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Objectives This study aims to elucidate the genomic dynamics driving the emergence of antimicrobial resistance (AMR), with a specific focus on the interplay between AMR and antimicrobial usage. Methods We conducted a comprehensive analysis using a ST239 methicillin-resistant Staphylococcus aureus (MRSA) dataset over a continuous 12-year period from a single hospital. Genomic analyses were performed tracking the changes in MRSA populations, particularly the emergence of reduced vancomycin susceptibility, and assessing the impact of glycopeptide use on these emergence events. Results Our findings reveal a significant correlation between hospital glycopeptide usage and the selection of MRSA strains with reduced vancomycin susceptibility. Genomic analyses provided insights into the molecular mechanisms driving resistance emergence, including the slowing of the molecular clock rate in response to heightened antimicrobial consumption. Conclusions In conclusion, this study the highlights the complex dynamics between AMR and antimicrobial use at the hospital level. The observed correlation between antimicrobial consumption and the development of less susceptible MRSA strains underscores the importance of antimicrobial stewardship programmes and the establishment of optimal consumption thresholds for mitigating AMR effectively. [ABSTRACT FROM AUTHOR]

There is an increasing use of non‐medicated wound dressing with claims of irreversible bacterial binding. Most of the data are from in vitro models which lack clinical relevance. This study employed a range of in vitro experiments to address this gap and we complemented our experimental designs with in vivo observations using dressings obtained from patients with diabetes‐related foot ulcers. A hydrophobic wound dressing was compared with a control silicone dressing in vitro. Test dressings were placed on top of a Pseudomonas aeruginosa challenge suspension with increasing concentrations of suspension inoculum in addition to supplementation with phosphate buffered saline (PBS) or increased protein content (IPC). Next, we used the challenge suspensions obtained at the end of the first experiment, where bacterial loads from the suspensions were enumerated following test dressing exposure. Further, the time‐dependent bacterial attachment was investigated over 1 and 24 h. Lastly, test dressings were exposed to a challenge suspension with IPC, with or without the addition of the bacteriostatic agent Deferiprone to assess the impacts of limiting bacterial growth in the experimental design. Lastly, two different wound dressings with claims of bacterial binding were obtained from patients with chronic diabetes‐related foot ulcers after 72 h of application and observed using scanning electron microscope (SEM). Bacteria were enumerated from each dressing after a 1‐h exposure time. There was no statistical difference in bacterial attachment between both test dressings when using different suspension inoculum concentrations or test mediums. Bacterial attachment to the two test dressings was significantly lower (p < 0.0001) when IPC was used instead of PBS. In the challenge suspension with PBS, only the hydrophobic dressing achieved a statistically significant reduction in bacterial loads (0.5 ± 0.05 log colony forming units; p = 0.001). In the presence of IPC, there was no significant reduction in bacterial loads for either test dressing. When bacterial growth was arrested, attachment to the test dressings did not increase over time, suggesting that the number of bacteria on the test dressings increases over time due to bacterial growth. SEM identified widespread adsorption of host fouling across the test dressings which occurred prior to microbial binding. Therein, microbial attachment occurred predominantly to host fouling and not directly to the dressings. Bacterial binding is not unique to dialkylcarbamoyl chloride (DACC) dressings and under clinically relevant in vitro conditions and in vivo observations, we demonstrate (in addition to previously published work) that the bacterial binding capabilities are not effective at reducing the number of bacteria in laboratory models or human wounds. [ABSTRACT FROM AUTHOR]

