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PubMed2026

Incidence of invasive group A streptococcal infections and comparison of emm types from invasive infections, pharyngitis, and throat carriage in American Indian communities in the Southwest United States.

BACKGROUND: American Indian/Alaska Native (AI/AN) communities in the US have high rates of group A streptococcal (GAS) infections. We determined the incidence of invasive infections in AI communities in the Southwest and compared emm types from invasive infections, pharyngitis, and throat carriage. METHODS: Activities conducted in the White Mountain Apache Tribal lands (WMA) and Navajo Nation (NN) included active, laboratory-based surveillance for invasive GAS infections (WMA: 2019─2024; NN: 2023─2024; all ages); surveillance for GAS pharyngitis (2023-2024; children 0─17 years); and culture for GAS from oropharyngeal carriage samples (2019 and 2022─2023; children 0─14 years). Emm types were determined by whole-genome sequencing. Annual incidence rates were calculated using Poisson regression. RESULTS: In WMA, age-standardized rates of invasive infections ranged from 80-270/100,000 persons between 2019-2024. Predominant emm types varied (n=74 isolates): 91 (59%) and 49 (32%) in 2019-2020, and 43 (40%) and 53 (30%) in 2023. In NN, rates were 40-60/100,000 persons in 2023-2024; common emm types (n=51) were 53 (28%), 101 (18%), and 12 (16%). In WMA and NN, emm types 1, 12, and 53 predominated in pharyngitis (n=190), and 1, 12, and 91 in throat carriage (n=119). CONCLUSIONS: Rates of invasive GAS infections in these communities were 3-35 times higher than the national US average (12.2/100,000 in 2024). Emm types varied over time with limited overlap in strains from throat carriage or pharyngitis isolates and those from invasive infections. Findings support continuing GAS surveillance and engaging AI/AN communities throughout vaccine development and evaluation.

Indigenous health↗

PubMed2026

Lineage dynamics of invasive Escherichia coli isolates in the Netherlands from 1975 to 2021: a retrospective longitudinal genomic analysis.

BACKGROUND: Escherichia coli is a common cause of invasive infections such as bloodstream and cerebrospinal fluid infections in neonates. Strains positive for the K1 capsule are considered the most common cause of such neonatal invasive infections. This assumption of K1 dominance, and indeed the population genomics of E coli causing invasive infections in general is largely unstudied. We aimed to provide a comprehensive characterisation of this pathogen population using a longitudinal isolate collection. METHODS: In this analysis we report the findings of the SENTINEL study, a longitudinal genomic analysis of 1790 invasive E coli isolates collected mainly from newborns in the Netherlands between 1975 and 2021 by the Netherlands Reference Laboratory for Bacterial Meningitis, Amsterdam University Medical Centre, Amsterdam, Netherlands. The dataset included all bacterial strains cultured from cerebrospinal fluid or blood in cases of (clinical) bacterial meningitis (1976 to 1980). In 1981 the criteria were expanded to include neonates (aged ≤4 weeks) with E coli sepsis, and from July, 2016 all infants younger than 1 year with E coli sepsis were included. All isolates were sequenced using either the HiSeq 2500 or HiSeq 4000 platforms (Illumina, San Diego, CA, USA). We confirmed species and identified sequence types (STs), detected antimicrobial resistance genes, virulence genes, and the presence of K1 capsule, and characterised the dynamics of these factors over time. FINDINGS: Our data show a highly dynamic bacterial population that is entirely unaffected by antimicrobial resistance determinants. Key pathogen population fluctuations include the complete disappearance of the dominant lineage ST567 and the swapping of dominant ST95 clones from a single serotype O18:H7 clone to two distinct serotype O1:H7 clones, with changes in virulence factors including major fimbrial adhesins. These findings, combined with only 58·8% (1053 of 1790) prevalence in K1-expressing isolates in the entire study population, point to host-pathogen interaction and immune selection pressures as key drivers of bacterial population dynamics in this largely antimicrobial-naive population. INTERPRETATION: Our data show the vital need for ongoing genomic surveillance of microbial pathogen populations to guide appropriate intervention strategies. Additionally, genomic insights of a pathogen population from one specific disease syndrome or patient population cannot always be generalised across other cohorts. FUNDING: Wellcome Antimicrobial and Antimicrobial Resistance Doctoral Training Programme and the National Institute for Health and Care Research Birmingham Biomedical Research Centre.

