Acta microbiologica et immunologica Hungarica最新文献

Severe community-acquired pneumonia (SCAP) remains a leading cause of infectious disease mortality worldwide. Timely identification of causative pathogens and appropriate antimicrobial therapy are critical determinants of patient outcomes. This retrospective cohort study investigated the etiological features of SCAP and their relationship with infection-related biomarkers, including C-reactive protein (CRP), procalcitonin (PCT), D-dimer (D-D), white blood cell count (WBC), and neutrophil percentage (NEUT), in an emergency department setting. A total of 146 patients with SCAP admitted to Tianjin Medical University General Hospital between March 2018 and March 2019 were included. Pathogen identification was performed through sputum or bronchoalveolar lavage fluid (BALF) cultures. Antimicrobial susceptibility testing was conducted using the Kirby-Bauer disk diffusion method. A total of 154 bacterial strains were isolated from 146 patients. Gram-negative bacteria predominated (145 strains, 94.2%), followed by Gram-positive bacteria (8 strains, 5.2%). The most frequently isolated pathogens were Klebsiella pneumoniae (25.3%), Acinetobacter baumannii (20.1%), and Pseudomonas aeruginosa (13.6%). Extended-spectrum beta-lactamase (ESBL)-producing strains were identified in 17 of 39 K. pneumoniae isolates (43.6%). High-risk clones of K. pneumoniae ST11, ST15, ST307, A. baumannii ST2, P. aeruginosa ST235 were detected in this study. Cefoperazone-sulbactam demonstrated low resistance rates in K. pneumoniae (7.7%), A. baumannii (9.7%), Enterobacter cloacae (8.3%), and P. aeruginosa (14.3%). Abnormal PCT levels were associated with higher proportions of K. pneumoniae and Stenotrophomonas maltophilia infections. Elevated CRP, D-D, WBC, and NEUT levels were more frequently observed in patients infected with K. pneumoniae and A. baumannii. Gram-negative bacteria, particularly K. pneumoniae and A. baumannii, are the predominant pathogens in SCAP. Infection-related biomarkers, especially PCT, show promise in predicting specific etiologies and may guide empirical antimicrobial selection.

Dysphagia constitutes a growing global health burden, particularly among geriatric and post-stroke populations. Although traditionally managed through biomechanical interventions, emerging evidence underscores the microbiota-immune axis as a critical modulator of systemic resilience and clinical outcomes. This review delineates how dysphagia drives systemic dysbiosis via three primary mechanisms: dietary modification, descending migration of oral pathogens along the oral-gut-lung axis, and iatrogenic pharmacological effects. A core pathological consequence is the depletion of microbial metabolites, especially short-chain fatty acids (SCFAs), which undermines neurological recovery and musculoskeletal integrity through the gut-brain and gut-muscle axes. Such dysbiosis further weakens intestinal barrier function, precipitating endotoxin translocation, chronic systemic inflammation, and elevated risk of life-threatening complications like aspiration pneumonia. Consequently, nursing practice should integrate microbiome-targeted strategies. Key interventions encompass nutritional modulation with specific probiotics (e.g., Lactobacillus rhamnosus GG) and prebiotics to restore SCFA levels, enhanced oral care to minimize pathogen reservoirs, and pharmacological stewardship to mitigate iatrogenic microbial disruption. Adopting these tailored approaches, these can transit nursing care from compensatory support to actively promoting physiological recovery and immune resilience in dysphagia patients.

