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.