Staphylococcus aureus is an opportunistic pathogen implicated in skin and soft-tissue infections and chronic inflammatory skin diseases, such as atopic dermatitis. These infections can range from mild to potentially life-threatening systemic illnesses progressing to bacteremia, endocarditis, and sepsis. Mast cells, traditionally recognized for their role in allergies, are highly abundant within the skin and are gaining recognition for their contribution to bacterial defense. Here, we discuss the role of mast cells in three models of S. aureus skin infection according to skin depth: epicutaneous sensitization, intradermal injections, and subcutaneous injections. During S. aureus skin infection, mast cells become activated and accumulate in infected skin, recognize bacterial toxins, and modulate the activity of other immune cells, including neutrophils and dendritic cells. We discuss areas of research that should be the target of future studies, such as neuroimmunology, infected excisional wounds, and risk of systemic illness. Our review aims to bring attention to the host-pathogen interaction between mast cells and S. aureus in the skin, both to encourage deeper investigation and inform the development of immunomodulatory-based therapeutics.

We report a bloodstream Burkholderia arboris isolate from a 75-year-old man without cystic fibrosis. The organism was recovered from both aerobic bottles of two separately collected blood-culture sets and was initially assigned to the Burkholderia cepacia complex (Bcc) by matrix-assisted laser desorption ionization-time-of-flight mass spectrometry. Whole-genome sequencing yielded three circular chromosomes and one circular plasmid. DFAST_QC identified B. arboris as the only type-strain match above the species threshold, with an average nucleotide identity of 99.48%; the next-highest match was B. seminalis at 93.33%. Multilocus sequence typing identified ST-2575, and ResFinder detected no acquired antimicrobial resistance genes. The patient improved after 14 days of meropenem therapy without recurrent B. arboris bacteremia. This report adds a clinically supported bloodstream infection, a complete genome resource, and detailed susceptibility data, while illustrating the importance of up-to-date reference genomes for species-level interpretation of unusual Bcc isolates.

The convergence of resistance and hypervirulence in Klebsiella pneumoniae poses a severe global health threat, yet the genomic mechanisms underlying adaptation to different clinical source remain incompletely understood. We conducted longitudinal genomic surveillance of 282 carbapenem-resistant K. pneumoniae (CRKP) isolates (225 sputum, 57 blood) between 2021and 2024 to characterize population structure, source-associated genomic adaptations, and plasmid evolution. ST11-CG258 dominated the cohort (77.3%), with 61.3% of isolates exhibiting the CR-hvKP phenotype. Longitudinal analysis revealed significant capsular plasticity within ST11, characterized by a temporal shift from KL64/47 to KL25 and the emergence of the highly invasive ST16-KL51 lineage, whereas non-ST11 clones displayed high capsular fidelity. Although blaKPC-2 predominated, blaOXA-181 was enriched among bloodstream isolates, whereas three blaNDM variants were more frequently detected in respiratory isolates. Comparative genomics identified enrichment of genes assigned to COG categories associated with energy production and amino acid transport in bloodstream isolates, whereas sputum isolates showed enrichment of genes involved in DNA repair and insertion sequences. Plasmid clustering of carbapenem-resistant plasmid revealed six antimicrobial clusters (Aclusters 1-6), identifying hybrid plasmids within Acluster 1 co-carrying blaKPC-2 and essential virulence determinants (iucABCD-iutA, rmpA, peg-344). Hypervirulent plasmids formed two major clusters, with Vcluster 2 diverging from Vcluster 1 via a 40kb deletion encompassing the ter (tellurium resistance) operon and metabolism-associated genes. These findings provide a comprehensive genomic characterization of CRKP from respiratory tract and bloodstream infections and support genome-based surveillance integrating clonal lineages, capsular types, and plasmid architectures to strengthen infection control and facilitate early identification of emerging high-risk CRKP lineages.

Infective endocarditis remains a life-threatening condition with high morbidity and mortality, particularly when caused by methicillin-sensitive Staphylococcus aureus. Early diagnosis is essential yet often challenging, especially when typical valvular vegetations are absent.We present the case of a 41-year-old man with methicillin-sensitive S. aureus bacteremia, complicated by retropharyngeal abscess, pyomyositis, empyema, and septic lung embolization. Multiple peripheral stigmata, including Osler nodes, Janeway lesions, and splinter hemorrhages fulfilled the modified Duke criteria for definite endocarditis, despite no imaging evidence of vegetations, in repeated echocardiograms, as well as fluorine-18 fluorodeoxyglucose positron emission tomography/computed tomography scan. Early antibiotic therapy and drainage of empyema and leg abscess led to a full recovery. This case illustrates the diagnostic limitations of imaging in native valve endocarditis, where small or mural vegetations may be overlooked. It underscores the critical role of clinical judgment in managing bacteremia with systemic involvement, ensuring timely and appropriate treatment despite negative imaging.

•B. clausii can cause bacteremia or sepsis in pediatric or immunocompromised patients.•In immunocompromised hosts, epithelial damage and adhesion favor bloodstream entry.•WGS revealed a close genomic relationship between both B. clausii isolates.•Multiple genomic methods consistently supported isolate relatedness.

Purpose: Bloodstream infections (BSIs) require prompt, targeted antimicrobial therapy, but traditional blood culture methods may delay optimal treatment. The BIOFIRE® Blood Culture Identification 2 (BCID2) panel provides rapid pathogen identification and mayreduce time to targeted therapy. This study evaluated the impact of BCID2 implementation at a community teaching hospital. Methods: A retrospective, quasi-experimental pre/post study was conducted at a for-profit community teaching hospital in adults aged ≥18 years with BSIs. Eligible patients had bacteremia, blood cultures collected, and empiric antibiotic therapy initiated during the study periods. Exclusion criteria included pregnancy, detection of multiple pathogens in a single culture, availability of susceptibility results before the designated timeline, and discharge, transfer, or leaving against medical advice before completion of testing. The pre-implementation group included 64 patients (October-December 2023), and the postimplementation group included 60 patients (October 2024-February 2025). The primary outcome was time from blood culture collection to initiation of targeted antibiotic therapy based on final susceptibility results. Secondary outcomes included pathogen identification, empiric and total antibiotic use, and length of stay. Results: The study included 124 patients (mean age, 70.5 ± 17.3 years; 67% ≥65 years; 50% male). Blood cultures were ordered for suspected sepsis/septic shock in 58% of patients and suspected secondary bacteremia in 42%. Pathogen distribution was similar between groups, with Escherichia coli, Staphylococcus epidermidis, Enterococcus faecalis, and Staphylococcus aureus identified most frequently. BCID2 implementation significantly reduced time to optimal therapy (3.73 ± 2.01 vs. 2.02 ± 1.48 days, p<0.001) and empiric antibiotic duration (3.73 ± 2.01 vs. 2.04 ± 1.48 days, p < 0.001). Total antibiotic duration and length of stay did not differ significantly between groups. Conclusion: BCID2 implementation at a community hospital significantly shortened time to optimal therapy and reduced empiric antibiotic use among older hospitalized adults.