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Group B Streptococcus (GBS) asymptomatically colonizes the vagina but can opportunistically ascend to the uterus and be transmitted vertically during pregnancy, resulting in neonatal pneumonia, bacteremia, and meningitis. GBS is a leading etiologic agent of neonatal infection and understanding the mechanisms by which GBS persists within the polymicrobial female genital mucosa has the potential to mitigate subsequent transmission and disease. Type VIIb secretion systems (T7SSb) are encoded by Bacillota and often mediate interbacterial competition using LXG toxins that contain conserved N-termini important for secretion and variable C-terminal toxin domains that confer diverse biochemical activities. Our recent work characterized a role for the GBS T7SSb in vaginal colonization and ascending infection but the mechanisms by which the T7SSb promotes GBS persistence in this polymicrobial niche remain unknown. Herein, we investigate the GBS T7SS in interbacterial competition and GBS niche establishment in the female genital tract. We demonstrate GBS T7SS-dependent inhibition of mucosal pathobiont Enterococcus faecalis both in vitro using predator-prey assays and in vivo in the murine genital tract and found that a GBS LXG protein encoded within the T7SS locus (herein named group B streptococcal LXG Toxin A) contributes to these phenotypes. We identify BltA as a T7SS substrate that is toxic to E. coli and S. aureus upon induction of intracellular expression along with associated chaperones. Finally, we show that BltA and its chaperones contribute to GBS vaginal colonization. Altogether, these data reveal a role for a novel T7b-secreted toxin in GBS mucosal persistence and competition.IMPORTANCECompetition between neighboring, non-kin bacteria is essential for microbial niche establishment in mucosal environments. Gram-positive bacteria encoding T7SSb have been shown to engage in competition through the export of LXG-motif-containing toxins, but these have not been characterized in group B Streptococcus (GBS), an opportunistic colonizer of the polymicrobial female genital tract. Here, we show a role for GBS T7SS in competition with mucosal pathobiont Enterococcus faecalis, both in vitro and in vivo. We further find that a GBS LXG protein contributing to this antagonism is exported by the T7SS and is intracellularly toxic to other bacteria; therefore, we have named this protein group B streptococcal LXG Toxin A (BltA). Finally, we show that BltA and its associated chaperones promote persistence within female genital tract tissues, in vivo. These data reveal previously unrecognized mechanisms by which GBS may compete with other mucosal opportunistic pathogens to persist within the female genital tract.
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Group B Streptococcus (GBS) is a Gram-positive pathobiont that commonly colonizes the gastrointestinal and lower female genital tracts but can cause sepsis and pneumonia in newborns and is a leading cause of neonatal meningitis. Despite the resulting disease severity, the pathogenesis of GBS is not completely understood, especially during the early phases of infection. To investigate GBS factors necessary for blood stream survival, we performed a transposon (Tn) mutant screen in our bacteremia infection model using a GBS mariner transposon mutant library previously developed by our group. We identified significantly underrepresented mutations in 628 genes that contribute to survival in the blood, including those encoding known virulence factors such as capsule, the ß-hemolysin, and inorganic metal ion transport systems. Most of the underrepresented genes have not been previously characterized or studied in GBS, including gloA and gloB, which are homologs for genes involved in methylglyoxal (MG) detoxification. MG is a byproduct of glycolysis and a highly reactive toxic aldehyde that is elevated in immune cells during infection. Here, we observed MG sensitivity across multiple GBS isolates and confirm that gloA contributes to MG tolerance and invasive GBS infection. We show specifically that gloA contributes to GBS survival in the presence of neutrophils and depleting neutrophils in mice abrogates the decreased survival and infection of the gloA mutant. The requirement of the glyoxalase pathway during GBS infection suggests that MG detoxification is important for bacterial survival during host-pathogen interactions.
