U. ROCHESTER (US) — Bacteria best known for causing cavities are also able to make their way into heart tissue, causing endocarditis, a dangerous and potentially lethal condition.
Identification of the protein that allows Streptococcus mutans to gain a foothold is reported in the journal Infection and Immunity, and may lead to a screening tool, like a swab of the cheek, or a spit test, to gauge a dental patient’s vulnerability to the condition.
S. mutans is a bacterium best known for causing cavities that reside in dental plaque—an architecturally sophisticated goo composed of an elaborate molecular matrix created by S. mutans that allows the bacteria to inhabit and thrive in the oral cavity. There, they churn out acid that erodes teeth.
Normally, S. mutans confines its mischief to the mouth, but sometimes, particularly after a dental procedure or even after a vigorous bout of flossing, the bacteria enter the bloodstream. There, the immune system usually destroys them, but occasionally, within just a few seconds, they travel to the heart and colonize its tissue, especially heart valves.
The bacteria can cause endocarditis, inflammation of heart valves, which can be deadly. Infection by S. mutans is a leading cause of the condition.
“When I first learned that S. mutans sometimes can live in the heart, I asked myself: Why in the world are these bacteria, which normally live in the mouth, in the heart? I was intrigued. And I began investigating how they get there and survive there,” says Jacqueline Abranches, Ph.D., research assistant professor of microbiology and immunology at the University of Rochester.
Abranches discovered that a collagen-binding protein known as CNM gives S. mutans its ability to invade heart tissue. In laboratory experiments, strains with CNM were able to invade heart cells, and strains without CNM are not.
When the team knocked out the gene for CNM in strains where it’s normally present, the bacteria were unable to invade heart tissue. Without CNM, the bacteria simply couldn’t gain a foothold; their ability to adhere was about one-tenth of what it was with CNM.
The team also studied the response of wax worms to the various strains of S. mutans and found that strains without CNM were rarely lethal to the worms, while strains with the protein were lethal 90 percent of the time. Then, when Abranches’ team knocked out CNM in those strains, they were no longer lethal—those worms thrived.
The work may someday allow doctors to prevent S. mutans from invading heart tissue. Even sooner, though, since some strains of S. mutans have CNM and others do not, the research may enable doctors to gauge a patient’s vulnerability to a heart infection caused by the bacteria.
Abranches has 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.
“It may be that CNM can serve as a biomarker of the most virulent strains of S. mutans,” says Abranches. “When patients with cardiac problems go to the dentist, perhaps those patients will be screened to see if they carry the protein. If they do, the dentist might treat them more aggressively with preventive antibiotics, for example.”
Researchers from the University of Florida contributed to the study, that was funded by the American Heart Association.
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