Streptococcus gordonii is a Gram-positive bacterium that represents a significant component of the micro-ecosystem within the human mouth. It belongs to the viridans group streptococci, which are common, non-harmful residents. This organism exists peacefully as a commensal microbe but possesses the genetic potential to become an opportunistic pathogen responsible for serious systemic infections. Understanding its transition from the oral cavity to the bloodstream explains its role in developing Infective Endocarditis (IE).
Its Role in the Oral Microbiome
This bacterium is a prominent member of the S. sanguinis group within the viridans streptococci, naturally residing on the tongue, dental plaque, and other surfaces of the oral cavity. As one of the earliest colonizers, S. gordonii plays a foundational part in establishing the complex bacterial communities that form dental plaque. It helps create the necessary attachment substratum, allowing other bacteria to subsequently adhere and build the mature biofilm.
In its normal state, the presence of S. gordonii helps maintain a healthy balance in the mouth, a concept known as colonization resistance. By occupying available niches and competing for nutrients, it actively prevents more harmful bacterial pathogens from establishing a foothold. The high affinity of S. gordonii for molecules in the salivary pellicle allows it to rapidly colonize clean tooth surfaces.
The Entry Point to the Bloodstream
The transition of S. gordonii from a localized oral resident to a systemic pathogen begins with a breach in the protective mucosal barrier, leading to a temporary condition called transient bacteremia. This entry into the circulation often happens during invasive dental procedures, which include tooth extractions, root canals, or any manipulation of the gingival tissue. During these procedures, the physical disruption of the tissue allows the high concentration of oral bacteria to enter the underlying blood vessels.
Bacteremia is not limited to clinical settings; routine daily activities can also facilitate bacterial entry into the bloodstream. Activities such as aggressive tooth brushing, flossing, or even chewing food can cause minor bleeding events that inoculate the circulation with oral flora. Some studies suggest that the continuous, low-grade bacteremia caused by these routine activities may pose a greater long-term risk than the short-duration, high-intensity bacteremia caused by a single dental extraction.
How It Causes Infective Endocarditis
After entering the bloodstream, S. gordonii must successfully adhere to the inner lining of the heart, known as the endocardium, to cause Infective Endocarditis. The bacterium often targets areas where the endocardium or heart valves are already damaged or diseased, as these sites provide exposed host proteins for initial attachment.
S. gordonii expresses specialized proteins on its surface, known as adhesins, that facilitate this binding. Serine-rich repeat adhesins, such as Gordonii surface protein B (GspB) and Hsa, are important for this process. GspB mediates binding by interacting with glycoprotein (GP) Ibα, a receptor found on the surface of blood platelets. Another protein, Platelet Adherence Protein A (PadA), specifically interacts with the platelet receptor GPIIb/IIIa.
The binding of S. gordonii to platelets is a significant step because it causes the platelets to activate and clump together. This activation is also supported by proteins SspA and SspB, which induce platelet aggregation. The resulting mass of bacteria, aggregated platelets, and fibrin forms a protective structure known as a vegetation on the heart valve.
This vegetation shields the bacteria from the host’s immune cells and makes the infection difficult to treat with antibiotics. Within this structure, the bacteria transition into a protected, organized community, effectively forming a mature biofilm. The continuous presence of this infected thrombus is the hallmark of Infective Endocarditis, leading to progressive damage and destruction of the heart valves.
Prevention and Management
Preventing Infective Endocarditis linked to S. gordonii centers on reducing the bacterial load in the mouth and managing the risk of bacteremia. Maintaining consistent, effective daily oral hygiene, including regular brushing and flossing, is the most effective long-term strategy. Regularly scheduled dental visits support this approach by decreasing the overall incidence of bacteremia associated with routine activities.
For most individuals undergoing dental procedures, antibiotic prophylaxis is not routinely recommended due to concerns about the development of antibiotic-resistant bacteria. Current guidelines reserve preventative antibiotics for patients who face the highest risk of adverse outcomes from IE. This includes individuals who have prosthetic heart valves, a history of a previous IE infection, or certain forms of congenital heart disease.
For these high-risk patients, a single dose of an antibiotic, such as amoxicillin, is administered one hour before any dental procedure that involves manipulating the gingival tissue or perforating the oral mucosa. This single dose is timed to ensure a sufficient concentration of the drug is present in the bloodstream during the transient period of bacteremia. The goal of this targeted prophylaxis is to eliminate any S. gordonii that enters the circulation before it has the opportunity to colonize the susceptible heart tissue.