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Group B Streptococcus (GBS) asymptomatically colonizes the vagina but can opportunistically ascend to the uterus and be transmitted vertically during pregnancy, resulting in neonatal pneumonia, bacteremia and meningitis. GBS is a leading etiologic agent of neonatal infection and understanding the mechanisms by which GBS persists within the polymicrobial female genital mucosa has potential to mitigate subsequent transmission and disease. Type VIIb secretion systems (T7SSb) are encoded by Firmicutes and often mediate interbacterial competition using LXG toxins that contain conserved N-termini important for secretion and variable C-terminal toxin domains that confer diverse biochemical activities. Our recent work characterized a role for the GBS T7SSb in vaginal colonization and ascending infection but the mechanisms by which the T7SSb promotes GBS persistence in this polymicrobial niche remain unknown. Herein, we investigate the GBS T7SS in interbacterial competition and GBS niche establishment in the female genital tract. We demonstrate GBS T7SS-dependent inhibition of mucosal pathobiont Enterococcus faecalis both in vitro using predator-prey assays and in vivo in the murine genital tract and found that a GBS LXG protein encoded within the T7SS locus (herein named group B streptococcal LXG Toxin A) that contributes to these phenotypes. We identify BltA as a T7SS substrate that is toxic to E. coli and S. aureus upon induction of expression along with associated chaperones. Finally, we show that BltA and its chaperones contribute to GBS vaginal colonization. Altogether, these data reveal a role for a novel T7b-secreted toxin in GBS mucosal persistence and competition.
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Diabetic wound infections including diabetic foot ulcers (DFUs) are a major global health concern and a leading cause of non-traumatic amputations. Numerous bacterial species establish infection in DFUs, and treatment with antibiotics often fails due to widespread antibiotic resistance and biofilm formation. Determination of bacterial species that reside in DFU and their virulence potential is critical to inform treatment options. Here, we isolate bacteria from debridement tissues from patients with diabetes at the University of Colorado Anschutz Medical Center. The most frequent species were Gram-positive including Enterococcus faecalis, Staphylococcus aureus, and Streptococcus agalactiae, also known as Group B Streptococcus (GBS). Most tissues had more than one species isolated with E. faecalis and GBS frequently occurring in polymicrobial infection with S. aureus. S. aureus was the best biofilm producing species with E. faecalis and GBS isolates exhibiting little to no biofilm formation. Antibiotic susceptibility varied amongst strains with high levels of penicillin resistance amongst S. aureus, clindamycin resistance amongst GBS and intermediate vancomycin resistance amongst E. faecalis. Finally, we utilized a murine model of diabetic wound infection and found that the presence of S. aureus led to significantly higher recovery of GBS and E. faecalis compared to mice challenged in mono-infection.
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Streptococcus agalactiae [group B Streptococcus (GBS)] is a leading cause of neonatal meningitis, with late-onset disease (LOD) occurring after gastrointestinal tract colonization in infants. Bacterial membrane lipids are essential for host-pathogen interactions, and the functions of glycolipids are yet to be fully elucidated. GBS synthesizes three major glycolipids: glucosyl-diacylglycerol (Glc-DAG), diglucosyl-DAG (Glc2-DAG), and lysyl-Glc-DAG (Lys-Glc-DAG). Here, we identify the enzyme, IagB, as responsible for biosynthesis of Glc-DAG, the precursor for the two other glycolipids in GBS. To examine the collective role of glycolipids to GBS virulence, we adapted a murine model of neonatal meningitis to simulate LOD. The GBS∆iagB mutant traversed the gut-epithelial barrier comparable to wild type but was severely attenuated in bloodstream survival, resulting in decreased bacterial loads in the brain. The GBS∆iagB mutant was more susceptible to neutrophil killing and membrane targeting by host antimicrobial peptides. This work reveals an unexplored function of GBS glycolipids with their ability to protect the bacterial cell from host antimicrobial killing.
