Dataset Information

The microbiota of traumatic, open fracture wounds is associated with mechanism of injury.

ABSTRACT: Open fractures are characterized by disruption of the skin and soft tissue, which allows for microbial contamination and colonization. Preventing infection-related complications of open fractures and other acute wounds remains an evolving challenge due to an incomplete understanding of how microbial colonization and contamination influence healing and outcomes. Culture-independent molecular methods are now widely used to study human-associated microbial communities without introducing culture biases. Using such approaches, the objectives of this study were to (1) define the long-term temporal microbial community dynamics of open fracture wounds and (2) examine microbial community dynamics with respect to clinical and demographic factors. Fifty-two subjects with traumatic open fracture wounds (32 blunt and 20 penetrating injuries) were enrolled prospectively and sampled longitudinally from presentation to the emergency department (ED) and at each subsequent inpatient or outpatient encounter. Specimens were collected from both the wound center and adjacent skin. Culture-independent sequencing of the 16S ribosomal RNA gene was employed to identify and characterize microbiota. Upon presentation to the ED and time points immediately following, sample collection site (wound or adjacent skin) was the most defining feature discriminating microbial profiles. Microbial composition of adjacent skin and wound center converged over time. Mechanism of injury most strongly defined the microbiota after initial convergence. Further analysis controlling for race, gender, and age revealed that mechanism of injury remained a significant discriminating feature throughout the continuum of care. We conclude that the microbial communities associated with open fracture wounds are dynamic in nature until eventual convergence with the adjacent skin community during healing, with mechanism of injury as an important feature affecting both diversity and composition of the microbiota. A more complete understanding of the factors influencing microbial contamination and/or colonization in open fractures is a critical foundation for identifying markers indicative of outcome and deciphering their respective contributions to healing and/or complication.

SUBMITTER: Bartow-McKenney C

PROVIDER: S-EPMC6202213 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature

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The microbiota of traumatic, open fracture wounds is associated with mechanism of injury.

Bartow-McKenney Casey C Hannigan Geoffrey D GD Horwinski Joseph J Hesketh Patrick P Horan Annamarie D AD Mehta Samir S Grice Elizabeth A EA

Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society 20180301 2

Open fractures are characterized by disruption of the skin and soft tissue, which allows for microbial contamination and colonization. Preventing infection-related complications of open fractures and other acute wounds remains an evolving challenge due to an incomplete understanding of how microbial colonization and contamination influence healing and outcomes. Culture-independent molecular methods are now widely used to study human-associated microbial communities without introducing culture bi ...[more]

PMID: 29802752

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Project description:It is commonly observed that patients with bone fracture concomitated with traumatic brain injury (TBI) had significantly increased fracture healing while the underlying mechanisms were not fully revealed. Long non-coding RNAs (lncRNAs) were known for paly complicated roles in bone homeostasis while its role in TBI accelerated fracture were rarely reported. The present study was designed to determine the role of lncRNAs in TBI accelerated fracture via transcriptome sequencing and further bioinformatical analysis. Blood samples from 3 fracture only patients, 3 fracture concomitated with TIB patients and 3 healthy controls were harvested and were subsequently subjected to transcriptome lncRNAs sequencing. Differentially expression genes were identified, and pathway enrichment were performed by Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyze. High high-dimensional data portraying by self-organizing map (SOM) machine learning was applied to further interpret the data. A xCell method were then used to predict cellular behavior in all samples based on gene expression profiles and a lncRNA-cell interaction network were generated. A total of 874 differentially expressed genes were identified, of which about 26% were lncRNAs. Those identified lncRNAs were mainly enriched on traumatic brain injury related- and damage repair related-pathways. SOM analyzes revealed that those differentially expressed lncRNAs could be divided into three major module implications and were mainly enriched on transcriptional regulation and immune related signal pathways, which promote us to further explore cellular behaviors based on differentially expressed lncRNAs. We have predicted that basophils, CD8+ T effector memory cells, B cells, and naïve B cells were significantly down-regulated while microvascular endothelia cells were predicated significantly up-regulated with TBI/Fr group was the lowest or highest, respectively. ENSG00000278905, ENSG00000240980, ENSG00000255670, and ENSG00000196634 were the most differentially expression lcnRNA that related to all changes of cellular behavior. The present study has revealed for the first time that several critical lncRNAs may participate in TBI accelerated fracture potentially via regulating cellular behaviors of basophils, cytotoxic T cells, B cells and endothelia cells.