Netherlands↗

PubMed2025

Global spread of Streptococcus pyogenes A genomics-supported narrative review.

Group A Streptococcus (GAS) has recently reemerged as a leading cause of both mild and severe invasive infections worldwide, with recent upsurges in invasive disease among children and adults. Notwithstanding a partial synchronicity with the COVID-19 pandemic, this rapid global dissemination of more virulent GAS lineages has been promptly detected, as well as the molecular shifts underlying the observed changes in clinical patterns. Whole-genome sequencing (WGS)-based genomic epidemiology allowed us to gain relevant insights into this upsurge as it was happening. This review integrates the canonical research publication-based approach with genomic data and metadata and identifies a subset of genomic clusters playing a major role in invasive GAS (iGAS) infections worldwide, which were named as Global Pathogenic Lineages (GPLs). The four GPLs broadly coincide with five sequence types (STs): GPL1 with ST28, GPL2 with ST15 and ST315, GPL3 with ST52, and GPL4 with ST39. While non-GPLs clusters maintain a baseline reservoir of antimicrobial-resistance and virulence genes, GPLs show varying but noteworthy resistance profiles and are frequent causes of iGAS. The integration of WGS into routine diagnostics procedures is a forthcoming improvement, aimed not only at informing tailored therapy and implementing infection control strategies, but also to perform continuous surveillance. Ongoing WGS in clinical microbiology, as a matter of fact, will provide unparalleled insights into lineage emergence, transmission dynamics, and the geographic clustering of virulence and resistance determinants.

Streptococcus pyogenes↗

PubMed2026

Advancing the science of Staphylococcus aureus infection prevention in the neonatal intensive care unit.

Despite advances in infection prevention, infections due to Staphylococcus aureus continue to be an important cause of morbidity and mortality in NICUs. Whole genome sequencing (WGS) using advanced analytic approaches for defining transmission have shed new insights into transmission and persistence patterns in the NICU. WGS has also helped uncover important associations between transmission, persistence, and the risk of invasive infections. Current infection prevention strategies rely on hand hygiene compliance and surveillance and decolonization of patients positive for S. aureus. Parent decolonization may also play a role in decreasing parent-child transmission. In the future, precision surveillance of high-risk strains and targeted infection prevention efforts to decrease bacterial burden of those specific strains may provide a more effective and efficient approach to decreasing risk of invasive infections.

Humans↗

PubMed2026

An Aspergillus luchuensis isolated from a patient with hemoptysis insights from a comprehensive genome-based analysis: Case report.

RATIONALE: Asp luchuensis, a member of the A niger group, is widely used in food fermentation and rarely causes invasive pulmonary aspergillosis (IPA) in humans. Clinical cases of IPA induced by this strain are extremely scarce, and its genomic characteristics, virulence profiles, and pathogenic mechanisms remain poorly understood, resulting in insufficient clinical recognition of its invasive infection potential. PATIENT CONCERNS: A 57-year-old immunocompetent non-neutropenic male patient with a long-term smoking and drinking history presented with unexplained severe cough and massive hemoptysis (approximately100 mL) without other typical infectious symptoms. DIAGNOSES: Combined with chest computed tomography (CT) inflammatory lesions, positive galactomannan test, fungal PCR and metagenomic next-generation sequencing results, the patient was definitively diagnosed with probable A luchuensis-induced IPA. Genomic and transcriptomic analyses confirmed the pathogen as a variant A luchuensis strain with 3 key hypervirulence genes, highly active mitochondrial energy metabolism, and no specific antifungal resistance genes. INTERVENTIONS: The patient received standardized intravenous antifungal combination therapy with voriconazole and amphotericin B after confirmed diagnosis. OUTCOMES: The patient's cough and hemoptysis were significantly relieved after 10 days of treatment, with stable vital signs and no adverse drug reactions or disease progression. LESSONS: A luchuensis possesses strong invasive pathogenicity and can trigger IPA even in non-neutropenic immunocompetent individuals. Negative conventional microbial tests cannot exclude its infection, and mNGS is a reliable diagnostic tool. This strain is susceptible to routine antifungal drugs, and clinicians should raise awareness of atypical Asp species-induced invasive pulmonary infections.

