Abstract
Pseudomonas aeruginosa is one of the most frequent causative microorganisms of ventilator-acquired pneumonia (VAP). Tracheobronchial colonization (TBC) by Candida species is frequent ventilated patients. Clinical studies have found evidence of interactions between Candida and Pseudomonas, with Candida colonization possibly increasing the risk for Pseudomonas VAP. Very few animal studies have been performed stating either an indifferent or a facilitating role of previous C. albicans TBC on the development of murine P. aeruginosa pneumonia. In vitro, P. aeruginosa forms a biofilm on C. albicans filaments and ultimately kills them. In contrast, P. aeruginosa neither binds to nor kills yeast-forms C. albicans. In the presence of P. aeruginosa, C. albicans grows essentially as a yeast-form to avoid P. aeruginosa-dependant killing. This strategy of resistance operates through the detection of P. aeruginosa quorumsensing (QS) molecule 3OC12-HSL. Moreover, C. albicans produces farnesol, a cell-cell signaling molecule that induces decreased production of the QS molecule, Pseudomonas quinolone (PQS) signal and the virulence factor pyocyanin in addition to inhibit P. aeruginosa swarming mobility. By reviewing the advances made in the understanding of context-specific interactions of C. albicans and P. aeruginosa, we get an understanding on how these microorganisms mutually influence their lifestyle in the respiratory tract of critically ill patients.
Keywords: Pseudomonas aeruginosa, Candida albicans, ventilator-associated pneumonia, biofilm, farnesol
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