(RxWiki News) Streptococcus mutans is a bacterium most often associated with cavities. Now, researchers say that same bacteria can rapidly travel to the heart and create a potentially deadly condition.
Scientists at the University of Rochester Medical Center discovered that when the bacteria enter the bloodstream it can quickly cause inflammation of the heart valves, which can be fatal.
S. mutans resides in dental plaque, where it can thrive in oral cavities. Most often the bacteria remains in the mouth, but sometimes, particularly after a dental procedure or vigorous flossing, it can enter the bloodstream.
"Talk to your dentist about endocarditis."
It is usually destroyed by the immune system, but on occasion that doesn't happen and the bacteria travels to the heart within a matter of seconds and colonizes heart tissue, particularly heart valves. It can cause a deadly condition called endocarditis, or inflammation of the heart valves.
Scientists said the study raises the possibility of creating a screening tool such as a cheek swab to gauge a dental patient's susceptibility to the condition.
Dr. Jacqueline Abranches, Ph.D., a microbiologist and study author, and a team investigated how the bacteria arrived there and how it could continue to survive. Researchers and a team from the university’s Center for Oral Biology found that a collagen-binding protein known as CNM gives S. mutans its ability to invade heart tissue.
In lab experiments, scientists found that strains with CNM are able to invade heart cells, and strains without CNM are not.
The team also examined the response of wax worms to different strains of S. mutans. Strains without CNM were rarely lethal to the worms, while strains that contained the protein were fatal 90 percent of the time. But when CNM was removed from the strains, the worms thrived.
Abranches identified five specific strains of S. mutans that carry the CNM protein, out of more than three dozen strains examined. CNM is not found in the most common type of S. mutans found in people, type C, but is present in rarer types of S. mutans, including types E and F.
The research, which was published in Infection and Immunity, was funded by the American Heart Association.
