Background: The adenoid surface serves as a potential bacterial reservoir for upper respiratory tract pathologies, including Adenoid Hypertrophy (AH) and Otitis Media with Effusion (OME). While dysbiosis is implicated in the pathogenesis of these conditions, it remains unclear whether the microbiome of children with otitis media differs significantly from those with simple hypertrophy when compared against a healthy baseline. This study aimed to characterize the adenoid microbiome in children with adenoid hypertrophy with and without middle ear effusion, contrasting them with a healthy control group. Methods: We conducted a cross-sectional case–control study involving 58 pediatric participants divided into three groups: adenoid hypertrophy, adenoid hypertrophy and otitis media with effusion and healthy controls. Nasopharyngeal swabs were collected, and bacterial community composition was analyzed using 16S rRNA gene V4 sequencing. Alpha and beta diversity metrics, taxonomic composition, and differential abundance were evaluated. Results: Alpha diversity was significantly reduced in both disease groups compared to healthy controls (p < 0.001), indicating a collapse of microbial richness and evenness. Beta diversity analysis revealed a distinct separation between healthy and diseased cohorts; however, the microbial profiles of the AH and AH with OME groups were nearly identical. Taxonomic analysis demonstrated that disease was characterized by the depletion of health-associated commensals, specifically Veillonella, Actinomyces, and Gemella, and a concomitant expansion of Fusobacterium, Haemophilus, and Streptococcus. Conclusions: Adenoid hypertrophy is associated with a profound dysbiotic shift characterized by the loss of protective commensal flora and the dominance of pathobionts. The lack of significant microbial differentiation between the AH and AH with OME groups suggests that the adenoid surface acts as a centralized reservoir of dysbiosis, the composition of which is conserved regardless of the presence of middle ear effusion. These findings highlight the importance of restoring the commensal microbiome in the management of chronic adenoid disease.

Background: Chronic adenoidal disease and otitis media with effusion are prevalent pediatric conditions frequently associated with localized microbial dysbiosis. This study aimed to characterize the adenoid surface microbiome in children with isolated adenoid hypertrophy (AH) and AH with concurrent middle ear effusion, comparing them against a healthy pediatric nasopharyngeal baseline to elucidate the specific ecological shifts driving these interrelated pathologies. Methods: High-throughput 16S rRNA gene sequencing was performed on clinical samples from three distinct pediatric cohorts: isolated AH, AH with OME, and healthy controls. Microbial community architecture was evaluated using comprehensive alpha- and beta-diversity metrics. Taxonomic shifts and biomarker discovery were determined utilizing robust ANCOM-BC2, DESeq2, and LEfSe methodologies. Results: Alpha-diversity analyses revealed a profound, statistically significant reduction in microbial richness and community evenness across both disease cohorts compared to healthy controls (Observed ASVs p < 0.001; Shannon p < 0.001). Beta-diversity metrics demonstrated distinct, significant structural clustering (p < 0.001) that cleanly separated healthy microbiomes from diseased microbiomes. Differential abundance analyses confirmed this ecological collapse was driven by the severe depletion of health-associated commensals (including Streptococcus, Veillonella, Corynebacterium, and Rothia) and a uniform overgrowth of opportunistic pathogens, most notably Haemophilus, Moraxella, and Fusobacterium. Crucially, stringent ANCOM-BC2 comparative modeling between the isolated AH and AH with OME cohorts revealed highly homologous microbial architectures with no significant differential taxa. Conclusions: Pediatric adenoid hypertrophy is characterized by a profound collapse of the nasopharyngeal microbiome, marked by the depletion of commensals and an overgrowth of opportunistic pathogens such as Haemophilus, Moraxella, and Fusobacterium. Notably, the microbial architectures of isolated adenoid hypertrophy and adenoid hypertrophy with concurrent otitis media with effusion are highly homologous, lacking robust compositional differences.