The pathogenesis of cardiac microlesion formation during severe bacteremic infection

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Abstract
Cardiac microlesions are associated with a growing number of bacterial infections Community acquired pneumonia (CAP) caused by the gram-positive bacterium Streptococcus pneumoniae has been shown to predispose older individuals (aged 65 years and older) to adverse long-term cardiac sequelae such as new or worsened heart failure and cardiac arrhythmia [1,2]. To better understand these clinical observations, investigators sought to determine the interactions of S. pneumoniae with the heart during invasive pneumococcal disease (IPD). As a result, S. pneumoniae was found to form bacteria-filled vacuoles (i.e., cardiac microlesions) within the ventricles of mice, nonhuman primates, and humans, leading to an immunoquiescent immune response, altered electrophysiology, cardiomyocyte cell death, and heart failure in a mouse model [2]. As such, the formation of microlesions, subsequent healing, and formation of myocardial fibrosis have been hypothesized to be a pathology that could partially explain the adverse cardiac events observed in patients hospitalized with CAP [2]. More recently, the human commensal gram-positive bacterium Enterococcus faecalis was also shown to promote cardiac microlesion formation in mice, while suppressing the host cardiomyocyte inflammatory response in vitro [3]. Similar observations of microlesion formation were made with the gram-negative bacterium Franscisella tularensis subspecies novicida [4] and grampositive bacterium non-tuberculosis Mycobacterium avium [5]. Therefore, cardiac microlesion formation is becoming increasingly appreciated as a possible risk factor for adverse cardiac complications during severe bacterial infection [6]. This review seeks to shed light on these observations and the underlying mechanisms contributing to this newly described pathology.

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