Humans↗

PubMed2026

Emergence of Acinetobacter soli harboring three carbapenemase-encoding genes (blaNDM-1, blaIMP-14, and blaOXA-58) on a single plasmid in an ICU patient.

Acinetobacter soli is an environmentally adaptable species increasingly recognized as an emerging pathogen in hospital settings, particularly in intensive care units (ICUs). In this study, we report the first A. soli isolate from an ICU patient that co-harbors three carbapenemase-encoding genes (blaNDM-1, blaIMP-14, and blaOXA-58) on a single plasmid. Whole-genome sequencing revealed that multidrug resistance in this strain is mediated by a 294,790 bp plasmid, pSLAB-A, carrying 16 antimicrobial resistance genes, including all three carbapenemases. Comparative plasmid analysis showed a highly conserved backbone but identified a unique ~40 kb multidrug-resistance region containing blaNDM-1, blaIMP-14, and eight additional resistance genes. Genetic context analysis indicated that insertion sequences (ISAba125 and ISAba3) and class 1 integrons contribute to the mobilization and accumulation of carbapenemase-encoding genes. Plasmid stability assays demonstrated that pSLAB-A remained stably maintained for more than 90 generations without antibiotic selection. A global survey of the NCBI database identified 15 A. soli strains carrying carbapenemase-encoding genes, most of which were isolated from China, with clinical specimens representing the predominant source. Seven carbapenemase-encoding genes were detected, with blaNDM-1 being the most prevalent. Among eight isolates with complete genomes, all carried carbapenemase-encoding genes on plasmids. Phylogenetic analysis revealed regional dissemination of a clonal lineage across hospitals in Zhejiang Province and sustained nosocomial transmission within a hospital in Taiwan. These findings suggest that the spread of carbapenem resistance in A. soli is largely driven by multidrug-resistance plasmids, facilitating clonal expansion in hospital environments and posing a growing challenge for antimicrobial therapy and infection control in ICUs.IMPORTANCECarbapenem-resistant A. soli is an emerging clinical concern, capable of causing severe invasive infections, including bacteremia, in intensive care unit settings, and its emergence poses substantial challenges to antimicrobial therapy. In this study, we demonstrate that carbapenem resistance in A. soli is predominantly mediated by the acquisition of multidrug-resistance plasmids carrying carbapenemase-encoding genes. Owing to its strong environmental persistence, A. soli can readily undergo nosocomial clonal dissemination once carbapenem resistance is acquired. Moreover, the spread of multidrug plasmids co-harboring multiple carbapenemase-encoding genes may accelerate the evolutionary trajectory of resistance in A. soli, further exacerbating the threat to clinical management. Given its demonstrated capacity to cause hospital-associated infections and to rapidly acquire multidrug resistance, A. soli warrants heightened vigilance from both clinical and public health perspectives.

beta-Lactamases↗

PubMed2026

Loss of O-antigen due to wbbL mutations is common and associated with increased mortality in Escherichia coli bloodstream infections.

