Search Results (281)

Cronobacter spp. are opportunistic foodborne pathogens that can cause neonatal meningitis, necrotizing enterocolitis, and sepsis. This study conducted a systematic contamination survey and whole-genome epidemiological analysis of 562 low-water-activity food samples in Hunan Province of China. The results showed an overall Cronobacter spp. detection rate of 41.99% (236/562), with spices exhibiting the highest contamination rate (60.06%), and with high-level contamination samples (>110 MPN/g) concentrated in this category. The 236 isolates comprised 6 species, 120 sequence types, and 39 clonal complexes, with C. sakazakii being the most frequently isolated species (64.83%) and high-risk clones ST4, ST1, ST148, and ST64 prevailing. Multiple virulence genes (TraJ, fur, rcsAB, rpoS) and antimicrobial resistance genes (qnrS1, blaTEM-1, blaCTX-M-55, blaLAP-2, aac(3)-IId, aadA2, tet(A), floR, mcr-9.1, sul2) were detected. Core genome multilocus sequence typing (cgMLST) identified two clustering patterns: Cluster C, whose genetic clustering was consistent with transmission associated with potential common upstream raw materials across different brands and provinces, and Cluster G, whose clustering suggested potential persistent colonization in the production environment across multiple batches of the same brand. This study elucidates the contamination characteristics of Cronobacter spp. in low-water-activity foods from Hunan Province and provides a basis for WGS-based active surveillance and supply chain traceability. Full article

Tetrastigma hemsleyanum polysaccharide (TH-P) exhibited anti-inflammatory and intestinal protective activities, but its mechanism against ulcerative colitis (UC) remained unclear. This study used a multi-omics approach to elucidate the effects of TH-P in protecting against dextran sulfate sodium (DSS)-induced UC mice and the underlying mechanisms. In vitro, TH-P dose-dependently suppressed LPS-induced ROS production and pro-inflammatory cytokine release in RAW264.7 cells. In vivo, TH-P alleviated DSS-induced weight loss, disease activity index, colon shortening, edema, and mucosal damage. Transcriptomic analysis and Western blotting revealed that TH-P significantly reversed DSS-induced gene expression alterations, with particular enrichment of the PI3K/AKT signaling pathway. Serum metabolomics showed that TH-P restored metabolic disturbances in glycerophospholipid and arachidonic acid metabolism. The results of 16S rRNA sequencing indicated that TH-P increased microbial diversity, enriched beneficial Bacteroidota, and reduced opportunistic Actinomycetota and Pseudomonadota. Untargeted metabolomics further demonstrated elevated acetate, propionate, and butyrate levels. Collectively, TH-P alleviated UC through a multi-target mechanism involving antioxidant and anti-inflammatory activities, gut microbiota modulation, enhanced SCFA production, and activation of the PI3K/AKT signaling pathway. Full article

The human gut microbiome comprises a diverse community of bacteria whose interactions with the host range from beneficial mutualism to opportunistic pathogenicity. These interactions are shaped by genomic plasticity and ecological pressures that influence whether microbes support host health, remain conditionally harmless, or contribute to disease. Understanding the mechanisms underlying these shifts is essential for clarifying the balance between cooperation and pathogenicity within the gut ecosystem. This review explores the genomic and evolutionary mechanisms that shape microbial adaptation across the mutualism–pathogenicity spectrum in the human gut. Key processes, including horizontal gene transfer (HGT), host-mediated selection, and niche specialization, enable microbes to acquire, regulate, or retain traits that influence colonization, metabolic function, and virulence. These adaptive mechanisms allow gut bacteria to respond dynamically to ecological pressures such as inflammation, antibiotic exposure, and dietary change, resulting in context-dependent microbial behaviors. The review also considers how concepts from insect endosymbiosis may provide insight into gut microbial adaptation. While both systems exhibit host specialization, major differences in transmission mode, ecological flexibility, and genome evolution limit direct comparisons. Rather than following a fixed progression toward parasitism, gut microbes exhibit flexible adaptive strategies shaped by host and environmental conditions. By integrating ecological and evolutionary perspectives, this review presents a balanced framework for understanding how genomic adaptation influences microbial behavior in the gut. This perspective improves our understanding of dysbiosis and microbial pathogenesis and may support the development of microbiome-informed therapeutic strategies for maintaining host health. Full article

