconsistent between studies. Here, we investigate microbial engraftment in a previous randomized controlled trial (NCT01545908), in which FMT was sourced from a single donor, using amplicon-based profiling, shotgun metagenomics, and culture-enriched metagenomics. Placebo samples were included to estimate engraftment noise, and a significant level of false-positive engraftment was observed which confounds the prediction of true engraftment. We show that analyzing engraftment across multiple patients from a single donor enhances the accuracy of detection. We identified a unique set of genes engrafted in responders to FMT which supports strain displacement as the primary mechanism of engraftment in our cohort.

Abstract Background Celiac disease (CeD) is a T-cell mediated enteropathy driven by gluten in people with risk genes HLA-DQ2 or DQ8. Many patients experience symptoms such as constipation and/or persistent mucosal inflammation despite adherence to a gluten-free diet (GFD) and are advised to increase dietary fibre. Preliminary results from gluten-immunized NOD-DQ8 mice revealed that supplemented inulin could improve mucosal healing. However, whether fibre is tolerated and metabolized in CeD is unknown. Aims To investigate whether (1) fibre consumption in untreated and treated CeD compared to healthy volunteers (HV); (2) characterize microbial carbolytic capacity in the duodenum and feces. Methods We conducted an analysis of CeD patients (newly diagnosed and GFD-treated) and HV attending our specialized McMaster adult CeD clinic. To investigate fibre consumption, participants completed a validated food frequency questionnaire (Victoria DQES v2), and the chloroplast trnL-P6 plastid marker was used to analyze the presence and diversity of plant DNA in feces at the time of sample collection (FoodSeq). To characterize fibre metabolism, fecal SCFA were measured using gas chromatography mass-spectrometry, and microbiota composition from duodenal aspirates was investigated by 16S rRNA gene Illumina sequencing of the V3V4 region. In silico predictions of metabolic functions and relative abundances of key enzymes were completed with PICRUSt2. Results Most participants consumed fibre below the minimum recommendation (66% < 25g/day, Health Canada), despite diverse dietary plant consumption. Fibre did not correlate with self-reported gastrointestinal symptoms. Fecal SCFAs were lower in new CeD compared to HV, while GFD was partially rescued (CeD: 2799±927 vs HV: 5199±1616 μg/g, p<0.001; GFD: 4058±1283). Duodenal microbiota composition differed between all groups (Aitchinson Distance β-diversity, p<0.05). Abundance of enzymes related to fibre degradation (α-amylase K07405, fructan β-fructosidase K03332) were decreased in both CeD and GFD groups compared to HV (p<0.001), as was the abundance of several members of the Prevotellaceae family that had the greatest predicted contribution to this function (p<0.05). Conclusions Newly diagnosed CeD patients have inadequate fibre consumption and lower microbial capacity to metabolize fibre in the lower and upper GI tract. Despite patients on GFD having the lowest fibre intake, microbial carbolytic activity was improved. Taken together with unpublished findings of inulin accelerating mucosal healing in mouse models of gluten sensitivity, the data should encourage clinical studies to define the effects of fibre supplementation on symptom management and mucosal healing in CeD during GFD. Funding Agencies CIHRCeliac Canada

BACKGROUND:Serratia marcescens is an opportunistic AmpC β-lactamase-producing Enterobacterales associated with intensive care unit outbreaks, causing high morbidity and mortality. The spatiotemporal dynamics of Serratia species and their implications for hospital infection prevention and control remain understudied. METHODS:We prospectively identified patient culture specimens in a multihospital academic healthcare system from 2022 to 2024. We included first-time isolates of S. marcescens identified via culture and confirmed by matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS). Isolates underwent whole-genome sequencing on the Illumina NextSeq 2000 platform. We queried assembled genomes using the Comprehensive Antibiotic Resistance Database to identify resistance genes and predict resistomes. We constructed a maximum-likelihood phylogenetic tree using GTDB-Tk-assigned taxonomies. We identified possible links between patients if there was a spatiotemporal overlap and the average nucleotide identity (ANI) of a sequence pair was > 99.0%. We collected relevant patient characteristics via retrospective chart review and analyzed data using descriptive statistics. RESULTS:Of 147 identified isolates, we included 125. Phenotypic testing suggested either inducible or derepressed AmpC expression in all isolates. Whole-genome sequencing found species-level discordance with MALDI-TOF MS in 64 (51.2%) isolates, suggesting the presence of multiple members of the recently described S. marcescens complex causing hospital- or community-associated infections. Only 1 isolate pair had a spatiotemporal link and ANI > 99.0%. CONCLUSIONS:Between-patient transmission of S. marcescens complex outside of outbreaks is likely rare. Current MALDI-TOF MS-based identification methods are insufficient to identify S. marcescens complex and laboratory reporting should be modified to report only to the level of the complex.