Escherichia coli bloodstream infections are common and associated with high mortality. A key feature of E. coli is the lipopolysaccharide (LPS) O-antigen, which contributes to immune evasion during invasive infection. We analyzed serial isolates from patients with relapsed E. coli bacteremia and identified frequent disruption of O-antigen synthesis due to mutations in wbbL, resulting in a rough LPS phenotype. Rough LPS isolates were more serum sensitive and less pathogenic in mice. Despite this apparent attenuation, 11 of 61 (18%) E. coli sequence type 131 bloodstream isolates in our cohort harbored disruptive wbbL mutations and were associated with significantly worse clinical outcomes, including septic shock and mortality. Using a murine model of recurrent bacteremia, we show that rough LPS isolates partially evade protective immunity generated against smooth LPS E. coli, highlighting the importance of host immune context in invasive disease.

O Antigens↗

PubMed2025

The Streptococcus pyogenes mannose phosphotransferase system (Man-PTS) influences antimicrobial activity and niche-specific nasopharyngeal infection.

Streptococcus pyogenes is a human-adapted pathogen that can cause multiple diseases, including pharyngitis and skin infections. Although this bacterium produces many virulence factors, how S. pyogenes competes with the host microbiota is not well understood. Here, we detected antimicrobial activity from S. pyogenes MGAS8232 that prevented the growth of Micrococcus luteus. This activity was produced when cells were grown in 5% CO2 in M17 media supplemented with galactose; however, the addition of alternative sugars coupled with genome sequencing experiments revealed that the antimicrobial phenotype was not related to classical bacteriocins. To further determine genes involved in the production of this activity, a transposon mutant library in S. pyogenes MGAS8232 identified the mannose phosphotransferase system (Man-PTS), a major sugar transporter, as important for the antimicrobial phenotype. Loss-of-function transposon mutants linked to the antimicrobial activity were identified to also be involved in alternative sugar utilization, and additionally, the Man-PTS was further identified from an inadvertent secondary mutation in a bacteriocin operon mutant. Sugar utilization in the Man-PTS mutants demonstrated that galactose, mannose, and N-acetylglucosamine utilization was impaired. RNA-seq experiments in high and low glucose concentrations further characterized the Man-PTS as a glucose transporter; however, transcriptional regulators or virulence factors were not affected with the loss of the Man-PTS. Deletion of Man-PTS demonstrated defects in a mouse model of nasopharyngeal infection but not skin infection. This work suggests that the ability of S. pyogenes to utilize alternative sugars presented by glycans may play a role in acute infection and interactions with the endogenous microbial population existing in the nasopharynx.IMPORTANCEStreptococcus pyogenes is responsible for over 500,000 deaths per year primarily due to invasive infections and post-infection sequelae, although the most common manifestations include pharyngitis and impetigo. S. pyogenes can adapt to its environment through alternative sugar metabolism. Here, we identified an antimicrobial phenotype that was not bacteriocin-related but a by-product of alternative sugar metabolism. The mannose phosphotransferase system was involved in the production of the antimicrobial and was also important for S. pyogenes to utilize alternative sugars and establish nasopharyngeal infection but not skin infection. Overall, this study identified potential strategies used by S. pyogenes for interactions with the endogenous microbiota and further elucidated the importance of sugar metabolism in acute upper respiratory tract infection.

Streptococcus pyogenes↗

PubMed2026

Gene Contribution of Streptococcus dysgalactiae Subspecies equisimilis, an Emerging Pathogen, to Experimental Primate Necrotizing Myositis.

