The Streptococcus milleri group, often abbreviated as SMG, is a collection of bacteria recognized for their distinct ability to cause serious, deep-seated infections. Though historically viewed as harmless commensals, these streptococci are now acknowledged as opportunistic pathogens. Unlike Streptococcus pyogenes or Streptococcus agalactiae, the SMG is uniquely associated with the formation of localized, pus-filled pockets known as abscesses. Understanding the classification of this group and its developing antibiotic resistance profile is paramount for effective patient treatment.
Taxonomy and Nomenclature of the Group
The name Streptococcus milleri group is technically outdated but remains in common clinical use, reflecting historical confusion. The officially preferred taxonomic designation is the Streptococcus anginosus group (SAG). This group is comprised of three distinct species: S. anginosus, S. constellatus, and S. intermedius. They share a close genetic relationship and similar biochemical characteristics.
The SAG is categorized as a subgroup of the viridans streptococci, which is a broad collection of alpha-hemolytic or non-hemolytic streptococci. In the laboratory, these bacteria often form minute colonies and can sometimes emit a characteristic odor described as butterscotch or caramel, which aids in identification.
Ecological Role and Normal Habitat
The Streptococcus anginosus group is a normal and abundant part of the human body’s microflora, living in a symbiotic relationship with the host. They colonize multiple mucosal surfaces, including the oral cavity, the upper respiratory tract, the gastrointestinal tract, and the female genitourinary tract. This widespread colonization means that the source of an infection is often an individual’s own normal bacterial population.
Specific species often show a preference for certain anatomical sites; for instance, S. intermedius is frequently isolated from dental plaque, while S. anginosus is more prevalent in the gastrointestinal tract. The transition from a harmless colonizer to an invasive pathogen occurs when the mucosal barrier is compromised, such as through trauma, surgery, or underlying disease. The bacteria can then enter the bloodstream or deep tissues, where they cause infection.
Pyogenic Infections and Clinical Significance
The hallmark of infection caused by the Streptococcus anginosus group is its propensity for forming pus-filled abscesses, which distinguishes it from most other streptococcal infections. These deep-seated, suppurative infections can occur in almost any organ, creating significant diagnostic and therapeutic challenges. Common sites for abscess formation include the liver, brain, and spleen, collectively known as visceral abscesses.
In the thoracic cavity, the group is a frequent cause of empyema, which is an accumulation of pus in the pleural space, and lung abscesses. S. intermedius is particularly noted for its association with central nervous system abscesses and complicated dental infections. Infections caused by SAG are often polymicrobial, involving other bacteria like anaerobes, which synergistically enhance the abscess formation process. The group is also recognized as an agent of bacteremia and infective endocarditis, particularly in patients with pre-existing heart valve damage or those who are immunocompromised.
Mechanisms of Antibiotic Resistance
Treatment for serious SAG infections typically involves antimicrobial therapy, such as penicillin or a cephalosporin, and surgical drainage of the abscess. The bacteria are generally susceptible to beta-lactam antibiotics, which target bacterial cell wall synthesis. However, treatment efficacy is often limited by the physical presence of the abscess, which antibiotics struggle to penetrate, making drainage a critical component of care.
Reduced susceptibility to beta-lactams is emerging, primarily driven by alterations in the penicillin-binding proteins (PBPs). PBPs are bacterial enzymes that beta-lactam antibiotics bind to and inactivate. Rare strains of SAG exhibit amino acid substitutions in the PBP motifs, which reduces the antibiotic’s affinity for the target enzyme. This mechanism, similar to resistance in other streptococci, can lead to decreased effectiveness, particularly for certain cephalosporins.
Resistance to macrolides (e.g., erythromycin) and tetracyclines is more common and mediated by distinct genetic mechanisms. Macrolide resistance is often conferred by erm genes, which cause methylation of the ribosomal target site, blocking the antibiotic’s action. Alternatively, mef genes can confer resistance by encoding an efflux pump that actively expels the drug from the bacterial cell.
Tetracycline resistance is frequently mediated by the tet(M) gene, which protects the bacterial ribosome from the antibiotic’s binding. For serious infections like endocarditis, combination therapy is often required to achieve a faster and more complete killing effect. This typically involves combining a beta-lactam (like penicillin) with an aminoglycoside (like gentamicin) to achieve synergistic bactericidal activity.