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The environmental spread of antibiotic-resistant bacteria has been recognised as a growing public health threat for which hospitals play a significant role. The aims of this study were to investigate the prevalence of antibiotic resistance and antibiotic resistance genes (ARGs) in Escherichia coli isolates from hospital wastewater in Vietnam. Wastewater samples before and after treatment were collected using continuous sampling every month over a year. Standard disk diffusion and E-test were used for antibiotic susceptibility testing. Extended-spectrum beta-lactamase (ESBL) production was tested using combined disk diffusion. ARGs were detected by polymerase chain reactions. Resistance to at least one antibiotic was detected in 83% of isolates; multidrug resistance was found in 32%. The highest resistance prevalence was found for co-trimoxazole (70%) and the lowest for imipenem (1%). Forty-three percent of isolates were ESBL-producing, with the blaTEM gene being more common than blaCTX-M. Co-harbouring of the blaCTX-M, blaTEM and qepA genes was found in 46% of isolates resistant to ciprofloxacin. The large presence of antibiotic-resistant E. coli isolates combined with ARGs in hospital wastewater, even post-treatment, poses a threat to public health. It highlights the need to develop effective processes for hospital wastewater treatment plants to eliminate antibiotic resistant bacteria and ARGs.

Introduction. Multidrug-resistant (MDR) Gram-negative bacilli including carbapenem-resistant Gram-negative Enterobacteriaceae (CRE) threaten global health. Little is known, however, about the distribution of antimicrobial resistance genes in MDR isolated from patients in Vietnamese hospitals. In this study, we collected MDR Escherichia coli, defined as E. coli resistance against all fluoroquinolones, aminoglycosides, and carbapenems. Aim. This study was designed to clarify the molecular epidemiology of Escherichia coli isolates resistant to carbapenems, fluoroquinolones, and aminoglycosides isolated from patients admitted to one of the largest hospitals in Vietnam in 2014–2019 based on both whole-genome sequencing (WGS) and phenotypic data. Methodology. Sixty-seven Vietnamese isolates screened by drug resistance by the disk test were subjected to WGS, and their sequences were analyzed to determine their multilocus sequence type (MLST), O-types, H-types, distribution of drug resistance genes, plasmid types, pathogenicity islands (PIs), virulence factor distribution, and phylogenetic evolution using the WGS data. Results. Among the STs detected, ST410 was relatively dominant. Dominant O-types and H-types were O102 and H9 and showed some links, such as those between O102 and H8. The most dominant plasmid type and carbapenemase type were 4 and NDM-5, respectively. MLST, O-types, H-types, plasmid types, and types of carbapenemases were very heterogeneous among the isolates, with no clear correlation between them. Dominant plasmid type carrying drug resistance gene was IncQ1_1. The percentage of isolates positive for drug resistance genes, such as anti-beta-lactams and aminoglycosides, was relatively high because the isolates screened were resistant to carbapenems, fluoroquinolones, and aminoglycosides. Conclusions. MDR E. coli isolates isolated at a high-volume Vietnamese hospital were very heterogeneous, suggesting that they were acquired from different sources, including nosocomial infection, animals, and water. Eradication of MDR E. coli from hospitals and other clinical environments is very challenging because a single measure may be ineffective.