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Glucolípidos , Infecciones Estreptocócicas , Streptococcus agalactiae , Streptococcus agalactiae/patogenicidad , Streptococcus agalactiae/inmunología , Streptococcus agalactiae/metabolismo , Animales , Glucolípidos/metabolismo , Glucolípidos/inmunología , Ratones , Virulencia , Infecciones Estreptocócicas/inmunología , Infecciones Estreptocócicas/microbiología , Humanos , Modelos Animales de Enfermedad , Interacciones Huésped-Patógeno/inmunología , Neutrófilos/inmunología , Neutrófilos/metabolismo , MutaciónRESUMEN
Objective: To perform a geospatial analysis of food insecurity in a rural county known to have poor health outcomes and assess the effect of the COVID-19 pandemic. Methods: In 2020, we mailed a comprehensive cross-sectional survey to all households in Sullivan County, a rural county with the second-worst health outcomes among all counties in New York State. Surveys of households included validated food insecurity screening questions. Questions were asked in reference to 2019, prior to the pandemic, and for 2020, in the first year of the pandemic. Respondents also responded to demographic questions. Raking adjustments were performed using age, sex, race/ethnicity, and health insurance strata to mitigate non-response bias. To identify significant hotspots of food insecurity within the county, we also performed geospatial analysis. Findings: From the 28,284 households surveyed, 20% of households responded. Of 4725 survey respondents, 26% of households reported experiencing food insecurity in 2019, and in 2020, this proportion increased to 35%. In 2020, 58% of Black and Hispanic households reported experiencing food insecurity. Food insecurity in 2020 was also present in 58% of unmarried households with children and in 64% of households insured by Medicaid. The geospatial analyses revealed that hotspots of food insecurity were primarily located in or near more urban areas of the rural county. Conclusions: Our countywide health survey in a high-risk rural county identified significant increases of food insecurity in the first year of the COVID-19 pandemic, despite national statistics reporting a stable rate. Responses to future crises should include targeted interventions to bolster food security among vulnerable rural populations.
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On a single night in 2023, more than 653,000 people experienced homelessness in the United States. In this overview, we highlight structural and individual risk factors that can lead to homelessness, explore evidence on the relationship between homelessness and health, discuss programmatic and policy innovations, and provide policy recommendations. Health system efforts to address homelessness and improve the health of homeless populations have included interventions such as screening for social needs and medical respite programs. Initiatives using the Housing First approach to permanent supportive housing have a strong track record of success. Health care financing innovations using Medicaid Section 1115 waivers offer promising new approaches to improving health and housing for people experiencing homelessness. To substantially reduce homelessness and its many adverse health impacts, changes are needed to increase the supply of affordable housing for households with very low incomes. Health care providers and systems should leverage their political power to advocate for policies that scale durable, evidence-based solutions to reduce homelessness, including increased funding to expand housing choice vouchers and greater investment in the creation and preservation of affordable housing.
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Personas con Mala Vivienda , Humanos , Estados Unidos , Vivienda , Políticas , MedicaidRESUMEN
BACKGROUND: Nursing assistants working in long-term care (LTC) often report that their job is stressful. To reduce their work stress, a better understanding of their stress profile is needed. OBJECTIVE: We aimed to pilot test methods to identify and understand stressors that LTC nursing assistants experience. METHODS: We asked each participant to provide wearable sensor/watch data, ecological momentary assessment (EMA) surveys and end of day review data over two eight-hour working shifts. RESULTS: Eight nursing assistants participated. All participants worked in a common continuing care retirement community in Maryland, United States of America. Our stress assessment method revealed 83 stressful events that were classified under 10 categories. Most of the reported events were rated as having a mild to low-moderate intensity. The three most common causes of stress were work demands and pressure (28.35%), heavy workload and staffing (19.69%), and safety issues and COVID-19 concerns (17.32%). We also explored the difference between stress events and intensity among different shifts. Disrespect from residents (22.73%) was the most commonly reported stressor during day shifts. Feeling rushed was the most commonly reported stressor during the evening (22.47%) and the night (38.46%) shifts. CONCLUSIONS: We found stress was commonly reported. Stress intensity conflicted with prior literature, and we explored possible explanations. IMPLICATIONS FOR PRACTICE: We discuss potential implications for these findings, modification of our methods to increase feasibility, the utility of these data collection methods for future work and suggest next steps.
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Asistentes de Enfermería , Dispositivos Electrónicos Vestibles , Humanos , Cuidados a Largo Plazo , Evaluación Ecológica Momentánea , Carga de TrabajoRESUMEN
Group B Streptococcus (GBS) is known to colonize the female reproductive tract and causes adverse pregnancy outcomes and neonatal disease. DNA methylation is a common mechanism for both phage defense and transcriptional regulation. Here, we report the m6A and m4C methylomes of four clinical GBS isolates, CJB111, A909, COH1, and NEM316.
