Aaron Barnes (left) and Kristi Frank (right – Photo by Uniformed Services University)
We interviewed all the authors to find out more about the inspiration behind this paper:
Could you provide a bit of context into what Enterococcus faecalis is?
Enterococcus faecalis is the Dr. Jekyll and Mr. Hyde of bacteria: a common, benign member of our gut microbiome that can become a dangerous pathogen in the bloodstream. Most prominently, E. faecalis in the blood – or bacteremia – can infect the lining of the heart, leading to infectious endocarditis. Infectious endocarditis is an uncommon disease but one that can lead to significant illness or even death. Prior to the discovery of antibiotics, bacterial IE was considered to be uniformly fatal. Even now, advanced antibiotic therapy is often complex and protracted, and the mortality rate of bacterial IE has not fallen in decades.”
Could you provide a brief, simple overview of the topic your paper covers?
We investigated several new and unexpected findings that were at odds with the standard models of how bacteria attach to the lining of the heart and cause disease. The classic model of bacterial IE pathogenesis is that bacteria adhere to sites of damage in the endocardium. We demonstrated that E. faecalis can attach to the surface of the lining of the heart without the need for previous damage. In particular, we found that bacterial microcolonies form on undamaged surfaces and did not appear to require host platelets or immune cells from the animal host to attach or develop.”
Enterococcus faecalis forms microcolonies in vivo on undamaged rabbit endovasculature.
What encouraged you to perform research in this area of microbiology?
We joke that enterococci are “the third leading cause of everything in the clinical micro lab” – enterococci are rather like a Jack-of-All-Trades. Specifically, however, this project came about as many good scientific projects do: we had some results that didn’t make sense. We knew the bacteria in the bloodstream must be attaching in the heart, but they were frequently not on the valves where the literature told us they should be.”
What do you see as the next steps in this area of research?
While our research for this paper was extensive — as it has to be for such novel data — it is still only in a single animal model system. We need to verify that it holds true in other mammals, then tackle the next really big questions: How do enterococci attach to the undamaged surface of the heart lining? What genes have to be expressed as they change from a free-floating, planktonic lifestyle to a pre-pathogenic, stuck-to-the-surface bacteria biofilm? And how can we interfere with this disease state so we can eventually develop therapies for patients with these infections?”
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