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Contribution of the collagen adhesin Acm to pathogenesis of Enterococcus faecium in experimental endocarditis

Sreedhar R Nallapareddy1, Kavindra V Singh, Barbara E Murray

  • 1Department of Internal Medicine, Division of Infectious Diseases, Center for the Study of Emerging and Re-Emerging Pathogens, University of Texas Medical School, Houston, Texas 77030, USA.

Infection and Immunity
|July 2, 2008
PubMed

Insights

The collagen adhesin Acm is the first identified virulence factor for Enterococcus faecium, crucial for causing endocarditis in rats. Antibodies targeting Acm show potential for controlling this multidrug-resistant pathogen.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Pathogenesis

Background:

  • Enterococcus faecium is a multidrug-resistant bacterium causing nosocomial infections like endocarditis.
  • No specific virulence factors for E. faecium have been experimentally demonstrated.
  • A cell wall-anchored collagen adhesin (Acm) has been identified in some clinical isolates.

Purpose of the Study:

  • To experimentally demonstrate the role of Acm in E. faecium pathogenesis.
  • To investigate Acm's contribution to endocarditis and collagen adherence.
  • To explore Acm as a potential immunotarget for therapeutic strategies.

Main Methods:

  • Utilized a rat endocarditis model to assess the virulence of an E. faecium acm deletion mutant (TX0082 Deltaacm::cat) compared to wild-type TX0082.
  • Employed quantitative reverse transcription-PCR to analyze acm mRNA levels in non-adherent isolates.
  • Used flow cytometry to detect Acm expression on bacterial cells from infected vegetations.
  • Tested the efficacy of anti-Acm antibodies in reducing bacterial collagen adherence.

Main Results:

  • The acm deletion mutant was significantly attenuated in the rat endocarditis model, showing reduced valve colonization and vegetation burden.
  • Acm was confirmed as the first experimentally demonstrated factor essential for E. faecium pathogenesis.
  • While some isolates showed reduced in vitro acm transcription, Acm expression was observed during infection in vivo.
  • Anti-Acm antibodies significantly reduced E. faecium collagen adherence, indicating Acm's functional role.

Conclusions:

  • Acm is a critical virulence factor for Enterococcus faecium, particularly in experimental endocarditis.
  • Downregulation of acm transcription in vitro does not preclude Acm expression and function during infection.
  • Acm represents a promising target for developing immunotherapies against E. faecium infections.

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