Two patients with severe eosinophilic asthma on anti-IL-5 biologics (mepolizumab and benralizumab) who developed unexpected hypereosinophilia during *Pseudomonas aeruginosa* airway infection, evaluated to explore whether bacterial infection can drive eosinophil rebound independent of IL-5 pathway blockade.
Both patients showed marked eosinophil rebound (1,400 and 1,690 cells/μL, respectively) coinciding with *P. aeruginosa* infection, which resolved after targeted antipseudomonal antibiotic therapy — suggesting IL-5-independent mechanisms of eosinophil elevation.
Case series of only 2 patients limits generalizability; causal mechanism linking *P. aeruginosa* to IL-5-independent eosinophilia is proposed but not experimentally confirmed; full text not available to assess additional confounders.
In patients on anti-IL-5 or IL-5R biologics who develop breakthrough hypereosinophilia during an exacerbation, send sputum cultures to rule out *P. aeruginosa* infection before assuming biologic failure. Antipseudomonal treatment may resolve eosinophilia without changing the biologic regimen.
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