Abstract

BackgroundMicrobial biofilms have been associated with the development of chronic human infections and represent a clinical challenge given their increased antimicrobial tolerance. Staphylococcus aureus is a major human pathogen causing a diverse range of diseases, of which biofilms are often involved. Staphylococcal attachment and the formation of biofilms have been shown to be facilitated by host factors that accumulate on surfaces. To better understand how host factors enhance staphylococcal biofilm formation, we evaluated the effect of whole human plasma on biofilm formation in clinical isolates of S. aureus and the expression of seven microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) known to be involved in biofilm formation by quantitative real-time PCR. We also evaluated whether plasma augmented changes in S. aureus biofilm morphology and antimicrobial resistance.ResultsExposure of clinical isolates of S. aureus to human plasma (10%) within media, and to a lesser extent when coated onto plates, significantly enhanced biofilm formation in all of the clinical isolates tested. Compared to biofilms grown under non-supplemented conditions, plasma-augmented biofilms displayed significant changes in both the biofilm phenotype and cell morphology as determined by confocal scanning laser microscopy (CLSM) and scanning electron microscopy (SEM), respectively. Exposure of bacteria to plasma resulted in a significant fold-increase in MSCRAMM expression in both a time and isolate-dependent manner. Additionally, plasma-augmented biofilms displayed an increased tolerance to vancomycin compared to biofilms grown in non-supplemented media.ConclusionsCollectively, these studies support previous findings demonstrating a role for host factors in biofilm formation and provide further insight into how plasma, a preferred growth medium for staphylococcal biofilm formation enhances as well as augments other intrinsic properties of S. aureus biofilms. Consequently, these findings indicate that incorporation of host factors may be necessary to better replicate in vivo conditions and for the best utility of a clinical biofilm assay to evaluate the process of biofilm formation and treatments.

Highlights

  • Introduction to biofilmInt J Antimicrob Agents 1999, 11:217–221. discussion 237–219. 2

  • Human plasma enhances biofilm formation by clinical isolates of S. aureus, in part through increased MSCRAMM expression Previous studies have shown that supplementing media, as well as coating surfaces, with human plasma can facilitate S. aureus attachment and promote biofilm accumulation in vitro [18,19]

  • For S. aureus MRSA3, the addition of plasma significantly enhanced biomass accumulation, whereas for S. aureus UAMS-1 the effect of plasma on biofilm formation seemed to be related to morphology, appearing more dense and compact compared to biofilms grown in only media (Figure 1A-B)

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Summary

Introduction

Introduction to biofilmInt J Antimicrob Agents 1999, 11:217–221. discussion 237–219. 2. Microbial biofilms have been associated with the development of chronic human infections and represent a clinical challenge given their increased antimicrobial tolerance. Staphylococcus aureus is a major human pathogen causing a diverse range of diseases, of which biofilms are often involved. To better understand how host factors enhance staphylococcal biofilm formation, we evaluated the effect of whole human plasma on biofilm formation in clinical isolates of S. aureus and the expression of seven microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) known to be involved in biofilm formation by quantitative real-time PCR. Biofilms are implicated as a significant factor contributing to chronic human infections [2,3,4], and represent a major challenge to modern medicine given their recalcitrance to antimicrobials and host mechanisms of clearance. A class of surface proteins known as the microbial surface components recognizing adhesive matrix molecules (MSCRAMMs), which in addition to virulence, are responsible for mediating initial attachment to both naïve tissues and various biomaterials [5,6,7]

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