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Housing insecurity can take multiple forms, such as unaffordability, crowding, forced moves, multiple moves, and homelessness. Existing research has linked homelessness to increased emergency department (ED) use, but gaps remain in understanding the relationship between different types of housing insecurity and ED use. In this study, we examined the association between different types of housing insecurity, including detailed measures of homelessness, and future ED use among a cohort of patients initially seen in an urban safety-net hospital ED in the United States between November 2016 and January 2018. We found that homelessness was associated with a higher mean number of ED visits in the year post-baseline. Other measures of housing insecurity (unaffordability, crowding, forced moves, and multiple moves) were not associated with greater ED use in the year post-baseline in multivariable models. We also found that only specific types of homelessness, primarily unsheltered homelessness, were associated with increased ED use.
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Inestabilidad de Vivienda , Problemas Sociales , Humanos , Servicio de Urgencia en Hospital , PacientesRESUMEN
Group B Streptococcus (GBS) colonizes the female reproductive tract (FRT) and causes adverse pregnancy outcomes and invasive disease following vertical transmission to the fetus or newborn. Despite this major public health burden, the mechanisms of GBS FRT colonization are understudied. A recent transposon sequencing screen identified GBS factors contributing to vaginal colonization and ascending spread, including a putative DNA-cytosine methyltransferase (Dcm). We constructed a Δdcm deletion strain and confirmed that dcm contributes to murine FRT colonization. Investigation of the evolutionary origin of the dcm gene reveals that it is widely distributed across GBS and is encoded as part of a prophage genome that displays evidence of horizontal transfer between GBS strains. We further show that Dcm contributes to 5mC methylation and global regulation of genes involved in carbohydrate metabolism, transcription regulation, and known adhesins and metabolic factors involved in GBS colonization. Interestingly, GBS genes that are induced in the presence of the highly glycosylated vaginal mucin MUC5B were significantly downregulated in the ∆dcm mutant. Furthermore, the ∆dcm mutant exhibited reduced binding to immobilized mucin and was attenuated in its ability to grow on numerous carbon sources including the carbohydrates found on mucins. While the ∆dcm mutant displayed enhanced clearance from the FRT in wild-type mice, there was no significant difference in MUC5B -/- mice, indicating that Dcm-mediated regulation requires MUC5B to promote GBS colonization. This is the first report to characterize the impact of a DNA methyltransferase on GBS gene regulation and FRT colonization. IMPORTANCE Group B Streptococcus (GBS) colonizes the female reproductive tract (FRT) in one-third of women, and carriage leads to numerous adverse pregnancy outcomes including the preterm premature rupture of membranes, chorioamnionitis, and stillbirth. The presence of GBS in the FRT during pregnancy is also the largest predisposing factor for the transmission of GBS and invasive neonatal diseases, including pneumonia, sepsis, and meningitis. The factors contributing to GBS colonization are still being elucidated. Here, we show for the first time that GBS transcription is regulated by an orphan DNA cytosine methyltransferase (Dcm). Many GBS factors are regulated by Dcm, especially those involved in carbohydrate transport and metabolism. We show that GBS persistence in the FRT is dependent on the catabolism of sugars found on the vaginal mucin MUC5B. Collectively, this work highlights the regulatory importance of a DNA methyltransferase and identifies both host and bacterial factors required for GBS colonization.
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BACKGROUND: Permanent supportive housing (PSH)-subsidized housing paired with support services such as case management-is a key part of national strategic plans to end homelessness. PSH tenants face high overdose risk due to a confluence of individual and environmental risk factors, yet little research has examined overdose prevention in PSH. METHODS: We describe the protocol for a hybrid type 3 stepped-wedge cluster randomized controlled trial (RCT) of overdose prevention practice implementation in PSH. We adapted evidence-based overdose prevention practices and implementation strategies for PSH using input from stakeholder focus groups. The trial will include 20 PSH buildings (with building size ranging from 20 to over 150 tenants) across New York City and New York's Capital Region. Buildings will be randomized to one of four 6-month intervention waves during which they will receive a package of implementation support including training in using a PSH Overdose Prevention (POP) Toolkit, time-limited practice facilitation, and learning collaboratives delivered to staff and tenant implementation champions appointed by each building. The primary outcome is building-level fidelity to a defined list of overdose prevention practices. Secondary and exploratory implementation and effectiveness outcomes will be examined using PSH staff and tenant survey questionnaires, and analysis of tenant Medicaid data. We will explore factors related to implementation success, including barriers and facilitators, using qualitative interviews with key stakeholders. The project is being conducted through an academic-community partnership, and an Advisory Board including PSH tenants and other key stakeholders will be engaged in all stages of the project. DISCUSSION: We describe the protocol for a hybrid type 3 stepped-wedge cluster RCT of overdose prevention practice implementation in PSH. This study will be the first controlled trial of overdose prevention implementation in PSH settings. The research will make a significant impact by testing and informing future implementation strategies to prevent overdose for a population at particularly high risk for overdose mortality. Findings from this PSH-focused research are expected to be broadly applicable to other housing settings and settings serving people experiencing homelessness. TRIAL REGISTRATION: ClinicalTrials.gov, NCT05786222 , registered 27 March 2023.