Inflammatory bowel disease (IBD) is a chronic inflammatory condition resulting from complex interactions between the immune system, genetic predisposition, and the gut microbiota. In this context, Escherichia coli (E. coli) plays a dual role in the human gut, ranging from harmless commensal strains to pathobionts capable of promoting intestinal inflammation. A growing body of evidence suggests that specific E. coli pathotypes, such as adherent-invasive E. coli (AIEC) and diffusely adherent E. coli (DAEC), contribute to the development and progression of IBD. This narrative review critically examines the microbiological, immunological, and clinical evidence supporting the role of E. coli in IBD, with particular emphasis on mechanisms of mucosal colonization, host–microbe interactions, and persistence within the inflamed intestinal environment. Furthermore, the lack of a standardized operational definition and the limited reproducibility of the AIEC phenotype are addressed, as well as uncertainty about the role played by E. coli as a primary initiator of the disease or as an opportunistic amplifier of intestinal inflammation, and the varying strength of evidence supporting associations with Crohn’s disease versus ulcerative colitis. Diagnostic implications, antimicrobial resistance, and therapeutic aspects are addressed as downstream and context-dependent consequences of E. coli–host interactions, with relevance for disease management and therapeutic response in patients with established IBD. By integrating data from experimental models, clinical studies, and translational research, the review identifies areas of consensus, ongoing controversy, and major knowledge gaps in IBD pathophysiology and clinical practice. Full article

Enterococcus lactis is increasingly recognized as an emerging mastitis pathogen, yet the functional basis of its virulence and associated health risks remain poorly defined. This study presents an integrated genomic and phenotypic characterization of E. lactis strain EL-A150 isolated from bovine subclinical mastitis. Whole-genome sequencing revealed a 2.49 Mb circular chromosome encoding multiple genes associated with adhesion (acm, bepA, fms, sagA), biofilm formation (empB, empC) and antimicrobial resistance, including determinants related to aminoglycosides and macrolides. Phenotypic assays demonstrated rapid growth, strong biofilm-forming capacity and high adhesion to bovine mammary epithelial cells, while internalization remained low and intracellular persistence was transient. Comparative genomic analyses confirmed the taxonomic placement of the strain within the E. lactis clade (ANI up to 99.5% against reference genomes) and revealed a limited resistome composed of chromosomally encoded genes, with no detectable plasmids or major mobile genetic elements. Collectively, these findings demonstrate that E. lactis EL-A150 possesses a coordinated set of traits conducive to intramammary colonization, supporting its classification as an opportunistic pathogen. The convergence of virulence potential and clinically relevant antimicrobial resistance within a single isolate underscores a One Health concern and highlights the need for surveillance frameworks that integrate functional validation with genomic risk assessment. Full article

An isolate of Peniophora lycii was obtained from grapevine, and its interactions with several grapevine-associated fungi and the plant host were examined. The fungus was not able to infect intact leaves, but necrotized the margins of foliar disks and caused necrosis and white rot in woody tissues. In dual cultures, P. lycii and Aureobasidium pullulans showed mutual antagonism. Mycoparsitism of P. lycii was observed on epiphytic Botrytis cinerea, Alternaria sp., and endophytic Botryosphaeria dothidea interaction partners. In contrast, P. lycii showed trophic growth towards endophytic Phaeomoniella chlamydospora without any signs of harmful interactions. Dual inoculations of foliar disks with epiphytic fungi revealed no effects of fungal interactions on necrosis development by pathogens and verified mycoparasitic interactions in planta. Co-infection assays of cuttings with endophytic pathogen fungi showed cumulative effects of fungal interactions on wood symptom expression, with the exclusive contribution of P. lycii to white rot development. In addition to providing the first isolation of P. lycii from grapevine and the description of its mycoparasitic behavior, the present study suggests that the fungus may act as an opportunistic grapevine pathogen, probably as a secondary colonizer in trunk diseases. The observed dual host preference may allow trunk disease pathogens to initially feed on fungi, followed by damage to the grapevine. This may be in connection with the exceptionally long latency of these syndromes. Full article