This single-centre cross-sectional study aimed to explore serum metabolomic and gut microbiota signatures in patients with Sjögren disease (SjD) complicated by anxiety disorder, with emphasis on microbe-metabolite crosstalk, to screen differential omics features and identify clinically relevant microbial and metabolic markers stratified by anxiety severity and SjD disease activity. A total of 59 SjD patients were enrolled, and all participants underwent serum untargeted metabolomics and faecal 16S rRNA gene sequencing. Participants were stratified according to the median Hamilton Anxiety Scale (HAMA) and European Alliance of Associations for Rheumatology (EULAR) Sjögren's Syndrome Disease Activity Index (ESSDAI) scores, and separate Pearson correlation analyses were performed between core clinical indicators and differential gut microbiota as well as serum metabolites. Five altered metabolites involved in purine and tyrosine metabolism were identified. SjD patients with anxiety exhibited enriched pro-inflammatory microbes and depleted anti-inflammatory commensals. Random-forest modelling identified Barnesiella, Lachnoclostridium and Veillonella as key discriminative genera; notably, Lachnoclostridium abundance showed a positive correlation with serum roccellic acid and N-(9-oxodecy) acetamide, indicating direct gut-circulating metabolite interplay. Subgroup analyses demonstrated gradient shifts of these core markers alongside increasing anxiety and disease severity, and Ligilactobacillus, Lachnoclostridium, xanthosine and 2,5-dihydroxybenzaldehyde were validated as anxiety-specific biomarkers. Collectively, SjD patients with anxiety display coordinated perturbations in serum metabolites and gut microbiota, and stratified correlation analyses yield novel microbiology-based, clinically interpretable biomarkers for identifying SjD patients complicated with anxiety disorder.

Carbapenem-resistant Klebsiella pneumoniae (CRKP) is a World Health Organization critical-priority pathogen, with a bloodstream-infection mortality of 40-70%. Ceftazidime-avibactam (CAZ-AVI) and colistin are key agents against CRKP, yet data on their minimum inhibitory concentrations (MICs) and association with carbapenemase genotypes in the Mekong Delta region of Vietnam are limited. This cross-sectional study on CRKP isolates from clinical specimens at hospitals in Can Tho City (November 2024-July 2025) determined the MICs of CAZ-AVI and colistin and their association with carbapenemase genotypes (blaKPC, blaOXA-48-like, blaNDM, blaIMP, blaVIM). MICs were measured by broth microdilution and interpreted per CLSI M100 (2024) and EUCAST (2024, for colistin); carbapenemases were detected by the modified carbapenem inactivation method (mCIM), the D73C disc, and singleplex polymerase chain reaction (PCR). Among 112 strains, susceptibility was 42.0% for CAZ-AVI (MIC50/MIC90 > 16/4 μg mL-1) and 82.1% for colistin (MIC50 = 1 μg mL-1, MIC90 = 8 μg mL-1). Among 92 PCR-tested strains, co-carriage of ≥2 carbapenemase genes were most common, and blaOXA-48-like was the most prevalent single gene. The CAZ-AVI MIC differed significantly among genotypes (p = 0.002): isolates carrying blaKPC or blaOXA-48-like retained the highest susceptibility, whereas all isolates carrying only a metallo-β-lactamase (blaNDM or blaVIM) were resistant; the colistin MIC did not differ among genotypes (p = 0.376). Carbapenemase genotyping should guide the use of CAZ-AVI in this setting, particularly for distinguishing serine carbapenemase producers from MBL producers, while the elevated colistin MIC90 supports continued surveillance of colistin susceptibility.