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Sobredosis de Droga , Personas con Mala Vivienda , Estados Unidos , Humanos , Sobredosis de Droga/prevención & control , Manejo de Caso , Ensayos Clínicos Controlados Aleatorios como AsuntoRESUMEN
Type VIIb secretion systems (T7SSb) in Gram-positive bacteria facilitate physiology, interbacterial competition, and/or virulence via EssC ATPase-driven secretion of small É-helical proteins and toxins. Recently, we characterized T7SSb in group B Streptococcus (GBS), a leading cause of infection in newborns and immunocompromised adults. GBS T7SS comprises four subtypes based on variation in the C-terminus of EssC and the repertoire of downstream effectors; however, the intraspecies diversity of GBS T7SS and impact on GBS-host interactions remains unknown. Bioinformatic analysis indicates that GBS T7SS loci encode subtype-specific putative effectors, which have low interspecies and inter-subtype homology but contain similar domains/motifs and therefore may serve similar functions. We further identify orphaned GBS WXG100 proteins. Functionally, we show that GBS T7SS subtype I and III strains secrete EsxA in vitro and that in subtype I strain CJB111, esxA1 appears to be differentially transcribed from the T7SS operon. Furthermore, we observe subtype-specific effects of GBS T7SS on host colonization, as CJB111 subtype I but not CNCTC 10/84 subtype III T7SS promotes GBS vaginal colonization. Finally, we observe that T7SS subtypes I and II are the predominant subtypes in clinical GBS isolates. This study highlights the potential impact of T7SS heterogeneity on host-GBS interactions.
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Infecciones Estreptocócicas , Sistemas de Secreción Tipo VII , Recién Nacido , Femenino , Humanos , Proteínas Bacterianas/genética , Proteínas Bacterianas/metabolismo , Sistemas de Secreción Tipo VII/genética , Virulencia , Operón/genética , Genitales Femeninos/metabolismo , Infecciones Estreptocócicas/microbiología , Streptococcus agalactiae/genética , Streptococcus agalactiae/metabolismo , Vagina/metabolismo , Vagina/microbiologíaRESUMEN
Group B Streptococcus (GBS) is a Gram-positive pathobiont that can cause adverse health outcomes in neonates and vulnerable adult populations. GBS is one of the most frequently isolated bacteria from diabetic (Db) wound infections but is rarely found in the non-diabetic (nDb) wound environment. Previously, RNA sequencing of wound tissue from Db wound infections in leprdb diabetic mice showed increased expression of neutrophil factors, and genes involved in GBS metal transport such as the zinc (Zn), manganese (Mn), and putative nickel (Ni) import systems. Here, we develop a Streptozotocin-induced diabetic wound model to evaluate the pathogenesis of two invasive strains of GBS, serotypes Ia and V. We observe an increase in metal chelators such as calprotectin (CP) and lipocalin-2 during diabetic wound infections compared to nDb. We find that CP limits GBS survival in wounds of non-diabetic mice but does not impact survival in diabetic wounds. Additionally, we utilize GBS metal transporter mutants and determine that the Zn, Mn, and putative Ni transporters in GBS are dispensable in diabetic wound infection but contributed to bacterial persistence in non-diabetic animals. Collectively, these data suggest that in non-diabetic mice, functional nutritional immunity mediated by CP is effective at mitigating GBS infection, whereas in diabetic mice, the presence of CP is not sufficient to control GBS wound persistence. IMPORTANCE Diabetic wound infections are difficult to treat and often become chronic due to an impaired immune response as well as the presence of bacterial species that establish persistent infections. Group B Streptococcus (GBS) is one of the most frequently isolated bacterial species in diabetic wound infections and, as a result, is one of the leading causes of death from skin and subcutaneous infection. However, GBS is notoriously absent in non-diabetic wounds, and little is known about why this species thrives in diabetic infection. The work herein investigates how alterations in diabetic host immunity may contribute to GBS success during diabetic wound infection.
