Cardiac Microlesions Form During Severe Bacteremic Enterococcus faecalis Infection.

Area of Science:

• Microbiology
• Pathogenesis
• Immunology

Background:

• Enterococcus faecalis is a common cause of hospital-acquired bacteremia.
• Cardiac microlesions are associated with severe bacterial infections.
• The mechanisms of E. faecalis-induced cardiac damage are not fully understood.

Purpose of the Study:

• To investigate the formation of cardiac microlesions during E. faecalis bacteremia.
• To identify bacterial factors involved in E. faecalis-mediated cardiac pathology.
• To elucidate the host immune response to E. faecalis cardiac microlesions.

Main Methods:

• Induction of severe bacteremic E. faecalis infection in a mouse model.
• Histopathological analysis of cardiac tissue to identify microlesions.
• Assessment of bacterial virulence using a Caenorhabditis elegans model.
• Analysis of cardiomyocyte cell death pathways (apoptosis and necroptosis).
• Quantification of host proinflammatory cytokine levels.

Main Results:

• E. faecalis infection in mice led to the formation of cardiac microlesions, similar to those seen in Streptococcus pneumoniae infections.
• Disulfide bond forming protein A (DsbA) was essential for E. faecalis virulence in C. elegans and cardiac microlesion formation in mice.
• E. faecalis induced apoptotic and necroptotic cell death in cardiomyocytes at microlesion sites.
• A mutant lacking DsbA resulted in increased proinflammatory cytokines, whereas the wild-type strain suppressed the immune response.

Conclusions:

• Enterococcus faecalis can cause cardiac microlesions during severe bacteremia.
• Bacterial DsbA is a key virulence factor required for cardiac microlesion formation.
• E. faecalis-induced cardiac microlesions involve host cardiomyocyte death and modulation of the immune response.