Carbapenem resistance driven by carbapenemase production in Gram-negative bacteria is a global threat. Carbapenem-resistant Acinetobacter baumannii (CRAb) is a critical priority pathogen listed by the World Health Organization (WHO). While blaOXA-23 and blaOXA-24/40-like are most frequently reported in CRAb, an increasing prevalence of blaNDM has been noted in recent years. This study aimed to investigate the distribution of carbapenemase genes among CRAb isolates obtained from three tertiary care centres in Türkiye.A total of 336 CRAb isolates recovered from various clinical specimens (blood, respiratory samples, wound/tissue swabs, urine, and catheter tip samples) between January 2023 and October 2024 were included (Centre-1:198; Centre-2:86; Centre-3:52). Antimicrobial susceptibility testing was performed using the VITEK2 or BD Phoenix system, with additional tests carried out using the disc diffusion or broth microdilution methods. The results were interpreted in accordance with EUCAST criteria. The presence of blaOXA-51, blaOXA-23, blaOXA-24/40-like, blaOXA-58, blaVIM, blaIMP, blaNDM and blaKPC was tested by qPCR. The clonal relationship among the isolates producing metallo-β-lactamase (MBL) was assessed using AP-PCR and PFGE methods.Our study detected blaOXA-23 in 305 isolates (90.8%), blaOXA-24/40-like in 88 (26.2%), blaNDM in 21 (6.3%), and blaVIM in one isolate. However, blaOXA-58, blaIMP and blaKPC were not detected. Dual gene combinations were observed in 73 isolates, while triple combinations were identified in three isolates (two blaNDM/blaOXA-23/blaOXA-24/40-like, one blaVIM/blaOXA-23/blaOXA-24/40-like). AP-PCR/PFGE demonstrated a clonal relationship among 18 isolates, all originating from a single intensive care unit at Centre-1. Because carbapenem resistance is endemic in this unit, the cluster was indistinguishable from the background resistant population and was detected only retrospectively by molecular typing; we therefore describe it as a silent outbreak.In this study blaOXA-23 and blaOXA-24/40-like were the predominant carbapenemase genes in CRAb, with blaNDM detected at a notable frequency. The detection of combined gene profiles and inter-centre differences highlight the potential impact of local antibiotic use and infection control practices on the dissemination of resistance, and the clonal cluster identified here shows that such dissemination can go unrecognised in endemic settings.

Klebsiella pneumoniae is a Gram-negative bacterium, which can cause a range of difficult-to-treat infections, like; wound infections, urinary tract infections (UTIs), pneumonia, and other diseases. Recent studies have shown that hypervirulent carbapenem-resistant K. pneumoniae (hv-CRKp) is a single, widespread "super-pathogen" that combines significant clinical complications. This convergence is not exclusive to hospitals, as plasmid-mediated virulence and resistance gene exchange occurs in wastewater and other aquatic habitats. Hospital effluents serve as the main hotspot for CRKp discharge, with substantial clonal spread, according to research from regional wastewater networks. Selective pressures from heavy metals, disinfectants, and antibiotic residues speed up horizontal gene transfer in these intricate microbial communities, encouraging the establishment of hv-CRKp. The molecular mechanisms underlying plasmid fusion and mobility, the role of the wastewater resistome and biofilms as sites of genetic exchange, and the One-Health implications of environmental dissemination are all summarized in this assessment of recent investigations from 2023 to 2025. We show how wastewater-based epidemiology may be utilized as an early warning system to discover novel hv-CRKp lineages by merging data from plasmidomics, metagenomics, and global surveillance. The ecological and molecular continuity that links hospitals, wastewater, and the larger environment must be understood when designing next-generation antimicrobial resistance control initiatives against hv-CRKp. This study concludes by discussing research gaps and intervention ideas to reduce environmental spread.

Oral squamous cell carcinoma (OSCC) is the most common malignancy of the oral cavity and a major public health concern worldwide. This study aimed to investigate the relationship between p53 and survivin expression, clinicopathologic parameters and HPV16 infection in OSCC in order to elucidate the potential role of HPV16 in its pathogenesis.The study enrolled 45 patients who underwent surgical treatment for histologically confirmed OSCC. Tumor specimens were formalin-fixed and paraffin-embedded (FFPE) and histologically analyzed using hematoxylin/eosin staining. Immunohistochemistry for p53 and survivin was performed using the DAKO system. DNA extracted from FFPE tumor tissues was analyzed for HPV16 genome presence using polymerase chain reaction (PCR). All patients were followed for three years after primary treatment.No statistically significant associations were observed between p53 or survivin expression and clinicopathologic parameters including age, gender, tumor site, grade, stage, recurrence, metastasis or HPV16 status (P > 0.05). Among HPV16-positive patients (11/45, 24.4%), low survivin expression (<5%) was found in 8/11 (73%) patients, while high p53 expression (>10%) was observed in 7/11 (64%) patients. Disease-free interval did not differ significantly between patients with low vs. high p53 (P = 0.220) or survivin expression (P = 0.580). A significant correlation was detected between p53 and survivin expression (P = 0.04). HPV16 positivity was significantly associated with the absence of p53 immunoreactivity.These findings suggest that HPV16-independent oncogenic pathways are likely predominant in OSCC, while HPV16 infection may be associated with a distinct molecular subset characterized by absent p53 expression (p53-; survivin+/-; HPV16+). These results underscore the biological heterogeneity of OSCC and may have implications for future biomarker-based stratification of patients.

