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Microbiology. 2017 Nov;163(11):1568-1577. doi: 10.1099/mic.0.000539. Epub 2017 Oct 6.

Pseudomonas phage inhibition of Candida albicans.

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2​Division of Infectious Diseases, Department of Medicine, Stanford University Medical School, Stanford, CA, USA.
1​California Institute for Medical Research, San Jose, CA, USA.
3​Cell Sciences Imaging Facility, Stanford University Medical School, Stanford, CA, USA.
4​Division of Biological Sciences, University of Montana, Missoula, MT, USA.
5​Immunology Program, Stanford University, Stanford, CA, USA.
6​Department of Chemistry, Stanford University, Stanford, CA, USA.


Pseudomonas aeruginosa (Pa) and Candida albicans (Ca) are major bacterial and fungal pathogens in immunocompromised hosts, and notably in the airways of cystic fibrosis patients. The bacteriophages of Pa physically alter biofilms, and were recently shown to inhibit the biofilms of Aspergillus fumigatus. To understand the range of this viral-fungal interaction, we studied Pa phages Pf4 and Pf1, and their interactions with Ca biofilm formation and preformed Ca biofilm. Both forms of Ca biofilm development, as well as planktonic Ca growth, were inhibited by either phage. The inhibition of biofilm was reversed by the addition of iron, suggesting that the mechanism of phage action on Ca involves denial of iron. Birefringence studies on added phage showed an ordered structure of binding to Ca. Electron microscopic observations indicated phage aggregation in the biofilm extracellular matrix. Bacteriophage-fungal interactions may be a general feature with several pathogens in the fungal kingdom.


Candida albicans; Pseudomonas aeruginosa; bacteriophage; biofilm; iron

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