Enterococci cause infections with various localizations, the most common being urinary infections. The purpose of the study was to identify the profile of the antimicrobial resistance of enterococci species (AMRE) isolated from patients hospitalized in three hospitals in Romania. We evaluated AMRE retrospectively (2019–2021) in various biological samples. The microbiological diagnosis was sustained by classical methods of bacteria culture and automatic identification. The sensitivity testing was performed by the Kirby–Bauer method, and the antibiotic minimum inhibitory concentration was tested by the automated Vitek system. We analyzed 86 strains of Enterococcus spp., identifying the following species: 47.7% E. faecalis, 47.7% E. faecium, 3.55% E. gallinarum, and 1% E. hirae. Most of the bacterial strains were isolated from urocultures (38.4%) and hemocultures (32.6%). Overall, the rate of vancomycin resistance was 5.8% for E. faecalis and 15.1%. for E. faecium. The prevalence of multidrug-resistant (MDR) strains was found to be 100% in E. gallinarum, 75.6% in E. faecium, and 21.9% in E. faecalis. The results confirm the high level of AMRE, which creates difficulties with adequate antibiotic prescriptions. The continuous monitoring of AMRE is essential for updating the local diagnostic and treatment protocols for enterococcal infections.

Staphylococcus aureus (MRSA) and vancomycin-resistant enterococci (VRE) are high-burden healthcare-associated pathogens that increase mortality, prolong hospitalisation, and drive substantial healthcare costs worldwide. These infections are associated with high morbidity, increased mortality, prolonged hospital stays, and significant costs, particularly among immunocompromised patients or those with extended hospitalizations. This systematic review was conducted and reported in accordance with PRISMA 2020, aiming to synthesise existing data on the epidemiology, resistance mechanisms, clinical manifestations, and strategies for the diagnosis, treatment, and prevention of MRSA and VRE infections. Data were qualitatively synthesised. A total of 113 records published between 2020 and 2025 met the inclusion criteria and were identified through searches in multiple bibliographic databases and publisher platforms (e.g., PubMed, Scopus, Web of Science). MRSA and VRE are implicated in numerous severe infections, including ventilator-associated pneumonia, catheter-associated urinary tract infections, endocarditis, and bacteraemia. Antimicrobial resistance is driven by the mecA, vanA, and vanB genes, while biofilm formation further complicates therapeutic efforts. Biofilm formation can promote antibiotic tolerance (slower killing without an increase in MIC) and persistence (survival of ‘persister’ cells), distinct from genetic resistance, and may complicate therapy in selected infections. Effective strategies include appropriate anti-MRSA/anti-VRE agents (e.g., ceftaroline for MRSA; linezolid or daptomycin for VRE), active screening, stringent infection prevention and control measures, and antimicrobial stewardship programmes. Implementation is often hindered by institutional barriers, limited resources, and insufficient staff training. A multidisciplinary, evidence-based approach is essential for the effective management of these infections. Reducing this burden requires coordinated implementation of rapid diagnostics, stringent infection prevention and control, and antimicrobial stewardship, supported by sustained institutional and public health investment.

Mycoplasma pneumoniae (MP) is a frequent cause of pediatric pneumonia, but the clinical relevance of respiratory coinfections remains incompletely defined. We conducted a retrospective cohort study of 192 hospitalized children with multiplex RT-PCR-confirmed MP infection between April 2023 and November 2025. Patients were classified as MP monoinfection (123/192, 64.1%), MP with viral coinfection (34/192, 17.7%), or MP with bacterial/mixed coinfection (35/192, 18.2%) and children with coinfection were younger than those with MP infection alone, with median ages of 6.5 years (IQR 1–11) in the viral coinfection group and 5 years (IQR 1–7) in the bacterial/mixed coinfection group, compared with 11 years (IQR 7–14) in children with MP alone (p < 0.001). Respiratory failure occurred in 36% of children with MP infection alone, 65% of those with viral coinfection, and 31% of those with bacterial/mixed coinfection. In adjusted logistic regression, viral coinfection was independently associated with higher odds of respiratory failure relative to MP infection alone (aOR 3.37, 95% CI 1.49–7.94; p = 0.004), whereas bacterial/mixed coinfection was not (aOR 0.85, 95% CI 0.35–2.03; p = 0.725). In multinomial regression, increasing age was inversely associated with both viral coinfection (RRR 0.86, 95% CI 0.79–0.94; p < 0.001) and bacterial/mixed coinfection (RRR 0.79, 95% CI 0.72–0.87; p < 0.001). In negative binomial regression, evidence for longer hospitalization in the viral coinfection group was weaker and imprecise (IRR 1.16, 95% CI 0.99–1.37; p = 0.069). Fibrinogen differed across etiologic groups, with the lowest values in bacterial/mixed coinfection (p = 0.004). In this hospitalized pediatric cohort, MP coinfection was more frequent in younger children, and viral co-detection showed the clearest association with respiratory failure. These findings should be interpreted in the context of the retrospective design, modest subgroup sizes, and the limitations of upper-airway multiplex PCR co-detection.