Authors ’ response

In a recent issue of Critical Care, Giglio and colleagues [1] reported that oral nystatin reduced Candida colonization in a cohort of critically ill surgical patients, even when colonization was present at baseline. Coloni zation is a prerequisite for systemic infection, which is associated with significant morbidity and mortality. Although it is possible to stratify individuals at risk of invasive fungal disease, diagnosing this condition is complex, and the present study [1] represents a potential mechanism for reducing the burden of fungal infection. Candida albicans has a complicated relation ship with potential bacterial respiratory pathogens and augments their growth in mixed biofilms [2,3]. Pseudomonas aeru ginosa is unable to bind yeast forms of C. albicans but forms a dense biofilm on C. albicans filaments [3]. This is relevant to clinical investigations in which respiratory tract coloni zation with C. albicans is associated with an increased risk of Pseudomonas ventilatorassociated pneu monia (VAP) [4], which is reduced with antifungal treatment [5]. The impact of nystatin on other infections, such as VAP caused by Pseudomonas or Staphylococcus, or indeed on other indices, such as length of stay and mortality, was not measured [1]. One might anticipate that the benefit of nystatin treatment will extend beyond infec tions caused directly by Candida, but there is an impor tant caveat. Nystatin generally is used as a sus pen sion with high sucrose content (49.8 % wt/vol), and growth of oral plaque is driven by sugars. Dental plaque becomes colonized with potential respiratory pathogens in critically ill patients and is important in the etiology of VAP. Future studies, therefore, should investigate the impact of nystatin on the oral microbiome, VAP, and mortality