Interactions between plants and bacterial communities are essential for host physiology and broader ecosystem functioning, but plant-microbiome interactions can be disrupted by environmental change like urbanization. Here, we evaluated how urbanization affected the diversity and assembly of soil and white clover Trifolium repens microbiome communities. We sampled 35 populations of white clover and associated roots and soil along an urbanization gradient. Soil alpha diversity was greater at the urban and rural limits of the gradient and lower in suburban habitats, while root alpha diversity was not influenced by urbanization. Root and soil bacterial communities had distinct compositions, with greater beta diversity for root compared to soil microbiomes. We found that urbanization directly and indirectly affected soil microbiome assembly, particularly through soil carbon. In contrast, root microbiome assembly was not linked to urbanization, which suggested that the host plant acted as an additional filter on microbiome assembly independent of urbanization. We also found that key pathogenic bacteria like Legionella and Clostridium varied in abundance with urbanization, which has implications for human health. Together, our study underscores the importance of examining how urban-driven environmental change alters the ecology and function of soil and root microbiomes.

Exclusive enteral nutrition (EEN) is effective in inducing remission in pediatric Crohn disease (CD). EEN alters the intestinal microbiome, but precise mechanisms are unknown. We hypothesized that pre-diagnosis diet establishes a baseline gut microbiome, which then mediates response to EEN. We analyzed prospectively recorded food frequency questionnaires (FFQs) for pre-diagnosis dietary patterns. Fecal microbiota were sequenced (16SrRNA) at baseline and through an 18-month follow-up period. Dietary patterns, Mediterranean diet adherence, and stool microbiota were associated with EEN treatment outcomes, disease flare, need for anti-tumor necrosis factor (TNF)-α therapy, and long-term clinical outcomes. Ninety-eight patients were included. Baseline disease severity and microbiota were associated with diet. Four dietary patterns were identified by FFQs; a “mature diet” high in fruits, vegetables, and fish was linked to increased baseline microbial diversity, which was associated with fewer disease flares (p < 0.05) and a trend towards a delayed need for anti-TNF therapy (p = 0.086). Baseline stool microbial taxa were increased (Blautia and Faecalibacterium) or decreased (Ruminococcus gnavus group) with the mature diet compared to other diets. Surprisingly, a “pre-packaged” dietary pattern (rich in processed foods) was associated with delayed flares in males (p < 0.05). Long-term pre-diagnosis diet was associated with outcomes of EEN therapy in pediatric CD; diet–microbiota and microbiota–outcome associations may mediate this relationship.

Breastfeeding and microbial colonization during infancy occur within a critical time window for development, and both are thought to influence the risk of respiratory illness. However, the mechanisms underlying the protective effects of breastfeeding and the regulation of microbial colonization are poorly understood. Here, we profiled the nasal and gut microbiomes, breastfeeding characteristics, and maternal milk composition of 2,227 children from the CHILD Cohort Study. We identified robust colonization patterns that, together with milk components, predict preschool asthma and mediate the protective effects of breastfeeding. We found that early cessation of breastfeeding (before 3 months) leads to the premature acquisition of microbial species and functions, including Ruminococcus gnavus and tryptophan biosynthesis, which were previously linked to immune modulation and asthma. Conversely, longer exclusive breastfeeding supports a paced microbial development, protecting against asthma. These findings underscore the importance of extended breastfeeding for respiratory health and highlight potential microbial targets for intervention.