Streptococcus dysgalactiae subspecies equisimilis (SDSE) is an emerging human pathogen closely related to group A Streptococcus. However, its genetic requirements for survival and growth in different conditions and for causing invasive infections remain poorly understood. To address this gap, transposon-directed insertion-site sequencing was used to identify genes contributing to fitness in experimental necrotizing myositis in nonhuman primates. Using two SDSE stG62647 human clinical isolates, MGCS36044 and MGCS36089, highly saturated transposon mutant libraries were generated and analyzed following in vitro growth and in vivo infection in eight nonhuman primates. A total of 398 essential genes were identified to be shared by both strains during growth in vitro and in vivo, and 17 and 7 conditionally essential genes required only in vitro or only in vivo, respectively. Additionally, 117 and 110 genes in MGCS36044 and MGCS36089, respectively, were found to be associated with fitness during necrotizing myositis. Transposon insertions in 34 MGCS36044 genes conferred increased fitness, whereas mutation of 83 genes conferred decreased fitness. Similarly, in MGCS36089, mutations in 38 and 72 genes conferred increased or decreased fitness, respectively. Importantly, both strains shared 46 fitness-associated genes, including an enrichment of transporter genes, highlighting nutrient acquisition as a dominant requirement during infection. The results provide critical information for guiding future translational efforts to develop preventive and therapeutic strategies against human SDSE infections.

Animals↗

PubMed2026

Human LFA-1 governs T cell immune surveillance of the skin.

The human integrin lymphocyte function-associated antigen 1 (LFA-1; αLβ2) is broadly expressed on leukocytes and involved in various intercellular adhesions. We report complete LFA-1 deficiency because of inherited αL (CD11a) deficiency in otherwise healthy adults of various ancestries with skin lesions due to commensal papillomaviruses. The patients had no history of invasive infections characteristic of children with inherited deficiency of β2 (CD18), which forms heterodimers with αL, αM (CD11b), αX (CD11c), or αD (CD11d). The development and function of leukocyte subsets are largely preserved in the absence of LFA-1. However, the transendothelial migration of skin-tropic cutaneous lymphocyte antigen (CLA)+ memory T cells is severely impaired, resulting in their selective sequestration in the blood. Conversely, alternative integrins mediate the extravasation of other leukocytes, including other T cell subsets, to other tissues. Human LFA-1 is required for steady-state T cell homing to the skin and control of papillomaviruses but is otherwise largely redundant. Integrin-mediated T cell compartmentalization is thus essential for organ-selective immune surveillance.

Humans↗

PubMed2025

An update on clinically relevant, rare, and emerging Candida and Saccharomycotina yeasts that have been recently reclassified from Candida.

SUMMARYMany yeast species causing life-threatening invasive infections that were formerly classified in the genus Candida have been reclassified due to their evolutionary and phylogenetic relationships elucidated by DNA sequencing methods that are increasingly using whole genomes. This review explores the evolving taxonomy, epidemiology, and clinical implications of clinically relevant, rare, emerging Candida and Saccharomycotina yeasts that have recently been reclassified from Candida. This article highlights the urgent need for intensified research efforts to enhance knowledge and improve outcomes in the management of infections caused by these yeasts. Communicating results from molecular phylogenetic studies of yeasts, which lead to their reclassification, is of great importance to the medical mycology community to implement such results in clinical practice.

Humans↗

PubMed2026

Functional analysis of Candida albicans protein kinases identifies Crk1 as a modulator of epithelial cell damage.