Background/Objectives: Non-tuberculous mycobacteria (NTM) are increasingly recognized as important opportunistic pathogens at the human–animal–environment interface. Their growing relevance is driven by increasing disease burden, environmental persistence, occurrence in multiple animal hosts and complex antimicrobial resistance (AMR) patterns. Unlike classical zoonotic pathogens, most NTM are primarily acquired from shared environmental reservoirs rather than through sustained host-to-host transmission. This review examines NTM from a One Health perspective, focusing on AMR, ecology, animal occurrence, cross-species exposure and public health relevance. Methods: A narrative review of the current literature was conducted to synthesize evidence on the ecology, environmental reservoirs, occurrence in animals, transmission patterns and AMR mechanisms of NTM. Particular attention was given to studies addressing the human–animal–environment interface and the implications of NTM for One Health surveillance and risk assessment. Results: The reviewed literature shows that NTM are widely distributed in water, soil, sediments and biofilms, creating repeated opportunities for exposure in both animals and humans. They have been reported in livestock, wildlife, companion animals, reptiles and aquatic organisms, where they may act as colonizers, opportunistic pathogens, or sources of diagnostic interference. Evidence for direct animal-to-human transmission remains limited, but animal and environmental findings are important for understanding ecological overlap, host range and circulation of resistant strains. AMR in NTM is shaped by intrinsic resistance, acquired mutations, efflux activity, and biofilm-associated tolerance, which together complicate treatment and resistance prediction. Conclusions: NTM should be considered environmentally maintained, multi-host organisms of increasing One Health importance rather than conventional zoonotic pathogens. Improved interdisciplinary surveillance, diagnostics and research are needed to clarify exposure pathways, resistance development and public health risk. Full article

Oral candidiasis (OC) is the most frequent fungal infection among users of dental prosthetic devices, immunocompromised patients, and those who underwent chemotherapy treatment and had a complication of long-term antibiotic therapy. About 150 species of Candida fungi have been described, whereas over 80% of oral fungal infections are attributed to the opportunistic pathogen Candida albicans. Pain, dryness of oral mucosa, pathological lesions, and intermittent mucosal bleeding are the main symptoms that worsen the daily functioning of the abovementioned fungal-infected patients. A promising adjunctive strategy may involve the use of probiotic bacteria to attenuate fungal colonization in the oral cavity in order to reduce the need for conventional treatment, which carries a risk of antifungal drug resistance—a significant problem worldwide. Probiotic formulations mostly incorporate commensal bacteria that naturally inhabit oral ecosystems such as Lactobacillus spp., Bifidobacterium spp., Bacillus spp., and others. Probiotic organisms may contribute to the restoration of oral microbiome homeostasis through numerous mechanisms, such as competitive control of Candida species numbers, better adhesion to oral mucosa and production of bioactive compounds and antimicrobial metabolites. Despite many studies, the current evidence base remains heterogeneous. Well-designed studies across diverse populations are required to determine whether probiotic-based interventions can be an effective and clinically useful alternative or adjunct to standard antifungal therapy of OC. Full article

Fusobacterium nucleatum (Fn) has emerged as one of the most extensively studied tumor-associated opportunistic pathogens in colorectal cancer (CRC). The central question in Fn–CRC research has shifted from species-level detection or enrichment toward identifying specific lineages with enhanced persistence and tumor-promoting potential under defined host and ecological contexts. Accumulating evidence suggests substantial heterogeneity within Fn at the subspecies and clade levels. Among these, the F. nucleatum subsp. animalis C2 (Fna C2) lineage has been proposed as a candidate high-risk clade with potentially greater adaptability to the gastrointestinal tract and tumor microenvironment. However, current support for Fna C2 is derived mainly from ecological enrichment, comparative genomics, inferred metabolic features, and limited functional observations, while direct clinical and mechanistic validation at the clade level remains limited. Fn has been implicated in CRC progression through multiple interconnected processes, including adhesion and colonization, host signaling activation, inflammatory amplification, immune suppression, and metabolic adaptation. Notably, these pathogenic outputs are unlikely to be uniformly distributed across all Fn lineages, but instead appear to be shaped by the combined influence of bacterial lineage, host molecular context, microbial community structure, and spatial organization within the tumor microenvironment. In this review, we summarize the lineage heterogeneity of Fn, its association with CRC, and the underlying host–pathogen interaction mechanisms. We further discuss implications for high-resolution stratification, risk classification, and clinical translation, emphasizing the need to move from species-level associations toward lineage-resolved and context-aware frameworks. Full article

