This Article Full Text (PDF) Other Versions of this Article: IAI.00509-07v1 75/9/4219    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Zhu, Y. Articles by Somerville, G. A. Search for Related Content PubMed PubMed Citation Articles by Zhu, Y. Articles by Somerville, G. A.

 Previous Article  |  Next Article 

Infect. Immun. doi:10.1128/IAI.00509-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Staphylococcus aureus metabolism in a biofilm: the influence of arginine on polysaccharide intercellular adhesin synthesis, biofilm formation, and pathogenesis

Department of Veterinary and Biomedical Sciences, University of Nebraska, Lincoln, NE 68583, Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198

^* To whom correspondence should be addressed. Email: gsomerville3{at}unl.edu.

	Abstract

Staphylococcus aureus and S. epidermidis are the leading causes of nosocomial infections in the USA and often associated with biofilms attached to indwelling medical devices. Despite the importance of biofilms, there is very little consensus about the metabolic requirements of S. aureus during biofilm growth. To assess the metabolic requirements of S. aureus growing in a biofilm, we grew USA200 and USA300 clonal types in biofilm flow cells, and measured the extraction and accumulation of metabolites. In spite of the genetic differences, both clonal types extracted glucose and accumulated lactate, acetate, formate, and acetoin, suggesting glucose was catabolized to pyruvate that was then catabolized via the lactate dehydrogenase, pyruvate formate-lyase, and butanediol pathways. Additionally, both clonal types selectively extracted the same six amino acids from the culture medium (serine, proline, arginine, glutamine, glycine, and threonine). These data and recent speculation about the importance of arginine in biofilm growth and the function of arginine deiminase in USA300 clones, led us to genetically inactivate the sole copy of the arginine deiminase operon by deleting the arginine/ornithine antiporter (arcD) in the USA200 clonal type and assess the effect on biofilm development and pathogenesis. Although inactivation of arcD did completely inhibit arginine transport and did reduce polysaccharide intercellular adhesin accumulation, arcD mutants formed biofilms and achieved cell densities in catheter infection studies equivalent to isogenic wild-type strains.

This article has been cited by other articles:

• Majerczyk, C. D., Sadykov, M. R., Luong, T. T., Lee, C., Somerville, G. A., Sonenshein, A. L. (2008). Staphylococcus aureus CodY Negatively Regulates Virulence Gene Expression. J. Bacteriol. 190: 2257-2265 [Abstract] [Full Text]