UNLABELLED: The commensal and pathogenic lifestyles of the opportunistic fungal pathogen Candida albicans require complex signaling networks regulated by protein kinases. To investigate the role of C. albicans protein kinases at the intestinal epithelial interface, we screened a comprehensive protein kinase deletion library for the capacity of the mutants to damage intestinal epithelial cells (IEC). Mutants showing altered IEC cytotoxicity relative to the wild type were further analyzed for their growth and morphology, focusing on hyper-damaging strains to identify kinases that rather prevent host cell damage. Deletion of CRK1 caused increased IEC-specific damage, despite slower growth, reduced hyphal length, and reduced adhesion as compared to wild-type cells. While tissue invasion levels and the formation of transcellular tunnels of the crk1Δ/Δ mutant were increased, the translocation capacity through the IEC barrier was reduced. Transcriptional and metabolic profiling suggested a role for Crk1 in metabolic adaptation to carbon and nitrogen sources, which was validated by showing that high glucose and amino acids are required for crk1Δ/Δ to cause increased IEC damage. Deletion of CRK1 rendered C. albicans more susceptible to cell wall and membrane stressors, but caused higher resistance to a catalase-specific and histidine biosynthesis inhibitor. This phenotypic pattern of medium- and epithelial cell type-specific cytotoxicity displayed by a C. albicans protein kinase mutant suggests that Crk1 regulates processes linked to carbon and amino acid metabolism that are relevant to interactions with intestinal epithelial cells. IMPORTANCE: Microbial signal transduction pathways regulate adaptation to changing environmental conditions and facilitate the success of many microbes during interactions with their hosts. The fungal pathobiont Candida albicans exists as a harmless commensal on mucosal surfaces of most humans but can also cause superficial and invasive infections under certain circumstances. Both lifestyles require complex signaling networks, predominantly regulated by protein kinases. The C. albicans genome was predicted to encode 108 protein kinases, yet nearly 50% remain uncharacterized. We aimed to dissect the role of C. albicans protein kinases during the transition from commensal to pathogen. We showed that multiple protein kinase genes are involved in epithelial cell damage. Particularly, the protein kinase gene Crk1 was of interest because deletion of CRK1 caused increased damage to intestinal epithelial cells under distinct conditions. Our study links Crk1 with regulation of metabolic processes relevant for commensalism and pathogenicity of C. albicans.

Candida albicans↗

PubMed2025

Landscape of essential growth and fluconazole-resistance genes in the human fungal pathogen Cryptococcus neoformans.

Fungi can cause devastating invasive infections, typically in immunocompromised patients. Treatment is complicated both by the evolutionary similarity between humans and fungi and by the frequent emergence of drug resistance. Studies in fungal pathogens have long been slowed by a lack of high-throughput tools and community resources that are common in model organisms. Here we demonstrate a high-throughput transposon mutagenesis and sequencing (TN-seq) system in Cryptococcus neoformans that enables genome-wide determination of gene essentiality. We employed a random forest machine learning approach to classify the C. neoformans genome as essential or nonessential, predicting 1,465 essential genes, including 302 that lack human orthologs. These genes are ideal targets for new antifungal drug development. TN-seq also enables genome-wide measurement of the fitness contribution of genes to phenotypes of interest. As proof of principle, we demonstrate the genome-wide contribution of genes to growth in fluconazole, a clinically used antifungal. We show a novel role for the well-studied RIM101 pathway in fluconazole susceptibility. We also show that insertions of transposons into the 5' upstream region can drive sensitization of essential genes, enabling screenlike assays of both essential and nonessential components of the genome. Using this approach, we demonstrate a role for mitochondrial function in fluconazole sensitivity, such that tuning down many essential mitochondrial genes via 5' insertions can drive resistance to fluconazole. Our assay system will be valuable in future studies of C. neoformans, particularly in examining the consequences of genotypic diversity.

Cryptococcus neoformans↗

PubMed2026

Invasive Wickerhamomyces anomalus Infections among Injecting Drug Users, France, 2012-20241.

Wickerhamomyces anomalus is a yeast rarely involved in human invasive fungal diseases (IFD). We retrospectively analyzed 44 episodes of W. anomalus IFD in France during 2012-2024. Injecting drug use (IDU) was the main risk factor among 26/35 (74.3%) incident cases. Most infections were community acquired; overall 3-month mortality rate was 1/30 (3.3%). Short tandem repeat (STR) genotyping and whole-genome sequencing analyses revealed substantial genetic diversity among isolates. However, 1 STR genotype was shared by 2 IDU patients, suggesting common exposure. In addition, 1 isolate obtained from a cotton filter used for drug preparation was identical by STR genotyping to the bloodstream isolate from the same patient, indicating direct inoculation via contaminated material or poor injection practices. Our findings highlight the increased risk for W. anomalus IFD among IDU patients and emphasize the importance of targeted preventive measures within that population.