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Diabetes Mellitus Experimental , Infecciones Estreptocócicas , Infección de Heridas , Ratones , Animales , Neutrófilos , Infecciones Estreptocócicas/microbiología , Streptococcus agalactiae/genéticaRESUMEN
Although effective evidence-based interventions (EBIs) exist, racial/ethnic minority individuals with lower income are less likely to have access to these interventions and may experience greater stigma in the health care system, resulting in disproportionate rates of morbidity and mortality. Peer recovery specialists (PRSs) may be uniquely suited to address barriers faced by those from impoverished areas; however, peers have not traditionally been trained in implementing EBIs. The current open-label trial (N = 8) was performed to evaluate implementation and preliminary effectiveness of an adapted EBI supporting recovery, linkage to treatment, and reduced depression. Results suggest the intervention was feasible, acceptable, and appropriate for linking individuals from a community setting to substance use treatment and could be delivered with fidelity by a peer interventionist. Participants who completed the intervention demonstrated clinically reliable decreases in substance use and depressive symptoms. Findings provide initial support for PRS dissemination of EBIs to increase linkage to care and support recovery in traditionally underserved populations. [Journal of Psychosocial Nursing and Mental Health Services, 61(11), 23-31.].
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Depresión , Trastornos Relacionados con Sustancias , Humanos , Depresión/terapia , Etnicidad , Estudios de Factibilidad , Grupos Minoritarios , Trastornos Relacionados con Sustancias/terapiaRESUMEN
Streptococcus agalactiae (Group B Streptococcus, GBS) is the leading cause of neonatal sepsis and meningitis but has been recently isolated from non-pregnant adults with underlying medical conditions like diabetes. Despite diabetes being a key risk factor for invasive disease, the pathological consequences during GBS infection remain poorly characterized. Here, we demonstrate the pathogenicity of the GBS90356-ST17 and COH1-ST17 strains in streptozotocin-induced diabetic mice. We show that GBS can spread through the bloodstream and colonize several tissues, presenting a higher bacterial count in diabetic-infected mice when compared to non-diabetic-infected mice. Histological sections of the lungs showed inflammatory cell infiltration, collapsed septa, and red blood cell extravasation in the diabetic-infected group. A significant increase in collagen deposition and elastic fibers were also observed in the lungs. Moreover, the diabetic group presented red blood cells that adhered to the valve wall and disorganized cardiac muscle fibers. An increased expression of KC protein, IL-1ß, genes encoding immune cell markers, and ROS (reactive oxygen species) production was observed in diabetic-infected mice, suggesting GBS promotes high levels of inflammation when compared to non-diabetic animals. Our data indicate that efforts to reverse the epidemic of diabetes could considerably reduce the incidence of invasive infection, morbidity and mortality due to GBS.
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The meninges are densely innervated by nociceptive sensory neurons that mediate pain and headache1,2. Bacterial meningitis causes life-threatening infections of the meninges and central nervous system, affecting more than 2.5 million people a year3-5. How pain and neuroimmune interactions impact meningeal antibacterial host defences are unclear. Here we show that Nav1.8+ nociceptors signal to immune cells in the meninges through the neuropeptide calcitonin gene-related peptide (CGRP) during infection. This neuroimmune axis inhibits host defences and exacerbates bacterial meningitis. Nociceptor neuron ablation reduced meningeal and brain invasion by two bacterial pathogens: Streptococcus pneumoniae and Streptococcus agalactiae. S. pneumoniae activated nociceptors through its pore-forming toxin pneumolysin to release CGRP from nerve terminals. CGRP acted through receptor activity modifying protein 1 (RAMP1) on meningeal macrophages to polarize their transcriptional responses, suppressing macrophage chemokine expression, neutrophil recruitment and dural antimicrobial defences. Macrophage-specific RAMP1 deficiency or pharmacological blockade of RAMP1 enhanced immune responses and bacterial clearance in the meninges and brain. Therefore, bacteria hijack CGRP-RAMP1 signalling in meningeal macrophages to facilitate brain invasion. Targeting this neuroimmune axis in the meninges can enhance host defences and potentially produce treatments for bacterial meningitis.