Objectives: Studies have revealed that a relatively high incidence of severe infection and mortality in COVID-19 patients is attributed to healthcare-associated infections (HAIs). We implemented a study in 2 field hospitals dedicated to COVID-19 treatment in Da Nang, Vietnam (July–August 2020), and Ho Chi Minh City, Vietnam (August–October 2021), to identify pathogens, risk factors, and outcomes associated with HAIs. Methods: We applied a prospective study tool to estimate HAI incidence among 1,454 patients. HAIs are diagnosed and ascertained using surveillance criteria established by the US Centers for Disease Control and Prevention. All patients hospitalized for COVID-19 for at least 2 days were enrolled in this assessment of HAI risks, pathogens, and outcomes. Results: Among 1,454 sampled patients, 391 patients had 423 HAIs (27.1%). The highest proportion occurred in ICUs, with 422 HAI patients (34.1%). Pneumonia (n = 331, 78.3%) and bloodstream infections (n = 55, 13.1%) were the most common HAIs. Multidrug-resistant (MDR) bacteria, such as Klebsiella pneumonia (27.9%) and Acinetobacter baumannii (25.3%), were the most commonly isolated organisms. Ventilators and central venous catheters were independently associated with HAIs. Regarding the mortality rates, 55% of deaths occurred in intensive care units. Patients with HAIs (70.3%) were twice as likely to die compared to patients without HAIs (38.8%). HAIs leading to septic shock caused almost triple mortality (n = 58, 90.6%) compared with non-HAI patients (n = 412, 38.8%). HAIs prolonged hospital stay: 24.7 days for patients with HAIs and 19.1 days for patients without HAIs ( P < .001). Conclusions: Patients with COVID-19–related critical illnesses are at high risk of HAIs from multidrug-resistant (MDR) bacteria. HAIs prolong hospitalization, whereas HAIs with septic shock almost tripled mortality. Guidelines and procedures to prevent and control HAIs caused by MDR bacteria as well as training and monitoring on aseptic-compliant techniques during invasive clinical procedures are needed.

Tick-borne viral infections, including severe fever with thrombocytopenia syndrome virus (SFTSV), are increasingly recognized as a significant threat to global public health owing to their rapid dissemination and high mortality rates. While isolated outbreaks within single species have been documented, reports of multi-host cluster cases remain scarce. This study describes a consecutive, cross-species outbreak of severe fever with thrombocytopenia syndrome disease between April and May 2024 on a remote island in Nagasaki Prefecture that involved four cats and four humans. An interdisciplinary investigation integrating molecular phylogenetic analysis of viral genomes—including previously identified Nagasaki strains of SFTSV—and haplotype network analysis provided insights into the infection dynamics. Despite the absence of confirmed direct contact between cats and humans, four animals and one patient succumbed to the infection. Genomic analyses demonstrated high similarity to circulating Nagasaki strains, whereas haplotype analysis indicated multiple viral introduction events and complex transmission pathways, reflecting diverse sources. These findings underscore the critical need for a One Health approach—integrating human, animal, and vector surveillance—to effectively monitor, understand, and control tick-borne viruses globally, in both endemic and emerging regions.

Trained immunity refers to a phenomenon in which innate immune cells undergo long-lasting functional adaptation following an initial challenge. This paradigm shift in pulmonary immunology reveals that classical innate cells such as alveolar macrophages and hematopoietic progenitors, as well as structural cells including epithelial and endothelial populations, can acquire memory-like traits through sustained epigenetic and metabolic reprogramming. In the lung, these reprogrammed circuits influence host defense, lung injury, repair, and fibrotic remodeling through mechanisms involving histone H3K4 trimethylation, mTOR–HIF-1α-dependent metabolic shifts, and KLF4–MERTK-driven efferocytosis. Recent studies highlight the dual nature of this response: whereas appropriately tuned training accelerates pathogen clearance and supports epithelial repair, excessive or persistent activation can exacerbate maladaptive inflammation and fibrosis. In this Mini-Review, we summarize advances from 2020 to 2025 on the cellular and molecular regulation of pulmonary trained immunity, its emerging roles in acute respiratory distress syndrome (ARDS) and lung fibrosis, and novel therapeutic approaches that aim to modulate innate immune reprogramming for lung repair.

