Vancomycin-intermediate Staphylococcus aureus strains have impaired acetate catabolism: Implications for polysaccharide intercellular adhesin synthesis and autolysis

Jennifer L. Nelson, Kelly C. Rice, Sean R. Slater, Paige M. Fox, Gordon L. Archer, Kenneth W Bayles, Paul D Fey, Barry N. Kreiswirth, Greg A Somerville

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

The most common mechanism by which Staphylococcus aureus gains resistance to vancomycin is by adapting its physiology and metabolism to permit growth in the presence of vancomycin. Several studies have examined the adaptive changes occurring during the transition to vancomycin-intermediate resistance, leading to a model of vancomycin resistance in which decreased cell wall turnover and autolysis result in increased cell wall thickness and resistance to vancomycin. In the present study, we identified metabolic changes common to vancomycin-intermediate S. aureus (VISA) strains by assessing the metabolic and growth characteristics of two VISA strains (vancomycin MICs of 8 μg/ml) and two isogenic derivative strains with vancomycin MICs of 32 μg/ml. Interestingly, we observed the parental strains had impaired catabolism of nonpreferred carbon sources (i.e., acetate), and this impairment became more pronounced as vancomycin resistance increased. To determine if acetate catabolism impairment is common to VISA strains, we assessed the ability of VISA and vancomycin-sensitive S. aureus (VSSA) clinical isolates to catabolize acetate. As expected, a significantly greater percentage of VISA strains (71%) had impaired acetate catabolism relative to VSSA (8%). This is an important observation because staphylococcal acetate catabolism is implicated in growth yield and antibiotic tolerance and in regulating cell death and polysaccharide intercellular adhesin synthesis.

Original languageEnglish (US)
Pages (from-to)616-622
Number of pages7
JournalAntimicrobial Agents and Chemotherapy
Volume51
Issue number2
DOIs
StatePublished - Feb 1 2007

Fingerprint

Autolysis
Vancomycin
Staphylococcus aureus
Acetates
Vancomycin Resistance
Cell Wall
Growth
polysaccharide intercellular adhesin
Cell Death
Carbon
Observation
Anti-Bacterial Agents

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)
  • Infectious Diseases

Cite this

Vancomycin-intermediate Staphylococcus aureus strains have impaired acetate catabolism : Implications for polysaccharide intercellular adhesin synthesis and autolysis. / Nelson, Jennifer L.; Rice, Kelly C.; Slater, Sean R.; Fox, Paige M.; Archer, Gordon L.; Bayles, Kenneth W; Fey, Paul D; Kreiswirth, Barry N.; Somerville, Greg A.

In: Antimicrobial Agents and Chemotherapy, Vol. 51, No. 2, 01.02.2007, p. 616-622.

Research output: Contribution to journalArticle

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