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Staphylococcus epidermidis ST2 strains associated with bloodstream infections contain a unique mobile genetic element

Amy A Gomez¹, Clara Kjerfve¹, Minseo Choi¹

¹Center for Infectious and Inflammatory Diseases, Institute of Biosciences and Technology (IBT), Texas A&M Health Science Center, Houston, Texas, USA.

|November 19, 2024

Abstract:

Staphylococcus epidermidis, a common commensal bacterium, is a leading cause of nosocomial catheter-associated bloodstream infections. S. epidermidis sequence type 2 (ST2) is specifically recognized globally for causing invasive disease. In this study, we identified a novel putative integrated conjugative element, pICE-Sepi-ST2, unique to the genomes of S. epidermidis ST2. Our investigation identified pICE-Sepi-ST2 in all ST2 isolates from bloodstream infections. Meanwhile, ST2 isolates from other infection sources, such as catheters, prosthetic joints, and fracture fixations, showed variable pICE-Sepi-ST2 prevalence. pICE-Sepi-ST2 encodes two putative cell wall anchored proteins that we have designated SesX and SesY. Biochemical characterization of SesY revealed that it binds both plasminogen (Plg) and plasmin (Pln) and inhibits Pln's ability to cleave a chromogenic substrate and degrade fibrin clots. Furthermore, all ST2 isolates containing a pICE-Sepi-ST2 also have a mutated sdrG gene. Thus, all ST2 isolates have two genetic modifications that target distinct steps in the hemostatic pathway. SdrG, which inhibits coagulation, is inactivated, and SesY, which inhibits fibrin, is introduced. These findings suggest that the hemostasis pathway is a strategic target for ST2 S. epidermidis bloodstream pathogenesis.

Importance:

This study uncovers a new virulence mechanism in Staphylococcus epidermidis ST2 bloodstream isolates. We identify a mobile genetic element (MGE) characteristic of an integrated conjugated element (ICE). pICE-Sepi-ST2 carries the genetic information needed to produce a cell wall-anchored (CWA) protein called SesY. The results indicate that SesY binds to plasminogen (Plg) and plasmin (Pln) and inhibits Pln's degradation of fibrin clots. Genetic analysis showed that all ST2 bloodstream isolates can express the plasmin inhibitor SesY and carry a mutation in the SdrG gene, resulting in the expression of inactive SdrG. Thus, we describe a molecular pathway targeting the coagulation pathway that may be required for S. epidermidis ST2 to cause bloodstream infections.

Insights

Staphylococcus epidermidis ST2 bloodstream infections are linked to a novel genetic element, pICE-Sepi-ST2. This element produces SesY, an inhibitor of fibrin degradation, and inactivates SdrG, aiding bacterial survival in the bloodstream.

Area of Science:

Microbiology
Molecular Biology
Pathogenesis

Background:

Staphylococcus epidermidis is a major cause of hospital-acquired infections, particularly catheter-associated bloodstream infections.
Sequence type 2 (ST2) of S. epidermidis is globally recognized for causing severe invasive diseases.
Understanding the virulence mechanisms of S. epidermidis ST2 is crucial for developing effective treatments.

Purpose of the Study:

To identify novel virulence factors and mechanisms employed by Staphylococcus epidermidis ST2 in bloodstream infections.
To characterize a unique mobile genetic element, pICE-Sepi-ST2, found in S. epidermidis ST2 isolates.
To elucidate the role of SesY and SdrG in the pathogenesis of S. epidermidis ST2 bloodstream infections.

Main Methods:

Genomic analysis to identify the novel integrated conjugative element (ICE) pICE-Sepi-ST2.
Biochemical characterization of the putative cell wall-anchored protein SesY.
Genetic analysis of the sdrG gene in S. epidermidis ST2 isolates.
Prevalence studies of pICE-Sepi-ST2 in isolates from various infection sources.

Main Results:

A novel ICE, pICE-Sepi-ST2, was identified and found to be unique to S. epidermidis ST2.
pICE-Sepi-ST2 encodes SesX and SesY, with SesY shown to bind plasminogen and plasmin, inhibiting fibrinolysis.
All bloodstream S. epidermidis ST2 isolates possessed pICE-Sepi-ST2 and a mutated, inactive sdrG gene.
ST2 isolates from other infection sources showed variable prevalence of pICE-Sepi-ST2.

Conclusions:

Staphylococcus epidermidis ST2 utilizes a dual strategy targeting the hemostasis pathway for bloodstream infection.
The introduction of SesY (plasmin inhibitor) and inactivation of SdrG (coagulation inhibitor) likely facilitates S. epidermidis ST2 survival and proliferation in the bloodstream.
The hemostasis pathway represents a key target for S. epidermidis ST2 pathogenesis.

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Keywords:

Staphylococcus epidermidis bloodstream infections coagulation pathway integrated conjugated element mobile genetic element molecular pathogenesis plasmin

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