MICROBIOLOGY-SGM微生物学（英国微生物学会刊）
MICROBIOLOGY-SGM(英文缩写 MICROBIOL-SGM),ISSN 1350-0872,eISSN 1465-2080,中文译名:微生物学（英国微生物学会刊） 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-28 至 2026-09-28，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 2.956 | Q3 |
| 2022 | 2.800 | Q3 |
| 2023 | 2.600 | Q3 |
| 2024 | 3.500 | Q2 |
| 2025 | 4.300 | Q2 |
MICROBIOLOGY-SGM 最新收录文献
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1. {"_":"Microbe Profile: , the gall-forming protist behind clubroot disease.","i":["Plasmodiophora brassicae"]}
PMID:日期:2026-09-01is a soil-borne intracellular obligate biotrophic protist and the causal agent of clubroot disease in Brassicaceae. Phylogenetically placed within the Rhizaria supergroup, it exhibits a complex two-stage life cycle leading to the formation of club-shaped galls, driven by phytohormone and effector-mediated host reprogramming. A recently obtained telomere-to-telomere genome assembly of the Canadian pathotype revealed a compact genome structure encoding a complex secretome. Despite its agronomic relevance, key aspects of its biology, including the existence of sexual reproduction, host specificity determinants and effector biology, remain poorly understood, due to its unculturable nature and limited genomic resources.
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2. Simulating the host niche: balancing complexity and control in the experimental evolution of antibiotic resistance and pathoadaptation.
PMID:日期:2026-09-01The 'ESKAPE' pathogens cause the majority of antibiotic-resistant infections in humans, with associated mortality expected to surpass that of cancer by 2050. Outbreak strains of these pathogens often demonstrate a remarkable ability to establish infection and easily acquire novel antimicrobial resistance mechanisms. Because the expression of virulence factors and antimicrobial resistance genes often imposes a fitness cost, successful host-adapted strains must evolve without compromising their ability to colonize the niches found in the human body. The ongoing spread of these multidrug-resistant strains suggests that these bacterial pathogens are actively adapting to antibiotic-treated hosts. With whole-genome sequencing, we can now identify the multiple genetic changes associated with host adaptation and increased antibiotic resistance. Yet, pinpointing the specific mutations responsible for phenotypic shifts through sequencing of clinical isolates remains challenging due to the high mutational load accumulated during infection. For this reason, our understanding of how pathogens evolve within specific host niches, both in the presence and absence of antibiotics, remains limited. Experimental evolution within host tissues now allows us to more accurately simulate the conditions under which antibiotic resistance and pathoadaptations emerge. In this Perspective article, we evaluate some of the systems currently employed, discuss their respective advantages and limitations and introduce engineered human microtissue models as a promising platform for bacterial experimental evolution.
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3. {"_":"Induction of the filamentous prophage, Pf4, is conditionally regulated by PA3572 () in biofilms.","i":["difP","Pseudomonas aeruginosa"]}
PMID:日期:2026-09-01is an opportunistic Gram-negative pathogen, often associated with airway infections in the lungs of people with cystic fibrosis (CF). Biofilms of many strains, such as PAO1, produce copious quantities of filamentous Pf4 phage. High titres of Pf4 phage are associated with a decline in lung function in people living with CF. We previously showed that genes encoding Pf4 and also an unlinked hypothetical protein, PA3572, form part of the core biofilm-associated transcriptome in PAO1. Here, using reporter gene assays, we confirm that PA3572 (which we designate - depresses induction of filamentous Pf4 prophage) is strongly induced in biofilms of PAO1. Transcriptomic analysis of a deletion mutant revealed elevated expression of several Pf4 ORFs, as well as elevated expression of the cell envelope stress-associated protein, CpxP. These modulations were confirmed by quantitative reverse transcription-PCR, indicating that DifP functions to depress Pf4 gene expression. Consistent with this, Pf4 phage titres were elevated in a Δ mutant, whereas over-expression of depressed Pf4 titres and Pf4 gene expression. This effect of was abolished in a mutant, indicating that DifP-dependent regulation of Pf4 production is likely linked with cell envelope stress sensing. Taken together and by contrast with most other regulators of Pf4 identified to date (which promote Pf4 production in biofilms), our data indicate that DifP plays a role in restraining Pf4 production in PAO1 biofilms.
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4. Detection of opportunistic bacterial pathogens with intrinsic amoxicillin- and cephalosporin-resistance in wild koala faecal microbiomes.
