Streptococcus salivarius is a common bacterium. Classified as a gram-positive, facultative anaerobic organism, it is one of the earliest microbial colonizers of humans. The bacterium primarily inhabits the oral cavity and upper respiratory tract. This organism belongs to the Streptococcus genus and is a part of the Viridans group streptococci, which are regarded as commensals.
Commensal Ecology and Protective Function
Streptococcus salivarius rapidly colonizes the oral and nasopharyngeal epithelia, often within the first few hours or days after birth, establishing itself as a permanent resident. This early and stable presence allows it to play a significant role in maintaining the ecological balance of the oral microbiome. Its primary mechanism for maintaining this balance is through competitive exclusion, where it effectively prevents the colonization and growth of more harmful bacterial species.
The organism achieves this protective function largely by producing potent antimicrobial peptides known as bacteriocins. These peptides provide a direct chemical defense against other microbes. Specific examples include salivaricins A2, B, and 9, which are active against a broad range of competing bacteria, including common respiratory pathogens like Streptococcus pyogenes, the bacterium responsible for strep throat.
S. salivarius helps to stabilize the microbial community and reduce the frequency of colonization by pathogenic organisms. The competitive advantage conferred by bacteriocin production is a central aspect of its role in promoting oral health.
Mechanisms of Pathogenesis
While S. salivarius is predominantly a harmless commensal, it is classified as an opportunistic pathogen capable of causing severe infection under specific conditions. Pathogenesis typically occurs when the organism gains access to a normally sterile site, such as the bloodstream. This translocation is usually triggered by a breach in the mucosal barrier, which acts as the body’s natural containment system.
A common mechanism for this breach involves traumatic or invasive procedures, such as dental surgery, tooth extraction, or routine endoscopy. Once in the circulation, the bacterium can seed various anatomical sites, leading to conditions like bacteremia, sepsis, and, rarely, meningitis. The risk of invasive infection is significantly elevated in individuals with underlying medical vulnerabilities, particularly those who are severely immunocompromised, such as patients with neutropenia.
The most serious manifestation of its pathogenic potential is infective endocarditis (IE), an infection of the heart valves. Although S. salivarius belongs to the Viridans group, which accounts for a substantial percentage of IE cases, S. salivarius itself is responsible for only about two percent of those infections. In endocarditis, the bacterium adheres to the damaged heart valve tissue, forming complex structures called biofilms. Biofilm formation is a key virulence factor, as these structures are highly resistant to both the host immune response and antibiotic treatments, making the resulting infection particularly difficult to clear.
Interaction with Host Immunity
S. salivarius actively engages with and modulates the host immune system. Studies show that the organism downregulates the innate immune responses of human epithelial cells. This immunomodulatory activity helps to maintain a state of non-inflammatory coexistence between the host and the resident microbial community.
The underlying molecular mechanism involves the inhibition of the nuclear factor-kappa B (NF-κB) signaling pathway. NF-κB is a protein complex that controls the transcription of DNA, cytokine production, and cell survival, acting as a major regulator of the inflammatory response. By suppressing the activation of this pathway, S. salivarius reduces the host’s ability to produce pro-inflammatory signaling molecules.
The suppression decreases the secretion of inflammatory cytokines, such as Interleukin-8 (IL-8) and Groα, even when the cells are challenged with known pathogens. Research suggests the organism may also induce changes in the systemic immune response, including the modulation of cytokines like Interleukin-12 (IL-12).
Antibiotic Susceptibility and Resistance
For invasive infections, the organism is typically susceptible to standard antibiotics used for streptococci, such as ceftriaxone, amoxicillin, and vancomycin. However, the susceptibility profile of S. salivarius is highly variable and can differ significantly from other members of the Viridans group.
A concerning trend is the high prevalence of resistance to certain classes of antibiotics, particularly macrolides like erythromycin and tetracyclines. Studies have reported that macrolide resistance can be found in more than 75% of commensal isolates and over 50% of clinical isolates, limiting the effectiveness of these common drugs. This resistance is mediated by specific genes, such as erm(B) and mef(A/E), which encode for different mechanisms that modify the drug target or pump the drug out of the cell.
Non-susceptibility to penicillin is also a significant issue. The presence of resistance genes in commensal strains highlights the role of S. salivarius as a potential reservoir for lateral gene transfer, where it can share these resistance mechanisms with other bacterial species in the oral and gastrointestinal tracts. Therefore, monitoring its antibiotic susceptibility is important for both clinical treatment and public health surveillance.