Fractional exhaled nitric oxide (FENO) is a biomarker of airway inflammation in asthma. The measurement of FENO is utilized to assist in the diagnosis and treatment of children with asthma, especially for those treated with inhaled corticosteroids. The aims of this study were to evaluate the correlations between FENO and atopic status, blood eosinophil levels, FCER2 mutation, and asthma control in Vietnamese children. This was a prospective and descriptive study approved by the local Ethical Board. All children with uncontrolled asthma, seen in the National Hospital of Pediatrics (Hanoi, Vietnam), were included. Exhaled breath FENO, blood eosinophils, skin prick test, total IgE, asthma control test (ACT), and FCER2 gene polymorphism were performed at inclusion. They were followed up at 3 months to evaluate clinical status, FENO levels, and ACT. Forty-two children with uncontrolled asthma with a mean age of 10±3 years (6-16 years) were included. The male/female ratio was 2.5/1. The mean FENO levels were 26±25 ppb. FENO was significantly higher in patients with a positive skin prick test for respiratory allergens ( <0.05). FENO was significantly correlated with blood eosinophil levels ( =0.5217; =0.0004). Five of the 32 subjects (15.6%) had a mutation of FCER2 gene (rs28364072 SNP). In this group, the levels of FENO were highest (37±10 ppb; <0.05). The levels of FENO were significantly decreased after 3 months of treatment (17±8 ppb vs 26±25 ppb; <0.05). Significant correlations between inhaled corticosteroid doses and FENO levels occurred at 1 and 3 months ( =0.415, =0.007; =0.396, =0.010; respectively). There were no correlations between FENO levels, ACT, and daily use of salbutamol. After 3 months, asthma remained uncontrolled in 22.2% of children. The measurement of FENO levels is a useful and feasible tool to predict clinical, biological, and asthma control in Vietnamese children.

Although osteoarthritis (OA) is regarded as a disease of the articular cartilage, recent research has demonstrated alterations in periarticular muscles that surround the affected joint. Here, we investigated changes in periarticular muscle during the progression of OA, as well as the cause-and-effect relationship between muscle weakness and OA, in a mouse model of OA by destabilization of the medial meniscus (DMM). Pathological phenotypes in the periarticular muscles were assessed in the early and late stages of OA by DMM. OA pathology and pain behavior in the mice after DMM induction were examined in response to periarticular muscle weakness induced by multiple rounds of barium chloride (BaCl 2 ) injections. The examinations were also performed in myostatin knockout mice with strengthened muscle phenotypes by muscle hypertrophy. Morphological alterations in the tibialis anterior (TA) and quadriceps muscles in DMM mice included variations in muscle-fiber size, aberrant extracellular matrix (ECM) deposition, inflammatory cell infiltration, and decreased muscle mass. Periarticular muscle fibers isolated from DMM mice showed reductions in the number of satellite cells and myogenic capacity of primary myoblast, as well as proliferation. DMM + muscle injury mice also showed exacerbated joint degeneration compared to the DMM vehicles. Myostatin knockout mice were characterized by attenuated OA and the complete abrogation of pain behavior after DMM. Our results suggest an association between muscle weakness and OA progression and pain.

