When I started grad school in the early 70’s, one of the hot new topics was Streptococcus mutans and its relationship to oral problems (cavities, infections, etc.). This gram positive microbe converts sugars (found in almost everything we eat) to lactic acid; it also uses sucrose to produce a biofilm that surrounds it, protecting it from outside interference (in dental parlance, this is called plaque). The combination of plaque and lactic acid formation is the driving force in dental decay.
[Biofilms are agglomerations of microbes and slime (extracellular polymeric substances) that afford protection to the microbial populations. They are important (not necessarily in a positive way) in many areas. The formation of biofilms in our drinking water systems can provide protection to the microbes against our disinfection processes; when found in cooling or heating systems, they detract from the desired results. Biofilms in our riverbeds serve as food sources for aquatic invertebrates, which then serve as food for our fish. Biofilms also form on catheters, which can lead to patient infection.]
On 9 September, UK
scientists Drs. Kerrigan and Jenkinson presented data at the meeting of the Society for General Microbiology that point to these same bacteria’s involvement in cardiac diseases. Streptococci in the blood stream leads to the formation of blood clots that provide significant risk for endocarditis and blood vessel inflammation; causes of heart attacks and stroke. Mastication and tooth-brushing afford these microbes the opportunity to enter the blood stream. Once the microbes enter the blood stream, they interact with platelets to form “clumps” that block blood flow or adhere to various vessels or valves.
When we don’t follow “prescribed” oral hygiene (brush twice daily, floss daily), we increase our chances for periodontal disease. This leads to elevated populations of Streptococci in the mouth and gum disease; when the gums bleed, the microbes invade the blood stream. Kerrigan and Jenkinson found a protein (PadA) on the microbial surface that affords the stratum for blood platelet clumping, leading to blood clots.
Using antibiotics against these microbes is not desired, since the biofilms around them preclude direct antibiotic contact; instead it may lead to increased antibiotic resistant biota. As such, the ability of PadA to “seed” the clumping action is being investigated, in concert with a new circulatory system model developed by Kerrigan.