The major Staphylococcaceae family is recognized as opportunistic pathogens colonizing human and animal skin, mucous membranes, and environments. Musca domestica, the house fly, plays a role in the transmission of AMR bacteria. This study focused on examining the epidemiology and antimicrobial-resistant genes of the family Staphylococcaceae in M. domestica through metagenomic analysis, using samples collected from three animal farms and two residential areas in southern Thailand. Fifty M. domestica were collected from five places surrounding Walailak University, including one chicken farm (CF1), two pig farms (PF2 and PF3), and two residential areas (H1 and H2). All samples were dispatched for analysis using shotgun metagenomic sequencing and analyzed using FastQC, MultiQC, FASTQ, MEGAHIT, QUAST, ABRicate, AMRFinderPlus, ResFinder, ARG-ANNOT, MEGARES, PlasmidFinder, VFDB, Kraken2, Krona and Python. Our findings describe the taxonomic composition of Staphylococcaceae taxa in M. domestica from different environments; the representation of the family Staphylococcaceae in CF1, PF2, PF3, H1, and H2 was recorded at 2%, 0.7%, 0.2%, 0.2%, and 2% of this phylum, respectively. The average populations discovered were Staphylococcus (37.4%), Mammaliicoccus (17.4%), and Macrococcus (10.3%), respectively. Trimethoprim-resistant genes (dfrG and dfrE) were found only in CF1, PF2, and H1. Interestingly, fosfomycin-resistant genes were found only in M. domestica within residential areas. Our findings pertain to the Staphylococcaceae population in M. domestica within residential areas, which exhibited varying multidrug-resistance genes, particularly those resistant to fosfomycin. Full article

Chronic Obstructive Pulmonary Disease (COPD) is characterized by persistent inflammation and structural alterations in the lung triggered mainly by oxidative stress. Colonization by the opportunistic fungus Pneumocystis has been associated with worse clinical outcomes in COPD, yet its role in airway remodeling remains unclear. To this end, an elastase-induced COPD model was established, followed by colonization with Pneumocystis. Lung tissue was analyzed histologically and molecularly to assess epithelial thickness, alveolar morphometric parameters (mean linear intercept [MLI], D₀, D₁, D₂), inflammation, collagen deposition, and the expression of remodeling and oxidative stress markers. Emphysematous damage parameters MLI, D₀, D₁, and D₂ were markedly elevated in co-exposed animals, indicating enhanced alveolar enlargement. Animals with COPD and Pneumocystis colonization showed a significant increase in airway inflammation compared with control, COPD, and Pneumocystis groups. Airway epithelial thickness, mucus metaplasia, and collagen deposition exhibited a summative increase in the COPD/Pneumocystis group. Redox-responsive markers, such as superoxide dismutase (SOD) and catalase, were upregulated. Moreover, protein and mRNA levels of nuclear factor erythroid 2–related factor 2 (Nrf2) and its downstream gene heme oxygenase-1 (Hmox1) were significantly increased, with the strongest activation observed in co-exposed animals. Integrative correlation analysis showed that Pneumocystis burden positively correlated with lung damage, inflammation, and epithelial remodeling. These structural alterations were accompanied by coordinated activation of the antioxidant pathway Nrf2. Taken together, Pneumocystis colonization is associated with enhanced pulmonary remodeling and modulation of antioxidant signaling in experimental COPD, promoting structural and molecular changes that may contribute to disease progression. These findings suggest that Pneumocystis acts as an amplifying factor in COPD-associated lung damage. Full article

Achromobacter spp. are opportunistic pathogens in people with cystic fibrosis (PwCF), yet the role of the upper airways in their persistence and adaptation remains poorly understood. We investigated whether the sinonasal compartment may act as reservoir and evolutionary niche for Achromobacter spp. during airway infection. Twenty-two isolates obtained from paired nasal lavage and sputum samples of seven PwCF were analysed by whole-genome sequencing. Within each PwCF, identical clone types were detected in both airway compartments, supporting bacterial exchange between upper and lower airways. Despite clonal relatedness, substantial genomic diversification was observed between paired isolates. Genomic signatures indicative of elevated mutation rates were detected in a high number of isolates (73%) and in both airway compartments, highlighting widespread genomic diversification across the respiratory tract. Mobilome analysis revealed compartment-specific variations in insertion sequences, prophages, and integrative elements, suggesting genome plasticity. Additionally, mutation in an aspartate kinase gene was consistently associated with loss of biofilm formation in vitro, highlighting a potential link between this pathway and biofilm phenotype. Overall, our findings indicate that upper and lower airways represent interconnected but partially independent ecological niches where Achromobacter populations can diverge during colonization, supporting the view that both compartments contribute to their persistence and evolution in CF airways. Full article

