Antagonistic effect of Pseudomonas aeruginosa on Candida auris

TL;DR

This study shows that Pseudomonas aeruginosa can inhibit the growth of Candida auris in laboratory conditions, possibly through secreted molecules affected by iron levels.

Contribution

The study reveals a previously unknown antagonistic interaction between Pseudomonas aeruginosa and Candida auris, mediated by secreted molecules modulated by iron.

Findings

Pseudomonas aeruginosa significantly inhibits Candida auris growth in co-culture experiments.

The inhibitory effect is fungistatic and persists for up to 72 hours.

Iron supplementation partially reverses the growth suppression of Candida auris.

Abstract

Candida (Candidozyma) auris and Pseudomonas aeruginosa are frequently found in hospital environments and on medical equipment, where they commonly colonize and infect hospitalized patients, contributing to healthcare-associated infections (HAIs). Although they share similar ecological niches and may interact, the mechanisms underlying their interspecies communication remain largely unknown.

This study investigated the in vitro interaction between planktonic cells of C. auris and P. aeruginosa through co-culture experiments in various growth media, with or without iron supplementation. Fluorescence microscopy was employed to assess yeast viability, and the effect of lyophilized, cell-free P. aeruginosa supernatants on C. auris was also evaluated.

P. aeruginosa significantly inhibited the growth of C. auris, regardless of the initial microbial concentrations. Growth suppression began after 8 hours of co-culture and persisted for up to 72 hours. Fluorescence microscopy suggested that this antagonistic effect was predominantly fungistatic, as most C. auris cells remained viable in the presence of the bacterium. The inhibitory effect was consistent across different culture media, and iron supplementation partially restored C. auris growth. Similarly, concentrated cell-free supernatants from P. aeruginosa inhibited C. auris, further supporting the role of secreted molecules. In this case as well, iron addition partially reversed the inhibitory effect.

These findings suggest that P. aeruginosa produces and secretes molecules with fungistatic activity against C. auris, and that this effect is at least partially modulated by iron availability. This discovery provides a foundation for future research into the identity and mechanisms of action of these secreted compounds, as well as the broader clinical implications of microbial interactions during co-colonization or co-infection.

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