Rapid degradation of Streptococcus pyogenes biofilms by PlyC, a bacteriophage-encoded endolysin.

Printer-friendly versionPrinter-friendly versionPDF versionPDF version
TitleRapid degradation of Streptococcus pyogenes biofilms by PlyC, a bacteriophage-encoded endolysin.
Publication TypeJournal Article
Year of Publication2013
AuthorsShen, Y, Köller, T, Kreikemeyer, B, Nelson, DC
JournalJ Antimicrob Chemother
Date Published2013 Aug

OBJECTIVES: Streptococcus pyogenes, or Group A streptococcus (GAS), has a propensity to colonize human tissues and form biofilms. Significantly, these biofilms are a contributing mechanism of antibiotic treatment failure in streptococcal disease. In this study, we evaluate a streptococcal-specific bacteriophage-encoded endolysin (PlyC), which is known to lyse planktonic streptococci, on both static and dynamic streptococcal biofilms.

METHODS: PlyC was benchmarked against antibiotics for MIC, MBC and minimum biofilm eradication concentration (MBEC). A biomass eradication assay based on crystal violet staining of the biofilm matrix was also used to quantify the anti-biofilm properties of PlyC. Finally, conventional fluorescence microscopy and laser scanning confocal microscopy were used to study the effects of PlyC on static and dynamic biofilms of GAS.

RESULTS: PlyC and antibiotics had similar MIC (range 0.02-0.08 mg/L) and MBC (range 0.02-1.25 mg/L) values on planktonic GAS. However, when GAS grew in biofilms, the MBEC values for antibiotics rose to clinically resistant values (≥400 mg/L) whereas PlyC had MBEC values two orders of magnitude lower by mass and four orders of magnitude lower by molarity than the conventional antibiotics. Laser scanning confocal microscopy revealed that PlyC destroys the biofilm as it diffuses through the matrix in a time-dependent fashion.

CONCLUSIONS: Our findings indicate that while streptococcal cells within a biofilm rapidly become refractory to traditional antibiotics, the biofilm matrix is readily destroyed by the lytic actions of PlyC.

Alternate JournalJ. Antimicrob. Chemother.
PubMed ID23557924