Humans↗

PubMed2026

Emerging trends in invasive Streptococcus dysgalactiae subsp. equisimilis infections in Denmark, 2014 to 2024: a nationwide genomic and registry-based study.

BACKGROUNDIncreasing incidence rates of invasive Streptococcus dysgalactiae subspecies equisimilis (iSDSE) have been detected worldwide.AIMWe aimed to investigate iSDSE infection incidence rates in Denmark during 2014-2024, and characterise the genomic population structure of a subset of iSDSE isolates and their antimicrobial resistance (AMR).METHODSUsing national register data, we estimated overall and sex-/age-stratified iSDSE incidences during 2014-2024, by retrospectively identifying cases of invasive infections with group C and G streptococci or S. dysgalactiae (including specified as subspecies equisimilis). From the voluntary national beta-haemolytic streptococci laboratory surveillance system, whole-genome-sequenced isolates from August 2020-September 2022 were used to investigate the iSDSE genomic population structure. Susceptibility to penicillin, erythromycin and clindamycin was determined and AMR genes identified.RESULTSDuring 2014-2024, iSDSE incidence rates increased significantly (linear trend analysis p < 0.001) with mean annual incidence ranging between 10.3 and 16.4 per 100,000, peaking in 2023. Incidence was higher in males, increasing with older age. Nearly 75% of the 1,223 iSDSE isolates belonged to four of 14 genetic clusters. Sequence types (STs) ST20 and ST17 were most prevalent, while emm-type stG62647, a variant associated internationally with higher virulence, dominated. All isolates were phenotypically susceptible to penicillin but approximately 10% were respectively erythromycin and clindamycin resistant. High erythromycin resistance prevalence (57%; 39/68), coinciding with gene ermA, occurred in one genetic cluster.CONCLUSIONThe findings illustrate the need for national registry-based surveillance to detect epidemiological changes and potential outbreaks. Further, continuous genomic surveillance can monitor the occurrence and expansion of genetic clades and AMR genes.

Denmark↗

PubMed2026

Clinical and Microbiological Characteristics of Invasive Group A Streptococcus Infection: Four Case Series of Re-Emerging Pathogens.

INTRODUCTION: Group A Streptococcus (GAS), particularly the M1UK lineage, has re-emerged as a major global public health concern following the COVID-19 pandemic, with a rise in invasive GAS (iGAS) and streptococcal toxic shock syndrome (STSS). Although STSS is under national surveillance in Japan, comprehensive molecular monitoring of iGAS infections remains limited, and the clinical characteristics of M1UK-associated iGAS have not been fully elucidated. METHODS: We retrospectively reviewed four consecutive iGAS cases requiring intensive care between March and May 2024. Detailed clinical, microbiological, and genomic investigations were performed to characterize the causative strains and their associated virulence profiles. RESULTS: All patients required respiratory and/or circulatory support with surgical debridement. Three cases involved necrotizing fasciitis, and one involved intra-abdominal infection secondary to ovarian tumor rupture. All four patients received penicillin G and clindamycin as definitive antimicrobial therapy, with two developing severe drug-related adverse events. Genotypic analysis identified three isolates as emm1 strains, including two M1UK lineage strains. The two M1UK isolates commonly harbored multiple superantigen genes. All isolates remained susceptible to β-lactam, clindamycin, and macrolide antibiotics. CONCLUSION: This case series documents the identification of the M1UK lineage among critically ill patients with iGAS infections in Japan. Our findings support the need for continued molecular surveillance while reinforcing the importance of prompt surgical source control and appropriate antimicrobial therapy in the management of severe iGAS.