PMID:日期:2026-09-01Opportunistic bacterial pathogens frequently associated with human clinical infections, including antimicrobial-resistant strains, are infiltrating the microbiomes of wild animals, where they have the potential to negatively impact wildlife health. Bacterial genes conferring resistance to amoxicillin have previously been reported in koala () faecal DNA. Koalas are facing several key threats, including wildfires, and affected individuals may receive amoxicillin therapy to treat burn wounds. This study aimed to identify the species of amoxicillin-resistant bacteria in koala gut microbiomes and determine if they are opportunistic pathogens. Faecal samples collected from 98 wild-caught koalas were cultured using amoxicillin-supplemented media to isolate amoxicillin-resistant Gram-negative enteric bacteria. Isolates were screened using 16S rRNA PCR and Sanger sequencing to identify opportunistic pathogenic species, which then underwent whole-genome sequencing and antimicrobial susceptibility testing. Intrinsically amoxicillin-resistant opportunistic pathogens were obtained from 9.2% (9/98) of koala faecal samples and comprised (6/98, 6.1%), (1/98, 1.0%) and spp. (2/98, 2.0%). Seven of nine amoxicillin-resistant opportunistic pathogens also exhibited cephalosporin resistance. Four isolates belonged to lineages associated with human clinical infections, which also have the potential to cause disease in koalas, including fatal systemic infections in pouch young. The presence of amoxicillin- and cephalosporin-resistant strains may also increase the risk of gut dysbiosis and opportunistic infections when penicillins or cephalosporins are required to treat bacterial infections in koalas, highlighting the importance of good antimicrobial stewardship. The study findings demonstrate the One Health perspective of microbial pathogens and the intertwined microbial ecology between humans and wildlife.
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5. Antimicrobial resistance in wastewater-impacted coastal waters: implications for environmental surveillance and public health.
PMID:日期:2026-09-01Antimicrobial resistance (AMR) is a global public health concern, and wastewater-impacted aquatic environments are recognized as reservoirs and dissemination pathways for antimicrobial-resistant bacteria (ARB) and genes (ARGs). However, harmonized environmental AMR surveillance frameworks that integrate culture-based ARB enumeration with molecular ARG monitoring across wastewater and receiving surface waters remain limited. This pilot study, conducted in Ireland as part of a European harmonized monitoring initiative, assessed ARB and ARG abundances in wastewaters and surface waters. Wastewater treatment plant influent (=3), effluent (=3) and surface waters upstream and downstream of the discharge point (=3 each) were sampled on three occasions in late 2024. Culture-based methods enumerated total and extended-spectrum -lactamase (ESBL)-producing , while quantitative real-time PCR quantified 16S rRNA and five AMR-associated genes (, , , and ). Total concentrations were highest in influent (~10-10 c.f.u. dl), decreased in effluent (~10-10 c.f.u. dl) and lowest in surface waters (~10¹-10² c.f.u. dl). ESBL-producing were consistently detected in influent (~10 c.f.u. dl) and effluent (~10-10 c.f.u. dl) but were not recovered from seawater. ARG abundances were highest in influent, reaching up to ~10 copies dl for , remained elevated in effluent (up to ~10 copies dl) and were ~2-3 orders of magnitude lower in surface waters relative to effluent. Downstream seawater exhibited higher ARG levels than upstream freshwater despite low culturable . Peak ARG concentrations in effluent and surface waters were observed following a period of heavy rainfall; however, the limited number of sampling events precluded assessment of any statistical association. These findings highlight the impact of wastewater discharges on environmental AMR dissemination and suggest that faecal indicator-based monitoring may underestimate emerging risks, supporting integration of AMR indicators into EU water quality frameworks.
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6. Implications of proteome allocation constraints for understanding interbacterial antagonism.
PMID:日期:2026-09-01Bacteria live in dense communities where competition influences the composition and, therefore, the function of these communities. Beyond competing for resources, bacteria engage in antagonism by deploying a range of molecular weapon systems to inhibit and kill other bacteria. Investing in antagonism is expected to incur a fitness trade-off, but the nature of this trade-off at the level of molecular physiology remains underexplained. Applying recent advances about the physiological constraints faced by bacterial cells may help us better understand existing studies and design new investigations into interbacterial antagonism. Bacterial cells face two important constraints: a finite amount of protein and a maximum translation speed for ribosomes. As a result, the only way for a cell to grow faster is to allocate more of its finite proteome to synthesizing ribosomes. A cell choosing to attack competitors must therefore allocate some of its limited proteome budget to antagonistic proteins instead of other functions. Conversely, being attacked and resisting the effects of such attacks also require an investment of proteomic resources. The extent to which proteome allocation constraints influence bacterial physiology is not fully understood; consequently, how these constraints influence interbacterial antagonism has not been investigated. Here, I will discuss how proteome allocation constraints can re-contextualize our existing understanding of the costs of both deploying and resisting attacks and how investigation of these constraints may further our understanding of interbacterial antagonism.