STUDY DESIGN:Cross-sectional survey study.OBJECTIVE:The aim was to determine if health literacy level is associated with patient-reported outcomes and self-reported health status among patients presenting to an academic outpatient spine center.SUMMARY OF BACKGROUND DATA:Patient reports are critical to assessing symptom severity and treatment success in orthopedic spine patients. Patient-reported outcome measures (PROMs) are important instruments commonly used for this purpose. However, the influence of patient health literacy on PROMs has not yet been given much consideration in spine literature.MATERIALS AND METHODS:Consecutive English-speaking patients over the age of 18 years and new to our clinic verbally completed the Newest Vital Sign health literacy assessment tool and a sociodemographic survey, including self-reported health status. In addition, seven Patient-Reported Outcomes Measurement Information System scores were extracted from patient records. Regression modeling was performed with PROMs considered as dependent variables, health literacy level as the primary predictor, and all other factors (age, sex, race, ethnicity, native English speaker, highest educational degree, grade-level reading, marital status, employment status, annual household income, and type of insurance) as covariates.RESULTS:Among the 318 included patients, 33% had limited health literacy. Adjusted regression analysis demonstrated that patients with limited health literacy had worse PROM scores across all seven domains (Physical Function: P =0.028; Depression: P =0.035; Global Health-Physical: P =0.001; Global Health-Mental: P =0.007; Pain Interference: P =0.036; Pain Intensity: P =0.002; Anxiety: P =0.047). In addition, patients with limited health literacy reported worse self-reported health status ( P <0.001).CONCLUSIONS:Spine patients with limited health literacy have worse baseline PROM scores confounders and report worse general health. Further investigations are necessary to elucidate if limited health literacy is a marker or the root cause of these disparities. Findings from this study urge the consideration of patient health literacy when interpreting PROMs as well as the implications for patient assessment and discussion of treatment options.

Abstract Background An imbalance in host proteases has been implicated in inflammatory bowel disease (IBD). Recent evidence implicates microbial proteolytic activity (PA) in ulcerative colitis but whether it also plays a role in Crohn’s disease (CD) remains unclear. Purpose We therefore investigated the colitogenic potential and underlying pathways of proteolytic CD microbiota. Method Adult germ-free (GF) C57BL/6 mice were colonized with CD microbiota selected based on high (CD-HPA) or low fecal proteolytic activity (CD-LPA), and from healthy controls with LPA (HC-LPA), after which total fecal proteolytic, elastolytic and mucolytic activity were analyzed in the mice. Microbial community was assessed by 16S rRNA gene sequencing. Immune function and colonic injury were investigated by inflammatory gene expression (NanoString) and histology. Colitis severity and underlying pathways were investigated in C57BL/6, Nucleotide-binding Oligomerization Domain-2 knock-out (Nod2-/-), and Protease-Activated Receptor 2 (PAR2) cleavage resistant mice (R38E-PAR2) subjected to 2% dextran sodium sulfate in drinking water for 5 days followed by 2 days on water. Result(s) Colonization with HC-LPA or CD-LPA lowered baseline fecal proteolytic activity compared with GF mice, which was paralleled by lower acute inflammatory cell infiltrate. CD-HPA further increased proteolytic activity compared with GF mice. Fecal supernatants from CD-LPA or HC-LPA colonized mice had lower in vitro PAR2 cleavage compared to supernatants from GF and CD-HPA colonized mice. Several genes, such as Map kinases, Rhoa, Myd88, and Tollip, were increased in GF mice compared to colonized mice. 18 genes related to inflammation and barrier function (e.g., Mapk2k6, Tnf, Claudin1) were differentially expressed between CD-LPA and CD-HPA. CD-HPA mice had lower alpha diversity, distinct microbial profiles, and higher fecal proteolytic activity compared with CD-LPA. Abundance of several beneficial species (e.g., Akkermansia muciniphilia) was decreased while other taxa were increased (e.g., Hungattella hathewayi) in CD-HPA compared to CD-LPA. H. hathewayi as well as the serine protease K04772 were transcriptionally increased in fecal samples from CD-HPA colonized mice. C57BL/6 and Nod2-/- mice, but not R38E-PAR2 mice, colonized with CD-HPA developed earlier and more severe colitis compared with mice colonized with CD-LPA. Conclusion(s) CD proteolytic microbiota is proinflammatory through a PAR2 pathway. H. hathewayi correlates with the proinflammatory phenotype through the serine protease K04772 in this model. The results support a role of microbial PA in CD, which could constitute a biomarker for identifying patients who would benefit from anti-proteolytic therapies. Disclosure of Interest None Declared

