Current and Emergent Control Strategies for Medical Biofilms - Antibiofilm Agents: From Diagnosis to Treatment and Prevention - page 130

several microorganisms involved in biofilm formation (Kudva et al. 1999 ). The
ability of these phages to inhibit and/or eradicate biofilms has been demonstrated
for biofilms of several pathogens including P. aeruginosa, K. pneumonia, E. coli,
Proteus mirabilis, and S. epidermidis , and these studies are summarized here
briefly.
Biofilms of E. coli strains 3000 XIII developed on the surfaces of
polyvinylchloride coupons in a modified Robbins device were infected and lysed
using bacteriophage T4D. Similar studies with phage E79 infecting P. aeruginosa
indicated that phages were infecting the surface organisms but access to the cells
deep in the biofilm was restricted (Doolittle et al. 1995 ). Investigators have dem-
onstrated the use of bacteriophages in killing S. aureus and P. fluorescens biofilms;
however, the infection of biofilm cells by phages is extremely conditional on their
chemical composition and environmental factors such as temperature, growth
stage, media, and phage concentration (Sillankorva et al. 2004 ; Chaignon
et al. 2007 ).
The crucial role of titers of specifically selected phages with a proper virion-
associated exopolysaccharide (EPS) depolymerase in the development of phage
therapy were shown by Cornelissen et al. ( 2011 ). They carried out an experiment to
investigate the in vitro degradation of single-species Pseudomonas putida biofilms,
PpG1 and RD5PR2, by the novel phage Q15, a “T7-like virus” EPS depolymerase.
Phage Q15 formed plaques surrounded by growing opaque halo zones, on seven out
of 53 P. putida strains. This has happened because of EPS degradation. Since halos
were absent on infection-resistant strains, they suggested that the EPS probably acts
as a primary bacterial receptor for phage infection. EPS degrading activity of
recombinantly expressed viral tail spike was also confirmed by capsule staining.
Application of bacteriophages in controlling mixed biofilms of Pseudomonas
fluorescens and Staphylococcus lentus has also been reported. Sillankorva
et al. ( 2010 ) challenged the biofilms with phage phiIBB-PF7A, specific for
P. fluorescens , and the results obtained showed that phiIBB-PF7A readily reached
the target host and caused a significant population decrease. This phage was also
capable of causing partial damage to the biofilms leading to the release of the
non-susceptible host ( S. lentus ) from the dual species biofilms.
Phage therapy has been successfully employed in the treatment of lung infec-
tions of cystic fibrosis caused by colonization of S. aureus and further predominant
growth of P. aeruginosa biofilms. The treatment is very difficult with antibiotics
due to several fold increased drug resistance (Brussow 2012 ). Applications of
bacteriophages NH-4 eliminated P. aeruginosa in the murine

lung and cystic fibrosis lung airway cells (Alemayehu et al. 2012 ).
Recently, potential of the bacteriophage-derived peptidase, CHAP K , for the
rapid disruption of biofilm was reported against staphylococci, associated with
the bovine mastitis (Fenton et al. 2013 ). Purified CHAP K was able to prevent
biofilm formation and also completely eliminated biofilms of S. aureus DPC5246
within 4 h. The CHAP K lysin also reduced S. aureus in a skin decolonization model.
Furthermore, Shen et al. ( 2013 ) found rapid degradation of S. pyogenes biofilms by
PlyC, a bacteriophage-encoded endolysin. Laser scanning confocal microscopy

ˆ MR299-2 and ˆ