Mechanism of injury influences early microbial trajectories and infection pathways in open fractures: A 16S rDNA study

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BACKGROUND: The mechanism of injury in open fractures-whether blunt or sharp- may significantly impact early microbial colonization and how those microbial communities develop in relation to wound microbiota, which leads to fracture-related infection (FRI). Nevertheless, the influence of trauma biomechanics on infection development and microbial community dynamics is poorly studied. This study aimed to assess how different injury mechanisms influence wound microbiota dynamics and susceptibility to FRI. METHODS: In this prospective cohort study, we recruited 155 patients with Gustilo-Anderson type II, IIIA, or IIIB open fractures. Deep tissue samples were obtained from all patients during their initial surgical debridement. In a subset of 28 patients who developed FRI, a second sample was collected at the time of re-debridement. The samples were matched and stratified into four groups based on trauma mechanism and infection status: Pre-debridement sharp, Pre-debridement blunt, Infection sharp, and Infection blunt. Microbial profiling was conducted using 16S rDNA sequencing. The sample metadata was analyzed in QIIME2, from which diversity indices (alpha and beta) were computed. The taxonomic composition and abundance were assessed at the genus level, while patterned relationships between groups were visualized through heatmap clustering. RESULTS: Beta diversity analysis showed that Pre-debridement sharp group clustered closely with both infection groups, significantly diverging from the Pre-debridement blunt group (p < 0.001). In terms of alpha diversity, the Pre-debridement sharp group exhibited the highest levels across richness, evenness (p < 0.05), as well as phylogenetic breadth. Taxonomic profiling showed that sharp trauma wounds were initially enriched with potentially pathogenic genera such as Pseudomonas, Acinetobacter and Staphylococcus, while blunt trauma wounds were dominated by low virulence taxa, like Bacillus. Heatmap analysis confirmed that the microbial composition of sharp samples was similar to those from both infection groups, suggesting that sharp trauma wounds possess a diverse microbial community that resemble the architecture seen in FRI. CONCLUSIONS: While the overall infection rate did not differ between blunt and sharp trauma, the mechanism of injury significantly influenced early microbial colonization patterns and infection development pathways. These findings emphasize the importance of trauma-specific microbiota profiling in understanding and potentially guiding the prevention of FRI.

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Related topics: Bone fractures and treatments · Orthopedic Infections and Treatments · Immune Response and Inflammation