Acinetobacter baumannii does not affect Candida albicans Susceptibility to Fluconazole in vitro

TL;DR

This study shows that Acinetobacter baumannii does not increase Candida albicans' sensitivity to fluconazole, unlike Pseudomonas aeruginosa.

Contribution

The novelty is showing that not all bacteria affect Candida drug resistance similarly, highlighting unique P. aeruginosa properties.

Findings

A. baumannii does not enhance fluconazole effectiveness against C. albicans in vitro.

P. aeruginosa produces unique molecules that influence C. albicans drug susceptibility.

Microbe-microbe interactions affect fungal pathogen virulence and antimicrobial susceptibility.

Abstract

Candida albicans
is the most common human fungal pathogen and is difficult to treat due to the scarcity of and increasing resistance to fungicidal drugs.
C. albicans
is commonly isolated with bacterial pathogens such as
Pseudomonas aeruginosa
and
Acinetobacter baumannii
that also cause multidrug-resistant hospital-acquired infections. We have recently described how the presence of
P. aeruginosa
makes the antifungal drug fluconazole (FLC) more effective and switches it from fungistatic to fungicidal against
C. albicans
, a process sensitive to iron chelation. Although different
P. aeruginosa
isolates enhance fluconazole sensitivity, it is unknown if other bacterial species have a similar effect.
A. baumannii
is similar to
P. aeruginosa
: it is gram-negative, drug resistant, produces siderophores and causes intractable nosocomial infections. In this study, we investigated if
A. baumannii
has a similar bacterial-drug synergy against
C. albicans
. We found that
A. baumannii
shows little to no enhancement of FLC against
C. albicans in vitro.
Our work indicates that not all opportunistic bacterial pathogens have the same effect on
Candida
drug susceptibility as
P. aeruginosa
. It further suggests that
P. aeruginosa
produces unique molecules that drive its interactions with
C. albicans
and contribute to the clearance of
C. albicans
in the presence of FLC. This work addresses the need to understand how microbe-microbe interactions regulate virulence and antimicrobial susceptibility of fungal pathogens, a still poorly understood aspect of infection and colonization.

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