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Encéfalo , Meninges , Meningitis Bacterianas , Neuroinmunomodulación , Humanos , Encéfalo/inmunología , Encéfalo/microbiología , Péptido Relacionado con Gen de Calcitonina/metabolismo , Meninges/inmunología , Meninges/microbiología , Meninges/fisiopatología , Dolor/etiología , Canal de Sodio Activado por Voltaje NAV1.8/metabolismo , Meningitis Bacterianas/complicaciones , Meningitis Bacterianas/inmunología , Meningitis Bacterianas/microbiología , Meningitis Bacterianas/patología , Streptococcus agalactiae/inmunología , Streptococcus agalactiae/patogenicidad , Streptococcus pneumoniae/inmunología , Streptococcus pneumoniae/patogenicidad , Nociceptores/metabolismo , Proteína 1 Modificadora de la Actividad de Receptores/metabolismo , Macrófagos/inmunología , Macrófagos/metabolismoRESUMEN
INTRODUCTION: Despite literature on a variety of social risks and needs screening interventions in emergency department (ED) settings, there is no universally accepted or evidence-based process for conducting such interventions. Many factors hamper or promote implementation of social risks and needs screening in the ED, but the relative impact of these factors and how best to mitigate/leverage them is unknown. METHODS: Drawing on an extensive literature review, expert assessment, and feedback from participants in the 2021 Society for Academic Emergency Medicine Consensus Conference through moderated discussions and follow-up surveys, we identified research gaps and rated research priorities for implementing screening for social risks and needs in the ED. We identified three main knowledge gaps: 1) screening implementation mechanics; 2) outreach and engagement with communities; and 3) addressing barriers and leveraging facilitators to screening. Within these gaps, we identified 12 high-priority research questions as well as research methods for future studies. RESULTS: Consensus Conference participants broadly agreed that social risks and needs screening is generally acceptable to patients and clinicians and feasible in an ED setting. Our literature review and conference discussion identified several research gaps in the specific mechanics of screening implementation, including screening and referral team composition, workflow, and use of technology. Discussions also highlighted a need for more collaboration with stakeholders in screening design and implementation. Additionally, discussions identified the need for studies using adaptive designs or hybrid effectiveness-implementation models to test multiple strategies for implementation and sustainability. CONCLUSION: Through a robust consensus process we developed an actionable research agenda for implementing social risks and needs screening in EDs. Future work in this area should use implementation science frameworks and research best practices to further develop and refine ED screening for social risks and needs and to address barriers as well as leverage facilitators to such screening.
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Investigación sobre Servicios de Salud , Proyectos de Investigación , Humanos , Servicio de Urgencia en Hospital , Lagunas en las Evidencias , ConsensoRESUMEN
INTRODUCTION: Emergency departments (ED) function as a health and social safety net, regularly taking care of patients with high social risk and need. Few studies have examined ED-based interventions for social risk and need. METHODS: Focusing on ED-based interventions, we identified initial research gaps and priorities in the ED using a literature review, topic expert feedback, and consensus-building. Research gaps and priorities were further refined based on moderated, scripted discussions and survey feedback during the 2021 SAEM Consensus Conference. Using these methods, we derived six priorities based on three identified gaps in ED-based social risks and needs interventions: 1) assessment of ED-based interventions; 2) intervention implementation in the ED environment; and 3) intercommunication between patients, EDs, and medical and social systems. RESULTS: Using these methods, we derived six priorities based on three identified gaps in ED-based social risks and needs interventions: 1) assessment of ED-based interventions, 2) intervention implementation in the ED environment, and 3) intercommunication between patients, EDs, and medical and social systems. Assessing intervention effectiveness through patient-centered outcome and risk reduction measures should be high priorities in the future. Also noted was the need to study methods of integrating interventions into the ED environment and to increase collaboration between EDs and their larger health systems, community partners, social services, and local government. CONCLUSION: The identified research gaps and priorities offer guidance for future work to establish effective interventions and build relationships with community health and social systems to address social risks and needs, thereby improving the health of our patients.