Project description:It is commonly observed that patients with bone fracture concomitant with traumatic brain injury (TBI) had significantly increased fracture healing, but the underlying mechanisms were not fully revealed. Long non-coding RNAs (lncRNAs) are known to play complicated roles in bone homeostasis, but their role in TBI accelerated fracture was rarely reported. The present study was designed to determine the role of lncRNAs in TBI accelerated fracture via transcriptome sequencing and further bioinformatics analyses. Blood samples from three fracture-only patients, three fracture concomitant with TBI patients, and three healthy controls were harvested and were subsequently subjected to transcriptome lncRNA sequencing. Differentially expressed genes were identified, and pathway enrichment was performed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. High-dimensional data visualization by self-organizing map (SOM) machine learning was applied to further interpret the data. An xCell method was then used to predict cellular behavior in all samples based on gene expression profiles, and an lncRNA-cell interaction network was generated. A total of 874 differentially expressed genes were identified, of which about 26% were lncRNAs. Those identified lncRNAs were mainly enriched on TBI-related and damage repair-related pathways. SOM analyses revealed that those differentially expressed lncRNAs could be divided into three major module implications and were mainly enriched on transcriptional regulation and immune-related signal pathways, which promote us to further explore cellular behaviors based on differentially expressed lncRNAs. We have predicted that basophils, CD8+ T effector memory cells, B cells, and naïve B cells were significantly downregulated, while microvascular endothelial cells were predicted to be significantly upregulated in the Fr/TBI group, was the lowest and highest, respectively. ENSG00000278905, ENSG00000240980, ENSG00000255670, and ENSG00000196634 were the most differentially expressed lncRNAs related to all changes of cellular behavior. The present study has revealed for the first time that several critical lncRNAs may participate in TBI accelerated fracture potentially via regulating cellular behaviors of basophils, cytotoxic T cells, B cells, and endothelial cells.

Project description:BackgroundAlthough many studies report the incidence and prevalence of surgical site infections (SSIs) after open fractures, there is limited information on the treatment and subsequent outcomes of superficial SSIs in patients with open fractures. Additionally, clinical studies describing the factors that are associated with persistent infection after nonoperative treatment with antibiotics for patients with superficial SSIs are lacking.Questions/purposesTherefore, we asked: (1) What proportion of patients with superficial SSIs after open fracture treatment developed persistent infection after nonoperative treatment (that is, treatment with antibiotics alone)? (2) What risk factors are associated with SSIs that do not resolve with nonoperative (antibiotic) treatment? As a secondary objective, we planned to analyze the microbiological information about participants wound cultures, when these were available, and the proportion of positive cultures for patients whose SSIs were not resolved by antibiotics alone.MethodsThis is a secondary analysis of the Fluid Lavage of Open Wounds (FLOW) trial dataset. The FLOW trial included 2445 patients with operatively managed open fractures. FLOW participants who had a nonoperatively managed superficial SSI diagnosed in the 12 months post-fracture were included in this analysis. Superficial SSIs were diagnosed in 168 participants within 12 months of their fracture. Of these, 83% (139) had their superficial SSI treated with antibiotics alone. Participants were grouped into two categories: (1) 97 participants whose treatment with antibiotics alone resolved the superficial SSI and (2) 42 participants whose treatment with antibiotics alone did not resolve the SSI (defined as undergoing surgical management or the SSI being unresolved at latest follow-up [12-months post-fracture for the FLOW trial]). Of the participants whose treatment with antibiotics alone resolved the SSI, 92% (89 of 97) had complete follow-up, 6% (6 of 97) were lost to follow-up before 12 months, 1% (1 of 97) withdrew consent from the study before 12 months, and 1% (1 of 97) experienced mortality before 12 months. Of the participants whose treatment with antibiotics alone did not resolve the SSI, 90% (38 of 42) had complete follow-up, 7% (3 of 42) were lost to follow-up before 12 months, and 2% (1 of 42) withdrew consent from the study before 12 months. A logistic binary regression analysis was conducted to identify factors associated with persistent infection despite superficial SSI antibiotic treatment. Based on biologic rationale and previous evidence, we identified a priori 13 potential factors (corresponding to 14 levels) to be included in the regression model.ResultsThe antibiotic treatment resolved the superficial SSI in 70% (97 of 139) of patients and did not resolve the SSI in 30% (42 of 139). After controlling for potential confounding variables, such as age, fracture severity, and time from injury to initial surgical irrigation and débridement, superficial SSIs diagnosed later in follow-up were associated with antibiotics not resolving the SSI (odds ratio 1.05 [95% CI 1.004 to 1.009] for every week of follow-up; p = 0.03). Sex, fracture pattern, and wound size were not associated with antibiotics not resolving the SSI.ConclusionsOur secondary analysis of prospectively collected FLOW data suggests that antibiotics alone can be an appropriate treatment option when treating superficial SSIs after an open fracture wound, especially when promptly diagnosed. Further research with longer follow-up time is needed to better identify the natural history of superficial SSIs and possibly some dormant or subclinical infections to help clinicians in the treatment decision-making process.Level of evidenceLevel III, therapeutic study.

Dataset Information

The microbiota of traumatic, open fracture wounds is associated with mechanism of injury.

Publications

The microbiota of traumatic, open fracture wounds is associated with mechanism of injury.

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