Candida species can shift from commensal organisms to opportunistic pathogens. Both Candida albicans and non-albicans Candida (NAC) species colonize oral biofilms and periodontal pockets, where they may contribute to inflammation and the progression of periodontal disease. This study aimed to determine the prevalence and antifungal susceptibility profiles of Candida species in individuals with different stages of periodontal disease. A cross-sectional study was conducted in 100 participants whose periodontal status was clinically evaluated. Saliva samples were cultured on chromogenic agar for yeast isolation, species identification was confirmed by MALDI-TOF MS, and antifungal susceptibility to fluconazole, clotrimazole, nystatin, and amphotericin B was assessed. Candida spp. was detected in 35% of participants, where C. albicans was the most prevalent species, followed by Nakaseomyces glabratus (formerly Candida glabrata), Candida parapsilosis, Candida dubliniensis, and Candida tropicalis. Species distribution varied according to periodontal status, with N. glabratus predominating in early periodontitis and C. albicans appeared more frequently in higher severe stages of periodontitis. Susceptibility testing showed resistance of C. albicans to clotrimazole (63.6%) and nystatin (22.7%), whereas amphotericin B and fluconazole remained effective. NAC species, particularly N. glabratus, exhibited resistance to nystatin and variable resistance to clotrimazole but remained susceptible to amphotericin B. These findings underscore the importance of early detection and personalized antifungal strategies for managing periodontal disease complicated by Candida colonization. Full article

The non-albicans Candida species Candida tropicalis is an opportunistic fungal pathogen that forms a robust gel-like biofilm on polymeric prosthetic materials. These biofilms are embedded in an extracellular polymeric substance that retains large amounts of water, resulting in a hydrogel-like matrix that protects fungal cells, increases antifungal resistance, and contributes to the biofouling of these prosthetic materials. Biofouling is the unwanted colonization and accumulation of microbial communities on material surfaces, which alters their function and compromises clinical performance. Clinically, it is significant because it is linked to recurrent urinary tract infections, bloodstream infections, and persistent device-related infections, which often result in therapeutic failure and device malfunction. Polymers such as silicone elastomer, polypropylene, polystyrene, polyurethane, polyethylene, and polyvinyl chloride are widely used in catheters, surgical meshes, implants, and prostheses because of their durability, flexibility, and biocompatibility, yet their surface properties often encourage microbial adhesion and biofilm formation. This review emphasizes that the gel-like biofilm architecture of C. tropicalis underpins its persistence and resistance, while also highlighting promising antifungal strategies being developed to mitigate these infections. Notably, palmitic acid has been shown to disrupt mature biofilms by lowering ergosterol and inducing oxidative stress, whereas C-10 massoia lactone damages the extracellular matrix and suppresses hyphal growth. Drug repurposing approaches, such as combining minocycline with fluconazole, restore susceptibility in resistant isolates and demonstrate synergistic antibiofilm activity. Additionally, biomaterial-based interventions, such as chitosan coatings on silicone surfaces, significantly reduce fungal adhesion and biofilm formation. Together, these findings reflect a translational shift toward integrating natural products, repurposed drugs, and functionalized biomaterials into antifungal development. Understanding biofouling and these emerging strategies is crucial for developing effective control measures against C. tropicalis biofilms and for guiding the design of infection-resistant prosthetic devices. Full article

Wuzhishan pigs are a typical Chinese indigenous miniature pig breed, with thin skin and high amino acid content in muscle; slow weight gain and long feeding phases limit their value. As the primary digestive and absorptive organ, the intestine is crucial for growth, yet current studies on its development are limited. This study aimed to investigate intestinal physiological differences in Wuzhishan pigs across four phases (pre-weaning: 7, 14 days; weaning: 35, 38, 45 days; fattening: 70, 100 days; maturity: 180, 240 days) by evaluating intestinal morphology, digestive enzyme activity, gut microbiota diversity via 16S rRNA gene sequencing, and metabolite characteristics via metabolomic analysis. Results showed poor intestinal morphology and enzyme activity during weaning, significant ileal and colonic microbial diversity differences across phases, increased beneficial bacteria with age, and enriched opportunistic pathogens (Streptococcus, Romboutsia, Terrisporobacter) during weaning; weaning also had lower lipid metabolites, correlated with decreased Fusobacterium, Lactobacillus, and Muribaculaceae. Fattening enhanced amino acid metabolism, with increased Lactobacillus correlated with higher amino acids and muscle-related metabolites, while maturity increased immune-related metabolites (e.g., pyridoxine) in the vitamin B6 pathway. These results explain delayed rapid weight gain in Wuzhishan pigs and provide a theoretical basis for maintaining intestinal stability and production performance. Full article