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How pneumonia bacteria can compromise heart health

Streptococcus pneumoniae, the bacterium responsible for most cases of bacterial pneumonia, can invade the heart and cause myocardial necrosis, according to a study recently published in PLOS Pathogens.1 This could help explain the link between pneumonia and adverse heart events, say the authors.

Associate Professor Carlos Orihuela (University of Texas Health Science Center, San Antonio, USA) and colleagues detected microlesions in experimentally infected mice and rhesus macaques, as well as in heart sections from humans who succumbed to invasive pneumococcal disease (IPD). Cardiac microlesion formation required interaction of the bacterial adhesin CbpA with host laminin receptor and bacterial cell wall with platelet-activating factor receptor.

Microlesion formation also required the pore-forming toxin pneumolysin, the authors say. When infected mice were rescued with antibiotics, they observed robust signs of collagen deposition at former lesion sites. Thus, microlesions and the scarring that occurs thereafter may explain why adverse cardiac events occur during and following IPD, they conclude.

Professor Orihuela, speaking to BJC Arrhythmia Watch, said: “It is well documented that hospitalisation of adults for pneumonia, in particular admission into an intensive care unit, is accompanied by ~20% frequency of an adverse cardiac event. There are lots of reasons for this, including rampant inflammation, underlying disease, etc… but one reason that had not been fully explored was that the bacteria actually invades the heart during bacteraemia and causes direct cardiac damage.”

Screen shot 2014-09-26 at 10.20.44

Attached is the picture of a mouse heart with a lesion next to a blood vessel

“Importantly, we identified the mechanisms by which S. pneumoniae is able to translocate across endothelial cells in the cardiac vasculature to invade the heart, and found that it is the same as that responsible for the bacteria crossing the blood brain barrier and development of meningitis,” Dr Orihuela added.

“We have with investigators at St. Jude Children’s Research hospital examined a candidate vaccine that…neutralises the adhesin that is required for translocation into the heart (choline binding protein A) as well as the toxin (pneumolysin) that is responsible for killing cardiomyoctes. Animals that were immunised were protected against cardiac lesion formation,” he continued.

“While the paper includes samples from deceased humans, it is a small sample size and the major question moving forward is what is the true incidence of this in humans…We are putting together a study to examine this in humans, are doing investigations in non-human primates, and are continuing our studies in mice to determine further molecular mechanisms,” Dr Orihuela concluded.

The authors conclude that “research is merited to determine the true frequency of cardiac microlesions in patients hospitalised with invasive pneumococcal disease, if modifications in antibiotic therapy improve long-term outcomes, and if prevention of cardiac damage is an indication for vaccination”.

References

1. Brown AO, Mann B, Gao G, et al. Streptococcus pneumoniae translocates into the myocardium and forms unique microlesions that disrupt cardiac function. PLoS Pathog 2014;10:e1004383. http://dx.doi.org/10.1371/journal.ppat.1004383

Published on: September 26, 2014

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