DOI: 10.1093/ajrccm/aamag286.101 ISSN: 1073-449X

B33-20 Blood Eosinophil Counts Are Associated With Airway Mold Growth and Pseudomonas Enrichment in Bronchiectasis

A Al-Itelat, S Chalmers, T R Aksamit, P Escalante, A N Kanj

Abstract

Rationale

Blood eosinophil count (BEC) has emerged as a marker of inflammatory endotypes in bronchiectasis. We examined whether bacterial and mold respiratory culture profiles differ by BEC, comparing patients with BEC ≥300 cells/μL to those with lower BEC.

Methods

We analyzed patients with bronchiectasis evaluated at a specialized clinic (2019-2025) who had contemporaneous respiratory bacterial and fungal cultures and BEC. Patients were stratified by BEC <300 vs ≥ 300 cells/μL; those with BEC <300 were further subclassified (<100 and 100-299 cells/μL) for figure presentation only. Cultures were evaluated for overall growth and organism-specific prevalence across eosinophil strata, focusing on the most frequently isolated organisms. Group comparisons were performed using Fisher’s exact test.

Results

A total of 608 patients met inclusion criteria (median age 69 years [IQR 61-77], 72% female); 138 (22.7%) had BEC ≥300 cells/μL. Bacterial growth occurred in 277 patients (45.6%) and mold growth in 366 (60.2%). The odds of bacterial growth were similar between BEC ≥300 and <300 groups (47.1% vs 45.2%). In contrast, BEC ≥300 was associated with higher odds of mold growth (68.1% vs 58.0%; OR 1.54, p = 0.038). Pseudomonas species (18.9%) were the most common bacterial isolates and comprised a greater proportion of all bacterial isolates in patients with BEC ≥300 compared with lower BEC (44.7% vs 30.0%; OR 1.89, p = 0.019). Penicillium species (27.5%), followed by Aspergillus (26.9%), were the most frequently isolated molds, with no differences in distribution across BEC strata.

Conclusions

BEC ≥300 cells/μL was associated with increased odds of respiratory mold growth and enrichment of Pseudomonas species, suggesting that eosinophil-defined endotypes may identify patients with distinct airway microbiologic patterns that could inform future phenotyping and treatment strategies.

This abstract is funded by: None

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