Pneumonia bacteria can kill off heart muscles cells, increasing the risk of adverse cardiac events in adults, but new research suggests potential methods for preventing this phenomenon.
In the past researchers knew contracting Streptococcus pneumoniaein adulthood increased the risk of events such as heart failure, but weren't sure why, PLOS reported. Carlos Orihuela, from the University of Texas Health Science Center in San Antonio, looked at how the bacteria behaved in mice and rhesus macaques to discover the process behind the phenomenon.
The team found mice with invasive pneumococcal disease showed elevated levels of troponin, which is a marker for heart damage found in the blood; the mice also had abnormal EKGs. The researchers noticed signs of microscopic injury sites called microlesions in the rodents' hearts containing S. pneumonia, suggesting the bacteria can "invade and multiply" within the organ. Looking upon the cellular level, these bacteria proved to be responsible for heart muscle death.
The team also found S. pneumoniae requires a molecule called CbpA to stray from the blood system and enter the heart. An experimental vaccine made up of composed of CbpA and a non-toxic version of pneumolysin created antibodies that helped protect the heart from the harmful and invasive bacteria.
The researchers looked at tissue samples from three rhesus macaques that had succumbed to pneumococcal pneumonia and observed similar lesions in the primate hearts, but minus the bacteria. The same situation proved to be true in the hearts of humans who had died from pneumococcal disease.
Since the macaques and humans had been treated with antibiotics, the researchers wondered if the bacteria had been killed off by the treatment after inflicting the lesions. To test this they infected mice with S. pneumoniae and treated them with a high-dose antibiotic as soon as they noticed the lesions occurring. The rodents' hearts still contained lesions but were bacteria-free following the treatment.
The findings suggest that since certain antibiotics such as the one used in the study break apart bacteria, these types of treatments could actually exacerbate the death of heart muscle cells. Alternatively, an antibiotic that does not break bacteria apart could be used to help keep heart cell death at a minimum.
"Research is merited to determine the true frequency of cardiac microlesions in patients hospitalized with invasive pneumococcal disease, if modifications in antibiotic therapy improve long-term outcomes, and if prevention of cardiac damage is an indication for vaccination," the researchers concluded.
The findings were published Sept. 18 the journal PLOS Pathogens.
