BackgroundCanine otitis externa provides a chronic, inflamed and frequently antimicrobial-exposed niche in which Pseudomonas aeruginosa can persist through a coordinated repertoire of adhesion, biofilm, iron-acquisition, secretion and toxin systems.MethodsWe characterized the virulence-associated genomic architecture of a historical Hungarian collection obtained from canine otitis cases in 2010 and 2017. Of the 70 isolate identifiers in the nominal range 70–139, 60 had corresponding long-read assemblies and linked VFDB screening records. One assembly was excluded after genome-based taxonomic validation showed that it did not meet the species-level criterion for P. aeruginosa.ResultsPrimary absence-sensitive analyses were restricted to 52 genome-confirmed P. aeruginosa assemblies meeting prespecified CheckM criteria (completeness ≥95%, contamination ≤5%), while seven additional genome-confirmed P. aeruginosa assemblies that did not meet the primary CheckM criteria were retained only for descriptive contextualization and were excluded from prevalence denominators and absence-sensitive analyses. The primary cohort contained 242 distinct virulence-associated genes, with a median of 230.5 genes per isolate. Of these, 217 (89.7%) were core-like, occurring in at least 95% of genomes. Alginate, type IV pilus, flagellar, siderophore, phenazine, quorum-sensing, type II, type III and type VI secretion backbones were broadly conserved. In contrast, type III effector content was heterogeneous: exoT occurred in 52/52 isolates, exoY in 50/52, exoS in 49/52 and exoU in 4/52; one isolate showed assembly-level co-detection of exoS and an exoU-homologous sequence. Whole-virulome composition did not differ detectably between 2010 and 2017 (square-root Jaccard PERMANOVA, R2 = 0.0134, p = 0.6083), and no individual gene remained associated with collection year after false-discovery-rate correction.ConclusionThese data define a conserved historical virulence-associated genomic backbone punctuated by isolate-level effector and surface-structure variation. The detected genes are interpreted as genomic homologues and repertoire features rather than as evidence of their expression or functional contribution to pathogenicity.