Abstract
Staphylococcus aureus frequently causes community- and hospital-acquired infections. S. aureus attachment followed by biofilm formation on tissues and medical devices plays a significant role in the establishment of chronic infections. Staphylococcal biofilms encase bacteria in a matrix and protect the cells from antimicrobials and the immune system, resulting in infections that are highly resistant to treatment. The biology of biofilms is complex and varies between organisms. In this review, we focus our discussion on S. aureus biofilms and describe the stages of their formation. We particularly emphasize genetic and biochemical processes that may be vulnerable to novel treatment approaches. Against this background, we discuss treatment strategies that have been successful in animal models of S. aureus biofilm-related infection and consider their possible use for the prevention and eradication of biofilm-related S. aureus prosthetic joint infection.
Highlights
20% and 60% of healthy adults are persistent and intermittent S. aureus nasal carriers, respectively [1]
Biofilms represent a mode of bacterial growth that acts as a multi-cellular structure, where each bacterial cell works in coordination to keep the structure alive and safe from adverse conditions [6]
S. aureus expresses up to 24 different cell-wall-anchored proteins, including MSCRAMMs (FnBPs, ClfB, and SdrC proteins) and other proteins, such as SasG, biofilm-associated protein (Bap), and SasC (Table 1) [13]. These intrinsic matrix molecules attach to the S. aureus cell wall after being cleaved by the membrane-associated protein Sortase A [14], and they interact with host matrix components, such as cytokeratin, fibronectin, collagen, and fibrinogen [15]
Summary
20% and 60% of healthy adults are persistent and intermittent S. aureus nasal carriers, respectively [1]. S. aureus carriers are at higher risk of endogenous infection. Sessile forms of bacteria are metabolically less active than planktonic forms and are protected by a filmy layer of “slime” referred to as the extra-polymeric substance (EPS) [4]. These properties of sessile forms of bacteria, when they form biofilms, make them recalcitrant to antibiotic treatment [4,5]. Free-floating planktonic cells attach to surfaces and multiply to form micro-colonies. During maturation, these micro-colonies produce an extracellular matrix and form solid three-dimensional biofilm structures. After full maturation of the biofilm, the extracellular matrix degrades and releases part of the bacteria to establish a new biofilm at another location (Figure 1)
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