Chemicals in food are widely used leading to significant human exposure. Allura Red AC (AR) is a highly common synthetic colorant; however, little is known about its impact on colitis. Here, we show chronic exposure of AR at a dose found in commonly consumed dietary products exacerbates experimental models of colitis in mice. While intermittent exposure is more akin to a typical human exposure, intermittent exposure to AR in mice for 12 weeks, does not influence susceptibility to colitis. However, exposure to AR during early life primes mice to heightened susceptibility to colitis. In addition, chronic exposure to AR induces mild colitis, which is associated with elevated colonic serotonin (5-hydroxytryptamine; 5-HT) levels and impairment of the epithelial barrier function via myosin light chain kinase (MLCK). Importantly, chronic exposure to AR does not influence colitis susceptibility in mice lacking tryptophan hydroxylase 1 (TPH1), the rate limiting enzyme for 5-HT biosynthesis. Cecal transfer of the perturbed gut microbiota by AR exposure worsens colitis severity in the recipient germ-free (GF) mice. Furthermore, chronic AR exposure elevates colonic 5-HT levels in naïve GF mice. Though it remains unknown whether AR has similar effects in humans, our study reveals that chronic long-term exposure to a common synthetic colorant promotes experimental colitis via colonic 5-HT in gut microbiota-dependent and -independent pathway in mice.

Emerging evidence implicates microbial proteolytic activity in ulcerative colitis (UC), but whether it also plays a role in Crohn's disease (CD) remains unclear. We investigated the effects of colonizing adult and neonatal germ-free C57BL/6 mice with CD microbiota, selected based on high (CD-HPA) or low fecal proteolytic activity (CD-LPA), or microbiota from healthy controls with LPA (HC-LPA) or HPA (HC-HPA). We then investigated colitogenic mechanisms in gnotobiotic C57BL/6, and in mice with impaired Nucleotide-binding Oligomerization Domain-2 (NOD2) and Protease-Activated Receptor 2 (PAR2) cleavage resistant mice (Nod2 (-/-); R38E-PAR2 respectively). At sacrifice, total fecal proteolytic, elastolytic, and mucolytic activity were analyzed. Microbial community and predicted function were assessed by 16S rRNA gene sequencing and PICRUSt2. Immune function and colonic injury were investigated by inflammatory gene expression (NanoString) and histology. Colonization with HC-LPA or CD-LPA lowered baseline fecal proteolytic activity in germ-free mice, which was paralleled by lower acute inflammatory cell infiltrate. CD-HPA further increased proteolytic activity compared with germ-free mice. CD-HPA mice had lower alpha diversity, distinct microbial profiles and higher fecal proteolytic activity compared with CD-LPA. C57BL/6 and Nod2 (-/-) mice, but not R38E-PAR2, colonized with CD-HPA had higher colitis severity than those colonized with CD-LPA. Our results indicate that CD proteolytic microbiota is proinflammatory, increasing colitis severity through a PAR2 pathway.