Group A Streptococcus↗

PubMed2026

Stenotrophomonas maltophilia in the Antimicrobial Resistance Era: Species-Complex Taxonomy, Pathogenesis, Evolving Therapeutic Priorities, and Genomic Surveillance.

Stenotrophomonas maltophilia is a globally distributed, aerobic, non-fermenting Gram-negative bacillus increasingly recognized as an opportunistic pathogen in hospitalized and immunocompromised patients. Clinical interpretation is challenging because respiratory and device-associated isolates may represent colonization, polymicrobial infection, or true invasive disease. Recent genomic studies further suggest that organisms historically identified as S. maltophilia comprise a genetically diverse species complex, with implications for epidemiology, virulence, resistance surveillance, and susceptibility testing. Treatment is difficult because of biofilm formation, persistence in water-associated healthcare reservoirs, and intrinsic or acquired resistance mediated by L1 and L2 β-lactamases, multidrug efflux pumps, reduced permeability, mobile resistance determinants, and biofilm-associated tolerance. Current IDSA guidance identifies cefiderocol monotherapy as the preferred treatment for invasive S. maltophilia infection, whereas aztreonam-avibactam and agents such as trimethoprim-sulfamethoxazole, levofloxacin, and minocycline occupy alternative or combination-based roles. Nevertheless, the therapeutic evidence base remains uneven, and clinical decisions should integrate infection severity, source control, susceptibility findings, pharmacokinetic/pharmacodynamic (PK/PD) exposure, toxicity, infection site, and host-related factors. This review summarizes advances in taxonomy, epidemiology, pathogenesis, diagnostics, resistance, treatment, infection prevention, and genomic surveillance, and highlights the need for standardized identification, validated breakpoints, prospective comparative-effectiveness studies, and pragmatic or adaptive trial designs.

L1 β-lactamase↗

PubMed2026

Biofilm-derived curli and Z-DNA shape anti-DNA antibody responses during Salmonella infections.

Antibodies to Z-DNA, a non-canonical DNA conformation with a left-handed zigzag backbone, are abundant in the serum of patients with systemic lupus erythematosus (SLE), with levels increasing with disease activity and flares. As SLE is associated with bacterial infections, and as extracellular DNA (eDNA) within biofilms of several bacterial species has been shown to adopt the Z-DNA conformation, bacterial Z-DNA may represent a source of immunogenic Z-DNA in SLE and other related autoimmune conditions. In these studies, we investigated whether eDNA in Salmonella biofilms also contained Z-DNA and whether such Z-DNA could elicit an antibody response. Using antibody-based staining approaches, we observed abundant eDNA in Salmonella enterica serovar Typhimurium (STm) biofilms in both the Z- and canonical B-DNA configurations, consistent with the highly Z-prone nature of the GC-rich Salmonella genome. To assess the functional contribution of these DNA conformations to biofilm integrity, biofilms were treated with DNase I, which lacks enzymatic activity against Z-DNA, or with benzonase, a nonspecific nuclease that degrades both B- and Z-DNA. DNase I treatment applied after biofilm maturation was less effective at thinning biofilms than treatment during early biofilm formation, a pattern also observed with benzonase treatment. Purified curli:DNA complexes contained Z-DNA and, when administered intraperitoneally to mice, elicited robust anti-Z-DNA antibody responses. Similarly, infection with invasive STm induced the production of anti-Z-DNA antibodies in vivo. Moreover, STm infection in mice fed a diet that promotes biofilm development was associated with increased Z-DNA levels in the cecal lumen and elevated anti-DNA antibody responses. Collectively, these findings suggest that Z-DNA, likely formed by extruded Salmonella genomic DNA, and embedded within curli:DNA complexes of STm biofilms, triggers a host immune response and drives anti-Z-DNA antibody production. This work provides mechanistic insight into how bacterial infections and diet-dependent modulation of biofilm formation may contribute to anti-Z-DNA antibody responses in autoimmune diseases like SLE.

Animals↗