In this proof‐of‐concept study of twenty participants, we sought to determine if a DACC (Dialkylcarbamoyl chloride)‐coated mesh dressing demonstrates an ability to adhere biofilm when placed on Diabetes Related Foot Ulcers (DRFUs) with chronic infection. The study also sought to determine if removal of the DACC‐coated mesh dressings contributes to reducing the total number of bacteria in DRFUs, by exploring the total microbial loads, microbial community composition, and diversity. Standard of care was provided in addition to the application of DACC or DACC hydrogel every three days for a total of two weeks. Wound swabs, tissue curettage, and soiled dressings were collected pre and post‐treatment. Tissue specimens obtained pre‐treatment were analysed with scanning electron microscopy (SEM) and peptide nucleic acid fluorescent in situ hybridisation (PNA‐FISH) with confocal laser scanning microscopy and confirmed the presence of biofilm in all DRFUs. SEM confirmed the presence of biofilms readily adhered to soiled DACC‐coated mesh dressings pre‐ and post‐treatment in all participants. Real‐time quantitative polymerase chain reaction (qPCR) demonstrated the mean total microbial load of DRFUs in 20 participants did not change after two weeks of therapy (pre‐treatment = 4.31 Log10 16 S copies (±0.8) versus end of treatment = 4.32 Log10 16 S copies (±0.9), P =.96, 95% CI −0.56 to 0.5). 16 S sequencing has shown the microbial composition of DACC dressings and wound swabs pre‐ and post‐treatment remained similar (DACC; R = −.047, P =.98, Swab; R = −.04, P =.86), indicating the microbial communities originate from the ulcer. Biofilms adhere to DACC‐coated mesh dressings; however, this may not reduce the total microbial load present within DRFU tissue. Wound dressings for use in hard‐to‐heal wounds should be used as an adjunct to a good standard of care which includes debridement and wound bed preparation. [ABSTRACT FROM AUTHOR]

Virtually all diabetes‐related foot ulcers (DRFUs) will become colonized by microorganisms that may increase the risk of developing an infection. The reasons why some ulcerations develop acute clinical infections (AI‐DRFUs) whilst others develop chronic infection (CI‐DRFUs) and the preceding host‐microbe interactions in vivo remain largely unknown. Establishing that acute and chronic infections are distinct processes requires demonstrating that these are two different strategies employed by microbes when interacting with a host. In this study, dual‐RNA seq was employed to differentiate the host‐microbe metatranscriptome between DRFUs that had localized chronic infection or acute clinical infection. Comparison of the host metatranscriptome in AI‐DRFUs relative to CI‐DRFUs identified upregulated differentially expressed genes (DEGs) that functioned as regulators of vascular lymphatic inflammatory responses, T‐cell signalling and olfactory receptors. Conversely, CI‐DRFUs upregulated DEGs responsible for cellular homeostasis. Gene set enrichment analysis using Hallmark annotations revealed enrichment of immune and inflammatory profiles in CI‐DRFUs relative to AI‐DRFUs. Analysis of the microbial metatranscriptome identified the DEGs being enriched within AI‐DRFUs relative to CI‐DRFUs included several toxins, two‐component systems, bacterial motility, secretion systems and genes encoding for energy metabolism. Functions relevant to DRFU pathology were further explored, including biofilm and bacterial pathogenesis. This identified that the expression of biofilm‐associated genes was higher within CI‐DRFUs compared to that of AI‐DRFUs, with mucR being the most highly expressed gene. Collectively, these data provide insights into the host‐microbe function in two clinically‐distinct infective phenotypes that affect DRFUs. The data reveal that bacteria in acutely infected DRFUs prioritize motility over biofilm and demonstrate greater pathogenicity and mechanisms, which likely subvert host cellular and immune pathways to establish infection. Upregulation of genes for key vascular inflammatory mediators in acutely infected ulcers may contribute, in part, to the clinical picture of a red, hot, swollen foot, which differentiates an acutely infected ulcer from that of a chronic infection. [ABSTRACT FROM AUTHOR]

Author(s): Maria A. Schumacher (corresponding author) [1]; Tiffany C. Glover [1]; Anthony J. Brzoska [2]; Slade O. Jensen [2]; Thomas D. Dunham [1]; Ronald A. Skurray [2]; Neville Firth [2] [...]

Results demonstrate that several Salmonella enterica strains exhibit a manB gene, which display a 93 to 99% DNA identity to the colanic acid manB gene of the bacterium. However, the manC genes differ from those of manB genes indicating that these two gene sets have evolved independently.

Cronobacter sakazakii neonatal infections can cause severe systemic infection and meningitis, resulting in mortality rates as high as 42% (1). C. sakazakii infections have been epidemiologically linked with contaminated powdered [...]