The microbiological characteristics of Staphylococcus aureus isolated from patients with native valve infective

Chung-Jong Kim1, Kyoung-Ho Song2,3, Pyoeng Gyun Choe3,4

  • 1Department of Internal Medicine, Ewha Womans University Seoul Hospital, Seoul, Republic of Korea.

Virulence
|November 14, 2019
PubMed

Insights

Staphylococcus aureus infective endocarditis (IE) is linked to higher fibronectin binding, potentially mediated by genetic variations in the fibronectin-binding protein A gene (fnbpA). This finding offers insights into S. aureus IE pathogenesis.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Genetics

Background:

  • Infective endocarditis (IE) caused by Staphylococcus aureus (S. aureus) is a serious condition.
  • The specific microbiological factors contributing to S. aureus IE remain incompletely understood.

Purpose of the Study:

  • To compare the microbiological characteristics of S. aureus isolates from patients with and without IE.
  • To investigate the role of virulence factors, specifically fibronectin and fibrinogen binding, in S. aureus IE.

Main Methods:

  • A case-control study involving S. aureus bacteremia (SAB) isolates from 10 hospitals over 7 years.
  • Matching of IE cases with non-IE controls based on infection type, acquisition, and methicillin susceptibility.
  • Analysis of virulence factor genes using multiplex polymerase chain reactions and in vitro binding assays for fibrinogen and fibronectin.
  • Sequencing of the fibronectin-binding protein A gene (fnbpA) to identify single-nucleotide polymorphisms (SNPs).

Main Results:

  • Of 2,365 SAB cases, 92 had IE. After matching, 37 pairs were compared.
  • The fibronectin-binding ratio was significantly higher in IE isolates (1.31 ± 0.42) compared to non-IE controls (1.06 ± 0.31; p=0.01).
  • Fibronectin-binding ratio positively correlated with the number of fnbpA SNPs in IE cases (p < 0.001), but not in controls (p=0.124).

Conclusions:

  • Fibronectin-binding by S. aureus may play a crucial role in the development of IE.
  • Genetic variability within the fnbpA gene appears to influence the degree of fibronectin binding and potentially IE pathogenesis.

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