Cardiovascular disease remains the leading cause of death and disability in the United States and globally. Disease burden continues to escalate despite technological advances associated with improved life expectancy and quality of life. As a result, longer life is associated with multiple chronic cardiovascular conditions. Clinical guidelines provide recommendations without considering prevalent scenarios of multimorbidity and health system complexities that affect practical adoption. The diversity of personal preferences, cultures, and lifestyles that make up one's social and environmental context is often overlooked in ongoing care planning for symptom management and health behavior support, hindering adoption and compromising patient outcomes, particularly in groups at high risk. The purpose of this scientific statement was to describe the characteristics and reported outcomes in existing person-centered care delivery models for selected cardiovascular conditions. We conducted a scoping review using Ovid MEDLINE, Embase.com, Web of Science, CINAHL Complete, Cochrane Central Register of Controlled Trials through Ovid, and ClinicalTrials.gov from 2010 to 2022. A range of study designs with a defined aim to systematically evaluate care delivery models for selected cardiovascular conditions were included. Models were selected on the basis of their stated use of evidence-based guidelines, clinical decision support tools, systematic evaluation processes, and inclusion of the patient's perspective in defining the plan of care. Findings reflected variation in methodological approach, outcome measures, and care processes used across models. Evidence to support optimal care delivery models remains limited by inconsistencies in approach, variation in reimbursement, and inability of health systems to meet the needs of patients with chronic, complex cardiovascular conditions.

OBJECTIVES:Prior research suggests that errors occur frequently for patients with medical complexity during the hospital-to-home transition. Less is known about effective postdischarge communication strategies for this population. We aimed to assess rates of 30-day (1) postdischarge incidents and (2) readmissions and emergency department (ED) visits before and after implementing a hospital-to-home intervention.METHODS:We conducted a prospective intervention study of children with medical complexity discharged at a children's hospital from April 2018 to March 2020. A multistakeholder team developed a bundled intervention incorporating the I-PASS handoff framework including a postdischarge telephone call, restructured discharge summary, and handoff communication to outpatient providers. The primary outcome measure was rate of postdischarge incidents collected via electronic medical record review and family surveys. Secondary outcomes were 30-day readmissions and ED visits.RESULTS:There were 199 total incidents and the most common were medication related (60%), equipment issues (15%), and delays in scheduling/provision of services (11%). The I-PASS intervention was associated with a 36.4% decrease in the rate of incidents per discharge (1.51 versus 0.95, P = 0.003). There were fewer nonharmful errors and quality issues after intervention (1.27 versus 0.85 per discharge, P = 0.02). The 30-day ED visit rate was significantly lower after intervention (12.6% versus 3.4%, per 100 discharges, P = 0.05). Thirty-day readmissions were 15.8% versus 10.2% postintervention (P = 0.32).CONCLUSIONS:A postdischarge communication intervention for patients with medical complexity was associated with fewer postdischarge incidents and reduced 30-day ED visits. Standardized postdischarge communication may play an important role in improving quality and safety in the transition from hospital-to-home for vulnerable populations.

Genomic epidemiology can facilitate an understanding of evolutionary history and transmission dynamics of a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak. We used next-generation sequencing techniques to study SARS-CoV-2 genomes isolated from patients and health care workers (HCWs) across five wards of a Canadian hospital with an ongoing SARS-CoV-2 outbreak. Using traditional contact tracing methods, we show transmission events between patients and HCWs, which were also supported by the SARS-CoV-2 lineage assignments. The outbreak predominantly involved SARS-CoV-2 B.1.564.1 across all five wards, but we also show evidence of community introductions of lineages B.1, B.1.1.32, and B.1.231, falsely assumed to be outbreak related. Altogether, our study exemplifies the value of using contact tracing in combination with genomic epidemiology to understand the transmission dynamics and genetic underpinnings of a SARS-CoV-2 outbreak. IMPORTANCE Our manuscript describes a SARS-CoV-2 outbreak investigation in an Ontario tertiary care hospital. We use traditional contract tracing paired with whole-genome sequencing to facilitate an understanding of the evolutionary history and transmission dynamics of this SARS-CoV-2 outbreak in a clinical setting. These advancements have enabled the incorporation of phylogenetics and genomic epidemiology into the understanding of clinical outbreaks. We show that genomic epidemiology can help to explore the genetic evolution of a pathogen in real time, enabling the identification of the index case and helping understand its transmission dynamics to develop better strategies to prevent future spread of SARS-CoV-2 in congregate, clinical settings such as hospitals.

