This study is a first report on the identification of multidrug-resistant (MDR) Acinetobacter bereziniae among non-baumannii acinetobacters that had previously escaped automated laboratory detection, and characterize their clinical courses of infection at two tertiary-care hospitals in Shenzhen city, China (2015-2017). Herein, definitive identification by PCR was performed with universal and species-specific primers targeting 16S rDNA and rpoB genes, respectively, followed by Sanger sequencing and blast analysis. Antimicrobial susceptibility of A. bereziniae isolates was assessed accordingly. Three of the five identified A. bereziniae isolates exhibited carbapenem-resistance and were subjected to a multiplex PCR assay to detect drug-resistance genes. Sequences of the rpoB amplicon were aligned with curated sequences from global databases for phylogenetic analysis on evolutionary relations. Five clinical isolates of A. bereziniae were thereby re-identified, whose infections were primarily nosocomial. Automated identification and susceptibility testing systems (Phoenix-100 and VITEK 2) proved insufficient for discriminating A. bereziniae from other acinetobacters such as Acinetobacter baumannii and Acinetobacter guillouiae. Among these isolates, three exhibited carbapenem-resistant phenotypes indistinguishable from that of carbapenem-resistant A. baumannii. The carbapenem-resistant A. bereziniae isolates were subsequently confirmed to carry a bla _NDM-1 (New Delhi metallo-β-lactamase-1) gene downstream of ISAba125. Phylogenetic analysis revealed that A. bereziniae isolates evolved slowly but independently in local habitats. A. bereziniae isolates are difficult to distinguish by traditional automated detection systems. PCR-based identification via amplification and sequencing of selected house-keeping genes provides sufficient resolution for discriminating the isolates.

BackgroundEarly diagnosis of atrial fibrillation is important as it is crucial for improving patient outcomes. Fibroblast growth factor-2 (FGF2) may serve as a diagnostic biomarker for heart failure due to its ability to promote cardiac fibrosis and hypertrophy; however, the relationship between FGF2 concentration and heart failure is unclear. Therefore, this study aimed to explore whether FGF2 could aid in distinguishing patients with heart failure from healthy controls and those with dyspnea without heart failure. Additionally, to evaluate the possible correlation between serum FGF2 levels and its diagnostic parameters in patients with heart failure. MethodsPlasma FGF2 concentration was measured in 114 patients with a complaint of dyspnea (enrolled in the study between January 2022 and August 2022). Based on heart failure diagnosis, the patients were assigned to three groups, as follows: heart failure (n = 80), non-heart-failure dyspnea (n = 34), and healthy controls (n = 36), following physical examination. Possible correlations between serum FGF2 levels and other prognostic parameters in patients with heart failure were analyzed. ResultsSerum FGF2 levels were higher in patients with heart failure (125.60 [88.95, 183.40] pg/mL) than in those with non-heart-failure dyspnea (65.30 [28.85, 78.95] pg/mL) and healthy controls (78.90 [60.80, 87.20] pg/mL) (p < 0.001). Receiver operating characteristic curve analysis identified FGF2 concentration as a significant predictor in heart failure diagnosis, with an area under the curve of 0.8693 (p < 0.0001). Importantly, in the heart failure group, serum FGF2 concentrations correlated with key prognostic parameters for heart failure, such as reduced left ventricular ejection fraction and elevated serum levels of N-terminal pro-B-type natriuretic peptide. ConclusionsElevated serum FGF2 level is strongly associated with an increased risk of heart failure and could serve as a useful biomarker to complement vital diagnostic parameters for heart failure.

Background: Multidrug-resistant Acinetobacter baumannii (MDR-AB) poses a critical threat in neonatal intensive care units (NICUs), however few studies have reported the molecular characterization of A. baumannii isolates from the NICU in China. This study aims to describe the molecular, biofilm and motility characteristics related to carbapenem resistance genes in A. baumannii isolates from the NICU. Methods: Following an outbreak in March–April 2024, 21 A . baumannii isolates from neonatal and environmental sources were collected. These isolates underwent antimicrobial susceptibility testing, whole-genome sequencing (WGS) for resistance gene profiling and multi-locus sequence typing (MLST). Biofilm formation and twitching motility were measured in representative strains exposed to subinhibitory concentrations of gentamicin, levofloxacin, and meropenem. Results: All 21 A . baumannii isolates were carbapenem-resistant Acinetobacter baumannii (CRAB), showing resistance to cephalosporins, aminoglycosides, and quinolones. WGS identified 25 resistance genes, including the universal bla _OXA-23 , bla _OXA-66 , bla _ADC-25 and bla _TEM-1D , aminoglycoside resistance genes ( armA , aph genes ), macrolide resistance genes ( mphE , msrE ), and tetracycline ( tetB ) resistance genes. Efflux pumps ( adeABC , adeFGH , adeIJK ) were ubiquitous. Two sequence types emerged: ST195 (20 isolates) and ST1959 (1 isolate), with high genetic similarity suggesting nosocomial transmission. ST1959 exhibited stronger biofilm formation than ST195. Biofilm formation of ST1959 was significantly enhanced by gentamicin but inhibited by levofloxacin. Meropenem suppressed only the ST195 biofilms. Twitching motility was markedly reduced in ST1959 and also decreased after levofloxacin exposure. Conclusion: This NICU outbreak was driven by CRAB ST195 harboring a conserved resistome. Strain-specific differences in biofilm formation and motility under antibiotic stress highlight the interplay between genetic lineage and phenotypic adaptability. Levofloxacin demonstrates dual anti-biofilm and anti-motility effects, which could guide targeted infection control strategies against high-risk A. baumannii clones.

Background: Prediction, early diagnosis, and treatment of heart failure are crucial. Fibroblast growth factor-2 (FGF2) may serve as a prognostic biomarker for heart failure owing to its ability to promote cardiac fibrosis and hypertrophy; however, the relationship between FGF2 concentration and heart failure is unclear. Therefore, this study aimed to explore whether FGF2 could aid in distinguishing patients with heart failure from healthy controls and those with dyspnea without heart failure and evaluate the possible correlation between serum FGF2 levels and its prognostic parameters in patients with heart failure. Methods: Plasma FGF2 concentration was measured in 114 patients with complaint of dyspnea (enrolled in the study between January 2022 and August 2022). Based on heart failure diagnosis, the patients were assigned to three groups, as follows: heart failure (n = 80), non-heart-failure dyspnea (n = 34), and healthy controls (n = 36), following physical examination. Possible correlations between serum FGF2 levels and other prognostic parameters in patients with heart failure were analyzed. Results: Serum FGF2 levels were higher in patients with heart failure (125.60 [88.95, 183.40] pg/mL) than in those with non-heart-failure dyspnea (65.30 [28.85, 78.95] pg/mL) and healthy controls (78.90 [60.80, 87.20] pg/mL) (p <0.001). Receiver operating characteristic curve analysis identified FGF2 concentration as a significant predictor in heart failure diagnosis, with an area under the curve of 0.8693 (p <0.0001). Importantly, in the heart failure group, serum FGF2 concentrations correlated with key prognostic parameters for heart failure, such as reduced left ventricular ejection fraction and elevated serum levels of N-terminal pro-B-type natriuretic peptide. Conclusion: Elevated serum FGF2 level is strongly associated with an increased risk of heart failure and could serve as a useful biomarker to complement vital prognostic parameters for heart failure.