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7. {"_":" promotes capsular polysaccharide shedding and fitness of Group B .","i":["ypmS","in vivo","Streptococcus"]}
PMID:日期:2026-09-01Group B (GBS) is a leading cause of neonatal sepsis and meningitis worldwide. Capsular polysaccharide (CPS) is a major virulence factor that aids GBS in colonizing the gastrointestinal (GI) and vaginal tracts, surviving in whole blood and evading the immune system. CPS is also the basis for a GBS CPS-protein conjugate vaccine candidate. In addition to its function on the surface of the bacteria, CPS can also be released and shed into the environment. In , shed CPS has been shown to absorb antimicrobial peptides and CPS-specific antibodies, allowing the bacteria to evade the innate immune system and potentially limiting vaccine protection. In this work, we show that CPS shedding occurs in ~75% of GBS isolates that we screened from a large library of clinical strains. We then identified as a genetic determinant of CPS shedding using an indexed transposon library. We used a clean in-frame deletion mutant of to assess the importance of shedding in GBS colonization and immune evasion. We explored the role of in colonization using murine models of GI and vaginal co-colonization and showed that the wild-type strain outcompeted the Δ mutant in both scenarios. We also assessed the effect of shed capsule on opsonophagocytosis. Free CPS was protective against bacterial killing in an opsonophagocytic killing assay using CPS-specific antibodies. With this work, we have identified a novel genetic cause of CPS shedding and shown its contribution to GBS colonization fitness and immune evasion.
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8. Distribution of poly(A) polymerase I in bacteria: an expanded role for horizontal gene transfer.
PMID:日期:2026-08-01Poly(A) polymerase I (PAP I), the product of the gene, catalyses the polyadenylation of RNA 3'-ends in . PAP I and were initially thought to be present only in the β, γ-Proteobacteria and a few other bacterial species. In the present study, blast searches using bacterial proteins bearing the PAP I signature sequence as queries have revealed the presence of proteins containing that signature sequence in a wide range of additional bacterial classes and phyla. Phylogenetic studies indicate that the genes in most of these newly identified species were not inherited by horizontal gene transfer (HGT) from β, γ-proteobacterial donors. Nevertheless, the present studies reveal a larger role for HGT in the inheritance of genes than was documented in previous studies. Together with the other studies cited here, the results presented below strongly suggest that the significant metabolic role for the polyadenylation of RNA 3'-ends in the domain Bacteria.
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9. {"_":"Interplay between different SHP/Rgg quorum sensing systems that control production of post-translationally modified peptides in .","i":["Streptococcus thermophilus"]}
PMID:日期:2026-08-01In , the Rap-Rgg-NprR-PlcR-PrgX-AimR (RRNPPA) superfamily of regulators mediates quorum sensing via autoinducing peptides (AIPs). AIPs are secreted, processed and reimported before interacting with their cognate regulators, modulating the latter's activity. Within RRNPPA families, short hydrophobic peptides (SHPs) interact with Rgg transcriptional regulators. A widely used bacterium in the dairy industry, , possesses an unusually high number of Rgg regulators (mean of 5 and max of 10 per genome). These regulators mainly control the expression of operons involved in the production of ribosomally synthesized and post-translationally modified peptides (RiPPs). Because SHP/Rgg systems display similarities at the amino acid level, we investigated potential crosstalk (i.e. cross-activation) among systems. We focused on five SHP/Rgg systems located upstream of operons involved in producing RiPPs that are modified by radical SAM enzymes as well as a putative RiPP that is modified by a ThiF-like adenylyltransferase/cyclase enzyme. Using genetic approaches (reporter fusions into different genetic backgrounds) and analytical chemistry (liquid chromatography tandem mass spectrometry), we found three key results: (1) each Rgg regulator activates the transcription of its proximal RiPP operon, (2) cross-activation also occurs, where one operon is co-regulated by two distinct Rgg regulators and (3) a single Rgg regulator can be activated by multiple SHPs. A particularly novel finding is that one of the five operons is expressed under the control of two independent quorum-sensing pathways: an SHP/Rgg system and the ComR/S competence system. The result is the production of a newly identified RiPP, named ThiF-like RiPP, that undergoes post-translational modifications catalysed by a ThiF-like adenylyltransferase/cyclase. Overall, our study has revealed that individual SHP/Rgg systems function autonomously but that their activity is further shaped by crosstalk involving both SHP- and DNA-binding. These findings underscore that these systems should be thoroughly characterized at the strain level to allow precise, targeted modifications.
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10. MCR-3 and MCR-9 confer species-specific increases in colistin MICs.
PMID:日期:2026-08-01For the clinical treatment of infections with , the development of resistance to last-resort antimicrobials like colistin is of concern, as it limits treatment options. Since 2015, ten families of () genes have been discovered; however, our understanding of MCR remains limited because (i) is the most studied variant, (ii) variants are rarely compared and (iii) variants are primarily studied in , even though studies have shown that variants can confer significantly different phenotypes and that lipid A (i.e. the target of colistin and modification) structurally differs between bacterial species. To fill this gap, we examined how and , as two less frequently studied variants, impact the colistin resistance of laboratory-adapted and real-world (i.e. clinical or food) isolates of , and . We found that while consistently conferred colistin resistance to all tested strains, only conferred resistance to two strains. The fold-change in colistin minimum inhibitory concentrations was significantly impacted by both the bacterial species and the variant but not by whether a strain was a laboratory-adapted or real-world isolate. Overall, our results suggest that while laboratory-adapted strains may provide a good estimate of -mediated colistin resistance of real-world isolates, findings of -mediated phenotypes in one bacterial species should not be extrapolated to another.