We evaluated Weifuchun tablets (composed of red ginseng, chamomile, and roasted shell) for preventing intestinal polyp recurrence and treating mucosal lesions after endoscopic resection, and to analyze its mechanism via gut microbiome regulation. This study prospectively enrolled 218 patients who underwent endoscopic intestinal polyp resection (April 2022-April 2024). The observation group (n = 109) received routine postoperative care plus oral Weifuchun tablets for three months, while the control group (n = 109) received routine care alone. Propensity score matching (PSM) was used to balance baseline characteristics. Primary outcomes included one-year polyp recurrence, mucosal injury scores, and gut microbiome alterations (16S rDNA sequencing). Safety and independent protective factors for recurrence (multivariate logistic regression) were also assessed. After PSM, the observation group had a significantly lower one-year recurrence rate than the control group (31.00% vs. 42.16%, P = 0.025). Weifuchun significantly reduced intestinal mucosal injury scores (P < 0.001). Crucially, microbiome analysis revealed that Weifuchun markedly increased gut microbial diversity (Sorensen index, P < 0.05) and significantly boosted the relative abundance of beneficial bacteria such as Bifidobacterium and Lactobacillus, while decreasing harmful bacteria including Escherichia coli and Bacteroides (all P < 0.001). Furthermore, Weifuchun significantly reduced postoperative complications (2.00% vs. 8.82%, P = 0.032) and was identified as an independent protective factor against recurrence (OR = 0.456, 95% CI: 0.304-0.683, P < 0.001). Weifuchun effectively prevents polyp recurrence and promotes mucosal repair post-endoscopic resection. Its mechanism is closely linked to beneficial modulation of the gut microbiome, restoring microbial balance and enhancing the intestinal microenvironment, and demonstrates a favorable safety profile.

Chronic obstructive pulmonary disease (COPD) is featured by persistent airflow limitation and chronic inflammation. Considerable evidence highlights the role of the gut-lung axis, suggesting that disruption of gut microbial balance may contribute to aggravated systemic and pulmonary inflammation. This research intended to assess the impacts of a structured gut-lung axis-targeted nursing intervention on immune-inflammatory parameters, gut microbiota, and clinical outcomes in patients with stable COPD. The study involved the randomization of 115 patients to either the intervention or control group in a 1:1 ratio. The intervention group received a 12-week multimodal program, which included personalized high-fiber/probiotic nutrition, customized exercise plans, and stress management techniques. Patients in the control group did not receive the multimodal program and instead received routine care. The findings indicated that the intervention notably lowered serum IL-6, TNF-α, and CRP. Microbiome analysis further revealed that the intervention significantly enhanced α-diversity (Shannon and Chao1), enriched beneficial butyrate-producing genera (Faecalibacterium, Roseburia, and Bifidobacterium), and reduced the relative abundance of potential pathogens (Enterobacteriaceae), indicating a favorable shift in gut microbial ecology. Compared with the control group, the intervention group also experienced fewer moderate-to-severe exacerbations and showed greater sustained improvement in quality of life (SGRQ and CAT scores). In summary, a comprehensive nursing strategy centered on the gut-lung axis can regulate gut microbiota, alleviate systemic inflammation, lead to a reduction in exacerbation frequency and an improvement in the quality of life among patients with stable COPD, thus presenting a promising supplementary strategy to conventional care.