Staphylococcal Biofilms

M. Otto

1 Introduction 208

2 Biofilms and Staphylococcal Infections 208

  1. 1 S. epidermidis Infections on Indwelling Medical Devices 209
  2. 2 S. aureus Biofilm-Associated Infection 209
  3. 3 Other Staphylococci 210
  4. 4 Interaction of Staphylococci with Other Pathogens in Mixed-Species Medical Biofilms 210

3 The Molecular Basis of Biofilm Formation in Staphylococci 210

  1. 1 Attachment 211
  2. 2 Maturation 212
  3. 3 Adhesive Forces: Aggregation 213
  4. 4 Disruptive Forces: Biofilm Structuring 215
  5. 5 Detachment 216
  6. 6 Cell Death and Extracellular DNA 217

4 Regulation of Biofilm Formation in Staphylococci 217

  1. 1 Environmental Influences 217
  2. 2 Regulation of Attachment Factors 218
  3. 3 Regulation of Exopolysaccharide Synthesis 218
  4. 4 Regulation of Phenol-Soluble Modulin Expression: agr 219

5 Physiology of Staphylococcal Biofilms: Lessons from Transcriptional Profiling 220

6 The Molecular Basis of Biofilm Resistance to Host Defenses and Antibiotics 221

7 Possible Anti-biofilm Therapeutics 221

  1. 1 Interfering with Essential Staphylococcal Biofilm Factors 222
  2. 2 Altering Adhesive Features of Indwelling Medical Devices 222
  3. 3 Vaccination 222

8 Conclusions and Outlook 223

References 223

Abstract Staphylococcus epidermidis and Staphylococcus aureus are the most frequent causes of nosocomial infections and infections on indwelling medical devices, which characteristically involve biofilms. Recent advances in staphylococcal molecular biology have provided more detailed insight into the basis of biofilm

M. Otto

Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, The National Institutes of Health, Rocky Mountain Laboratories, Hamilton, MT, USA [email protected]

T. Romeo (ed.), Bacterial Biofilms.

Current Topics in Microbiology and Immunology 322.

© Springer-Verlag Berlin Heidelberg 2008

formation in these opportunistic pathogens. A series of surface proteins mediate initial attachment to host matrix proteins, which is followed by the expression of a cationic glucosamine-based exopolysaccharide that aggregates the bacterial cells. In some cases, proteins may function as alternative aggregating substances. Furthermore, surfactant peptides have now been recognized as key factors involved in generating the three-dimensional structure of a staphylococcal biofilm by cell-cell disruptive forces, which eventually may lead to the detachment of entire cell clusters. Transcriptional profiling experiments have defined the specific physiology of staphylococcal biofilms and demonstrated that biofilm resistance to antimicrobials is due to gene-regulated processes. Finally, novel animal models of staphylococcal biofilm-associated infection have given us important information on which factors define biofilm formation in vivo. These recent advances constitute an important basis for the development of anti-staphylococcal drugs and vaccines.

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