Otitis media is among the most common pediatric illnesses globally, constituting a leading cause of antimicrobial prescriptions, recurrent medical consultations, and preventable hearing loss in early childhood. Traditionally regarded as a sterile cavity intermittently invaded by pathogens, the middle ear is now recognized as a dynamic ecological niche influenced by anatomical immaturity of the Eustachian tube, host immune development, and the composition of resident microbial communities. Increasing evidence demonstrates that microbial dysbiosis and the establishment of biofilms are central to the persistence and recurrence of disease. This review synthesizes current knowledge of the pediatric middle ear microbiome, highlighting how commensal organisms contribute to mucosal resilience and colonization resistance, whereas pathogenic bacteria exploit ecological disruption to establish biofilm communities. Biofilm formation provides bacteria with enhanced survival through immune evasion, altered microenvironments, and antibiotic tolerance, thereby transforming acute otitis media into recurrent or chronic states. Furthermore, studies demonstrate how adenoids act as reservoirs of biofilm-forming organisms, seeding the middle ear and perpetuating infection. The emerging ecological perspective emphasizes the limitations of conventional antibiotic-centered management and directs attention toward innovative strategies, including microbiome-preserving interventions, probiotic or live biotherapeutic approaches, and antibiofilm agents. By defining pediatric otitis media as a disorder of disrupted host–microbe equilibrium, future research may pave the way for precision-based preventive and therapeutic strategies aimed at reducing the global burden of this pervasive disease.

Serratia spp., particularly Serratia marcescens, have emerged as clinically important opportunistic pathogens and are increasingly recognized as causes of healthcare-associated infections, especially among critically ill and immunocompromised patients. Their remarkable ecological adaptability, persistence in hospital environments, and capacity to acquire multiple antimicrobial resistance determinants have contributed to the global emergence of multidrug-resistant strains and complicated therapeutic management. This review aims to comprehensively analyze the epidemiology, virulence mechanisms, antimicrobial resistance patterns, and current and emerging therapeutic strategies associated with Serratia spp. The manuscript is based on a critical review and analysis of previously published literature retrieved from electronic scientific databases focusing on clinically relevant Serratia spp. infections and resistance trends. The reviewed literature demonstrates that Serratia spp. combine intrinsic resistance mechanisms, particularly inducible chromosomal AmpC β-lactamases, with acquired resistance determinants including extended-spectrum β-lactamases, carbapenemases, aminoglycoside-modifying enzymes, and plasmid-mediated quinolone resistance. Horizontal gene transfer and biofilm formation further enhance bacterial persistence, dissemination, and adaptation within healthcare settings. Clinically, these pathogens are associated with device-related infections, bloodstream infections, pneumonia, urinary tract infections, and hospital outbreaks, where increasing multidrug and carbapenem resistance significantly limits therapeutic options. Novel β-lactam/β-lactamase inhibitor combinations and cefiderocol represent promising therapeutic approaches, although treatment success remains highly dependent on accurate identification of underlying resistance mechanisms. This review highlights the growing public health importance of Serratia spp. and underscores the need for improved surveillance, molecular diagnostics, antimicrobial stewardship, and the development of innovative therapeutic strategies in the context of the evolving antimicrobial resistance crisis.

Background/Objectives: Long-term data on the molecular epidemiology of methicillin-resistant Staphylococcus aureus (MRSA) from the Western Balkans remain limited. This study investigated temporal changes in the molecular population structure and antimicrobial resistance of MRSA in Serbia over more than four decades. Methods: A total of 395 non-duplicate MRSA isolates from four temporally distinct collections (1975–1985, 1997–2003, 2009–2010, and 2018–2019) were analyzed. Isolates were characterized by antimicrobial susceptibility testing, spa typing, SCCmec typing, and detection of Panton–Valentine leukocidin (PVL) genes. Clonal complexes and putative MLST associations were inferred from spa repeat patterns and previously established molecular epidemiological associations rather than determined by direct MLST or whole-genome sequencing. Results: Marked differences in the molecular composition of MRSA were observed across the four collection periods. The 1975–1985 collection was dominated by isolates assigned to CC8-MRSA-I and ST239-related CC8-MRSA-III backgrounds. By 1997–2003, the early CC8-MRSA-I background was no longer prominent, while ST239-related CC8-MRSA-III and South German-related CC5-MRSA-I predominated. In 2009–2010, CC5-MRSA-I was the most frequently identified background, while ST239-related MRSA remained represented, and SCCmec IV/V-associated backgrounds were increasingly detected. By 2018–2019, greater molecular heterogeneity was observed, including a higher representation of CC45-MRSA-IV, changes in the distribution of CC5 backgrounds compared with the previously dominant CC5-t041-SCCmec I profile, continued detection of ST239-related CC8-MRSA-III, and an increased representation of ST152/CC152-associated isolates. PVL-positive isolates were absent from the first two collections, detected in 2009–2010 (4.0%), and more frequent in 2018–2019 (17.0%), predominantly within ST152/CC152- and CC1-associated backgrounds. Ciprofloxacin resistance increased from 0% in 1975–1985 to 84.0% in 2018–2019, while aminoglycoside resistance also increased markedly. Resistance to erythromycin and clindamycin remained consistently high, whereas no resistance to vancomycin, teicoplanin, or linezolid was detected among the investigated isolates. Conclusions: Over four decades, the investigated MRSA collections from Serbia showed substantial changes in molecular population structure, including the repeated detection of ST239-related MRSA, shifts in the predominant hospital-associated backgrounds, and greater molecular diversity in the later collections, with increased representation of SCCmec IV/V-associated and PVL-positive isolates. Historical population movements and healthcare connections within the former Yugoslavia may have contributed to the circulation of internationally recognized MRSA lineages in Serbia, although their role could not be directly established. Although the sampling design and typing resolution do not permit definitive conclusions regarding continuous clonal persistence or direct lineage replacement, these findings provide a valuable long-term perspective on MRSA molecular epidemiology in Southeastern Europe and highlight the importance of historical strain collections for investigating changes in antimicrobial-resistant bacterial populations.