Standardized handoff tools improve communication and patient care; however, their widespread use in surgical fields is lacking. OrthoPass, an orthopaedic adaptation of I-PASS, was developed in 2019 to address handoff concerns and demonstrated sustained improvements across multiple handoff domains over an 18-month period. We sought to characterize the longitudinal effect and sustainability of OrthoPass within a single large residency program 3.5 years after its implementation. This mixed methods study involved electronic handoff review for quality domains in addition to survey distribution and evaluation. We conducted comparative analyses of handoff adherence and survey questions as well as a thematic analysis of provider-free responses. We evaluated 146 electronic handoffs orthopaedic residents, fellows, and advanced practice providers 3.5 years after OrthoPass implementation. Compared with 18-month levels, adherence was sustained across five of nine handoff domains and was markedly improved in two domains. Furthermore, provider valuations of OrthoPass improved regarding promoting communication and patient safety (83% versus 70%) and avoiding patient errors and near misses (72% versus 60%). These improvements were further substantiated by positive trends in Agency for Healthcare Research and Quality Surveys on Patient Safety Culture hospital survey data. Thematic analysis of free responses shared by 37 providers (42%) generated favorable, unfavorable, and balanced themes further contextualized by subthemes. At 3.5 years after its introduction, OrthoPass continues to improve patient handoff quality and to support provider notions of patient safety. Although providers acknowledged the benefits of this electronic handoff tool, they also shared unique insights into several drawbacks. This feedback will inform ongoing efforts to improve OrthoPass.

BACKGROUND: Limited health literacy exacerbates health inequity and has serious implications for patient care. It hinders successful communication and comprehension of relevant health infor-mation, which can lead to suboptimal care. Despite the evidence regarding the significance of health literacy, the topic has received little consideration in orthopedic spine patients. PURPOSE: To investigate the prevalence of and factors associated with limited health literacy among outpatients presenting to a tertiary urban academic hospital-based orthopedic spine center. STUDY DESIGN: Cross-sectionals. PATIENT SAMPLE: Patients 18 years of age or older seen at a tertiary urban academic hospital-based multi-surgeon outpatient spine center.OUTCOME MEASURES: The Newest Vital Sign (NVS) health literacy assessment. METHODS: Between December 2021 and March 2022, 447 consecutive English-speaking patients over the age of 18 years and new to the outpatient spine clinic were approached for partici-pation in a cross-sectional survey study, of which 405 agreed to participate. Patients completed the Newest Vital Sign (NVS) health literacy assessment tool, the Rapid Estimation of Adult Literacy in Medicine Short Form (REALM-SF), and a sociodemographic survey (including race/ethnicity, level of education, employment status, income, and marital status). The NVS scores were divided into lim-ited (0-3) and adequate (4-6) health literacy. REALM-SF scores were classified into reading levels below ninth grade (0-6) or at least ninth grade (7). Additional demographic data was extracted from patient records. Online mapping tools were used to collect the Social Vulnerability Index (SVI) and the Area Deprivation Index (ADI) for each patient. Subsequently, multivariable regression modeling was performed to identify independent factors associated with limited health literacy.RESULTS: The prevalence of limited health literacy in patients presenting to an urban academic outpatient spine center was 33% (135/405). Unadjusted analysis found that patients who were socioeconomically disadvantaged (eg, unemployed, lower household income, publicly insured and higher SVI) and had more unfavorable social determinant of health features (eg, housing concerns, higher ADI, less years of education, below ninth grade reading level, unmarried) had high rates of limited health literacy. Adjusted regression analysis demonstrated that limited health literacy was independently associated with higher ADI state decile, living less than 10 years at current address, having housing concerns, not being employed, non-native English speaking, having less years of education and below ninth grade reading level.CONCLUSIONS: This study found that a substantial portion of the patients presenting to an out-patient spine center have limited health literacy, more so if they are socially disadvantaged. Future efforts should investigate the impact of limited health literacy on access to care, treatment out-comes and health care utilization in orthopedic patients. Neighborhood social vulnerability meas-ures may be a feasible way to identify patients at risk of limited health literacy in clinical practice and offer opportunities for tailored patient care. This may contribute to prioritizing the mitigation of disparities and aid in the development of meaningful interventions to improve health equity in orthopedics.(c) 2022 Elsevier Inc. All rights reserved.

