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26-03-2012 | Cardiology | Article

Dental plaque bacteria implicated in infective endocarditis


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MedWire News: A bacterium that is normally present in the oral flora can cause infective endocarditis (IE) if allowed to enter the systemic system, research suggests.

IE is an inflammation of the inner tissue of the heart, including the heart valves, caused by a bacterial infection. If untreated, IE can lead to severe valvular insufficiency and congestive heart failure.

"About 30% of people with infective endocarditis die and most will require surgery for replacement of the infected heart valve with a metal or animal valve," said lead author Helen Petersen (University of Bristol, UK) in a press statement.

The researchers, from the Royal College of Surgeons in Ireland (RCSI) and the University of Bristol, have discovered that Streptococcus gordonii, a bacteria that is part of the normal oral flora and contributes to dental plaque, can cause IE if able to enter the systemic blood stream.

The bacteria gains entry to the blood through bleeding and damaged gums, such as those found in patients with periodontitis and gingivitis, they say.

Once in the circulation, S. gordonii is able to produce a molecule on its surface that mimics fibrinogen, a protein that is an essential component of the coagulation system and causes blood to clot. These blood clots can form on the heart valves, causing IE, or in the blood vessels that supply the heart and brain, potentially causing myocardial infarctions or strokes.

Speaking at the Society for General Microbiology Spring Meeting, Petersen explained that a better understanding of the interactions between bacteria and platelets could lead to the development of new treatments for IE, something which is especially important considering the growing problem of antibiotic resistance.

"In the development of infective endocarditis, a crucial step is the bacteria sticking to the heart valve and then activating platelets to form a clot. We are now looking at the mechanism behind this sequence of events in the hope that we can develop new drugs which are needed to prevent blood clots and also infective endocarditis," she said.

Co-author Steve Kerrigan from the RCSI continued: "Our team has now identified the critical components of the S. gordonii molecule that mimics fibrinogen, so we are getting closer to being able to design new compounds to inhibit it. This would prevent the stimulation of unwanted blood clots."

The team is looking more widely at other dental plaque bacteria that may have similar effects to S. gordonii. "We are also trying to determine how widespread this phenomenon is by studying other bacteria related to S. gordonii. What our work clearly shows is how important it is to keep your mouth healthy through regular brushing and flossing, to keep these bacteria in check," stressed Petersen.

By Iain Bartlett

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