Background Lower respiratory tract infection (LRTI) remains the leading infectious cause of morbidity and mortality globally. Key bacterial pathogens include Acinetobacter baumannii , Pseudomonas aeruginosa , Klebsiella pneumoniae , Escherichia coli , Staphylococcus aureus and Streptococcus pneumoniae . This study examined the prevalence and antimicrobial resistance patterns of major bacterial pathogens from community- and hospital-acquired LRTIs across six major hospitals in Vietnam. Methods Between January 2022 and May 2023, 1000 bacterial isolates were collected through an isolate-based surveillance. Species identification and antimicrobial susceptibility testing were performed by VITEK-2/Phoenix M50, with MICs determined by E-test or broth microdilution. Multiplex PCRs were used to detect common AMR genes. Results A. baumannii (49.6%), P. aeruginosa (21%), K. pneumoniae (18.6%) were predominant, followed by S. aureus (6.7 %) , E. coli (3.9%) and S. pneumoniae (0.2%). Most isolates (94.4%) were identified from hospital-acquired cases. High prevalence of MDR and carbapenem resistance were identified in A. baumannii (96% and 95%), P. aeruginosa (56.7% and 57.1%), and K. pneumoniae (78% and 69.2%), respectively. Notably, resistance to ceftazidime-avibactam was detected in K. pneumoniae (34.3%), P. aeruginosa (29%), and E. coli (7.7%), while colistin resistance was found in K. pneumoniae (18.2%) and A. baumannii (2.8%). MRSA prevalence was 79.1%, though S. aureus remained susceptible to vancomycin, linezolid and ceftaroline. Most bla NDM -positive K. pneumoniae (62/71, 87.3%), E. coli (2/2, 100%), and P. aeruginosa (23/25, 85.2%) showed resistance to ceftazidime-avibactam. Whole genome sequencing revealed that the bla NDM -positive but ceftazidime-avibactam susceptible isolates (9 K. pneumoniae and 2 P. aeruginosa ) carried truncated bla NDM . Overall, ceftazidime-avibactam was effective against K. pneumoniae , E. coli , and P. aeruginosa isolates carrying ESBL, ESBL and bla OXA−48 , or ESBL and bla KPC . Alternatively, no detectable AMR genes were found in 35 ceftazidime-avibactam resistant P. aeruginosa isolates. Conclusions Carbapenem-resistant Gram-negative pathogens were predominant among hospital-acquired LRTIs in Vietnam, with notable resistance to ceftazidime-avibactam and colistin. The lack of effective treatment for A. baumannii remains a major concern. We found a strong correlation between AMR phenotype and genotype among K. pneumoniae and E. coli , supporting gene-based therapy to guide ceftazidime-avibactam use. However, the presence of disrupted bla NDM underscores the need to re-evaluate commercial PCR assays for carbapenemase detection.

Osteoarthritis is a common chronic disease and major cause of disability and chronic pain in ageing populations. In this pathology, the entire joint is involved, and the regeneration of articular cartilage still remains one of the main challenges. Here, we investigated the molecular mechanisms underlying cartilage regeneration in young mice using a full-thickness cartilage injury (FTCI) model. FTCI-induced cartilage defects were created in the femoral trochlea of young and adult C57BL/6 mice. To identify key molecules and pathways involved in the early response to cartilage injury, we performed RNA sequencing (RNA-seq) analysis of cartilage RNA at 3 days after injury. Young mice showed superior cartilage regeneration compared to adult mice after cartilage injury. RNA-seq analysis revealed significant upregulation of genes associated with the immune response, particularly in the IFN-γ signaling pathway and qRT-PCR analysis showed macrophage polarization in the early phase of cartilage regeneration (3 days) in young mice after injury, which might promote the removal of damaged or necrotic cells and initiate cartilage regeneration in response to injury. IFN-γR1- and IFN-γ-deficient mice exhibited impaired cartilage regeneration following cartilage injury. DMM-induced and spontaneous OA phenotypes were exacerbated in IFN-γR1 −/− mice than in wild-type mice. Our data support the hypothesis that IFN-γ signaling is necessary for cartilage regeneration, as well as for the amelioration of post-traumatic and age-induced OA.

In the increasingly competitive context of non-public universities in Vietnam, effective human resource compensation policies are crucial for enhancing faculty engagement, with job satisfaction considered a key mediating mechanism. This study examines the relationships between multidimensional compensation, job satisfaction, and faculty commitment using survey data collected from 180 lecturers at Vietnamese private universities. Applying Partial Least Squares Structural Equation Modeling (PLS-SEM), we assessed the effects of five compensation components—salary, rewards, promotion opportunities, benefits, and organizational recognition—on job satisfaction and faculty commitment. Results indicate that the measurement model demonstrates strong reliability and validity. All five compensation components positively and significantly affect job satisfaction, with promotion opportunities exerting the strongest influence. Job satisfaction, in turn, substantially impacts faculty commitment, confirming its full mediating role in the relationship between compensation practices and organizational attachment. These findings offer important practical implications for private universities in Vietnam to design integrated compensation strategies that prioritize career development and recognition alongside financial incentives, thereby improving faculty retention and ensuring institutional sustainability.