#FEMSmicroBlog: Bacterial endocarditis without tissue damage


Endothelial tissue surrounding the heart can be infected by bacteria leading to dangerous illnesses. It was long thought that bacterial pathogens could only attach to damaged tissue thus colonizing a growing thrombus and causing disease. Now, a new study published in FEMS Microbes challenges the existing model. The authors of the study, Aaron Barnes and Gary Dunny explain for the #FEMSmicroBlog how Enterococcus faecalis could induce infectious endocarditis without previous tissue damage. #FascinatingMicrobes


Bacteria and infectious endocarditis

The endothelial tissue that lines the heart and other vascular components of the circulatory system is prone to infections. As such, infectious endocarditis can be caused by bacterial pathogens and can lead to significant illness or even death.

Prior to the discovery of antibiotics, bacterial infectious endocarditis was uniformly fatal. Even now antibiotic therapy is often complex and accompanied by weeks of hospitalisation.

For the past 50 years, the pathogenesis of bacterial infectious endocarditis has been based on the same model. When the endothelial layer is damaged, blood clot-inducing factors come in contact with the tissue below. Bacteria in the bloodstream can attach to the surface of this clot–the thrombus–and form biofilms in and on it.

A schematic model of how Enterococcus faecalis induces infectious endocarditis without previous tissue damage.
The enterococcal infection model. From Barnes et al. (2021).

Within this complex bacterially-derived matrix, the associated bacteria are protected. This so-called vegetation is likely the source of difficult treatment issues.

This classical model states that for clinical infectious endocarditis to establish, bacteria are already present in the bloodstream when the thrombus forms. Otherwise, without a thrombus, bacteria had no surface to attach to.


Bacterial infectious endocarditis can form without tissue damage

The article “Enterococcus faecalis Colonizes and Forms Persistent Biofilm Microcolonies on Undamaged Endothelial Surfaces in a Rabbit Endovascular Infection Model” published in FEMS Microbes aims to shed light on this process. The study reports that the bacterial species Enterococcus faecalis can build biofilm microcolonies on endothelial tissue without pre-existing damage.

The work uses a standard, catheter-based endothelial damage model of endocarditis in rabbits. This includes scraping and thus damaging the aortic valve of anaesthetized rabbits. After this minor damage, bacteria were injected and allowed to migrate to the site of injury.

It shows that Enterococcus faecalis also colonized areas that were impossible for the bacteria to reach with the catheter. These areas presumably did not suffer from surface tissue damage. This could mean that surface damage may not be an absolute requirement for the bacteria to spread.

Enterococcus faecalis also colonizes areas that did not suffer from tissue damage.

Further experiments showed that Enterococcus faecalis can form identical biofilm microcolonies on the endothelial surfaces in rabbits that never underwent surgical intervention. Of note, there might be historical reasons behind why this mechanism of endothelial colonization without pre-existing damage has been overlooked in previous studies.


Enterococcus faecalis in infectious endocarditis hides from the immune system

The paper further focuses on host components commonly presumed to play active roles in the bacterial infectious endocarditis process. Interestingly, platelets appeared to play no role in Enterococcus faecalis to form microcolony in this model system.

Furthermore, in animals with Enterococcus faecalis infections lasting as long as 14 days, tissue inflammation and white blood cells were almost completely absent. It seemed that the immune system was not activated. This likely means that bacteria in a thrombus-biofilm can effectively hide from the host immune system for long periods of time.

Microscopic picture of Entercoccus faecalis tissue damage after colonisation.
Enterococcal endothelial colonisation. From Barnes et al. (2021).

This ability of Enterococcus faecalis to hide out in microcolonies likely explains why enterococcal infections often become chronic and lead to clinical symptoms. However, the molecular details of this mechanism have not been investigated yet in vivo. Hence, elucidating this alternative colonization route will help us better understand the unusual Enterococci and their unique pathophysiology.


About FEMS Microbes

FEMS Microbes is a new Open Access journal from FEMS to support the needs of the microbiology community. In particular, it aims to be a venue for Early Career Scientists to read, publish, and contribute, and wants to recognize the crucial, and often unnoticed, contribution to peer review by Early Career Scientists. FEMS Microbes welcomes direct submissions. What are you waiting to submit your paper?

About this blog section

The section #FascinatingMicrobes for the #FEMSmicroBlog explains the science behind a paper and highlights the significance and broader context of a recent finding. One of the main goals is to share the fascinating spectrum of microbes across all fields of microbiology.

Do you want to be a guest contributor?
The #FEMSmicroBlog welcomes external bloggers, writers and SciComm enthusiasts. Get in touch if you want to share your idea for a blog entry with us!

Back to top

Leave a Reply

Your email address will not be published. Required fields are marked *

Share this news