Isolating and characterizing emerging SARS-CoV-2 variants is key to understanding virus pathogenesis. In this study, we isolated samples of the SARS-CoV-2 R.1 lineage, categorized as a variant under monitoring by the World Health Organization, and evaluated their sensitivity to neutralizing antibodies and type I interferons. We used convalescent serum samples from persons in Canada infected either with ancestral virus (wave 1) or the B.1.1.7 (Alpha) variant of concern (wave 3) for testing neutralization sensitivity. The R.1 isolates were potently neutralized by both the wave 1 and wave 3 convalescent serum samples, unlike the B.1.351 (Beta) variant of concern. Of note, the R.1 variant was significantly more resistant to type I interferons (IFN-α/β) than was the ancestral isolate. Our study demonstrates that the R.1 variant retained sensitivity to neutralizing antibodies but evolved resistance to type I interferons. This critical driving force will influence the trajectory of the pandemic.

The acidification of water in mining areas is a global environmental issue primarily catalyzed by sulfur-oxidizing bacteria (SOB). Little is known about microbial sulfur cycling in circumneutral pH mine tailing impoundment waters. Here we investigate biological sulfur oxidation over four years in a mine tailings impoundment water cap, integrating aqueous sulfur geochemistry, genome-resolved metagenomics and metatranscriptomics. The microbial community is consistently dominated by neutrophilic, chemolithoautotrophic SOB (relative abundances of ~76% in 2015, ~55% in 2016/2017 and ~60% in 2018). Results reveal two SOB strategies alternately dominate across the four years, influencing acid generation and sulfur speciation. Under oxic conditions, novel Halothiobacillus drive lower pH conditions (as low as 4.3) and lower [S 2 O 3 2− ] via the complete Sox pathway coupled to O 2 . Under anoxic conditions, Thiobacillus spp. dominate in activity, via the incomplete Sox and rDSR pathways coupled to NO 3 − , resulting in higher [S 2 O 3 2− ] and no net significant acidity generation. This study provides genomic evidence explaining acidity generation and thiosulfate accumulation patterns in a circumneutral mine tailing impoundment and has significant environmental applications in preventing the discharge of sulfur compounds that can impact downstream environments. These insights illuminate opportunities for in situ biotreatment of reduced sulfur compounds and prediction of acidification events using gene-based monitoring and in situ RNA detection.

Background:Residents in long-term care homes, who tend to be of advanced age and frail, are at increased risk of respiratory infections. The respiratory microbiota is known to change with age, but whether these changes contribute to the risk of infection is not known. Our goal was to determine how the nasal microbiota of frail older adults changes during symptoms of influenza-like illness (ILI) and how this may be impacted by enrolment in a placebo-controlled trial testing the feasibility of administering a Lactobacillus rhamnosus GG probiotic to prevent respiratory infection (2014-2017). Methods:The microbiome of the nasal (mid-turbinate) of 150 residents of long-term care homes was interrogated using 16S rRNA gene sequencing. Results:We identified a diverse and individualised microbiota which could be separated into nine distinct clusters based on Bray-Curtis distances. Samples collected during symptoms of ILI differed statistically from those collected pre- and post-cold and influenza season, and we observed decreased temporal stability (as measured by movement between clusters) in individuals who experienced ILI compared to those who did not. Conclusions:The use of probiotics decreased ILI-induced changes to the microbiota; however, it is not clear whether this decrease is sufficient to prevent respiratory illness.