Staphylococcal biofilm disassembly

Abstract

Staphylococcus aureus and Staphylococcus epidermidis are a frequent cause of biofilm-associated infections that are a tremendous burden on our healthcare system. Staphylococcal biofilms exhibit extraordinary resistance to antimicrobial killing, limiting the efficacy of antibiotic therapy, and surgical intervention is often required to remove infected tissues or implanted devices. Recent work has provided new insight into the molecular basis of biofilm development in these opportunistic pathogens. Extracellular bacterial products, environmental conditions, and polymicrobial interactions have all been shown to influence profoundly the ability of these bacteria to colonize and disperse from clinically relevant surfaces. We review new developments in staphylococcal biofilm disassembly and set them in the context of potential strategies to control biofilm infections.

Figure 1

Images of S. aureus biofilms on host surfaces. S. aureus cells (gold colored) attaching to and forming a biofilm on a heart valve (left) and an endotracheal tube (right).

Figure 2

Model of known Staphylococcal biofilm disassembly mechanisms. See text and Table 1 for details.

Figure 3

Susceptibility of S. aureus biofilms to proteinase K and bovine DNaseI. Flow cell biofilms formed by a methicillin-resistant S. aureus (MRSA) isolate expressing GFP were treated with either proteinase K or bovine DNaseI and imaged at 6 and 22 hr post treatment. GFP-expressing biofilms were visualized with confocal laser scanning microscopy (CLSM) and each side of a grid square in the images represents 20 μM. This figure was adapted from a previous publication [11].

Figure 4

AIP-mediated biofilm disassembly. Dual-labeled biofilms (P_sarA-RFP, P_agrP3-GFP) were grown for 2 days, and autoinducing peptide (AIP-I, 50 nM final) was added to the growth media. Biofilm integrity and RFP and GFP fluorescence were monitored with confocal laser scanning microscopy (CLSM) at Day 3 and 4. For the image reconstructions shown, AIP-I was added exogenously to either an agr type I wild type strain (A) or an agr deficient strain (B). The addition of AIP-I induces the agr system and dissembles the biofilm only in the wild type strain. Greenish yellow color indicates expression of the agr P₃-GFP reporter and each side of a grid square in the images represents 20 μM. This figure was adapted from a previous publication [10].